Bliss Lømo 2024 Per Andersen 12 January 1930 17 February 2020

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PER ANDERSEN
12 January 1930 — 17 February 2020
Biogr. Mems Fell. R. Soc.

Downloaded from https://royalsocietypublishing.org/ on 03 March 2024
PER ANDERSEN
12 January 1930 — 17 February 2020
Elected ForMemRS 1987
By Tim Bliss FRS1, * and Terje Lømo2,†

1
Group Leader Emeritus, The Francis Crick Institute, 1 Midland Road, London
NW1 1AT, UK
2
Institute for Basic Medical Sciences, University of Oslo, Sognsvannveien, 0372
Oslo, Norway
Per Andersen was one of the leading neuroscientists of the second half of the twentieth
century. He spent his entire career at the University of Oslo, apart from an exceptionally
productive postdoctoral period with Sir John Eccles FRS at the Australian National University
in Canberra between 1961 and 1963. As a PhD student he laid the foundation of field
potential analysis, which allowed synaptic function in laminated cortical structures such as
the hippocampus to be followed for long periods in intact animals, an essential technical
prerequisite for the study of the synaptic basis of memory. In Canberra he identified the
neurons responsible for feed-back inhibition in the hippocampus and feed-forward inhibition
in the cerebellum, the first inhibitory neurons to be functionally identified in the mammalian
brain. Per’s Canberra achievements catapulted him to superstar status, and enabled him
on his return to Oslo in 1963 to establish a laboratory that played a major role over the
following decades in characterizing the functional properties of hippocampal synapses. From
his laboratory emerged a string of significant advances, including the discovery of long-term
potentiation, a form of synaptic plasticity widely believed to support learning and memory,
and the introduction of the transverse hippocampal slice, which rapidly became the dominant
preparation for investigating the properties of hippocampal neurons. Young researchers, many
from the USA and Canada, flocked to his laboratory for postdoctoral training, adding to the
steady stream of Norwegian doctoral students, two of whom went on to win the Nobel Prize.
*Email: tim.bliss@crick.ac.uk
† Email: terje.lomo@medisin.uio.no
2024 The Author(s)

https://doi.org/10.1098/rsbm.2023.0041 3 Published by the Royal Society
4 Biographical Memoirs
Per was also committed to the importance of communicating scientific advances to the general
public, and contributed prolifically over the years to the Norwegian media, commentating on
advances in neuroscience and their relevance to neurological disorders.
Early life and education

Per Oskar Andersen was born in Oslo on 12 January 1930. His father David was a school
teacher who was imprisoned during the occupation of Norway in World War II for his
opposition to the Nazification of the school curriculum. He died when Per was 17. His
mother’s family included the nineteenth-century poet and politician Elias Blix, who was
responsible for the first translation of the Bible into Norwegian. As a schoolboy Per revelled
in the many outdoor pursuits available in the Oslo region—sailing, swimming, hiking and
fishing in the summer, and, in the winter, cross-country skiing in the extensive local forests.
He continued to enjoy these activities throughout his life. He was also an enthusiastic amateur
carpenter, constantly remodelling his holiday ‘hytte’ in the mountains northwest of Oslo. Per
excelled at school, particularly in physics and mathematics, and achieved the high grades
needed to enter medical school at the University of Oslo in 1948. He graduated in 1954,
and for his compulsory military service he was commissioned as a second lieutenant in the
Norwegian Navy, where he immersed himself in the physiological aspects of deep-sea diving.
During this period he wrote manuals for Navy divers, and two popular books on diving as a
hobby.
Per’s career as a neurophysiologist began in 1951, when he was awarded a student
assistantship to work with Birger Kaada, who had recently returned from postdoctoral studies
in the USA and Canada to set up a neurophysiological laboratory in the Anatomical Institute
at the University of Oslo. Also on the staff of the Anatomical Institute were Jan B. Jansen,
with whom Per took an extra job as a research assistant, and Alf Brodal. ‘These three’, Per
was to recall in the memoir he wrote for the series History of Neuroscience in Autobiography,
‘set me on the path to neuroscience’ (21)∗ . One of the younger researchers at the Anatomical
Institute was the neuroanatomist Theodor Blackstad. A life-changing moment occurred when
Blackstad showed Per a histological section of the rabbit hippocampus using a method that
stained degenerating cortical fibres. Per writes in his memoir:
After an entorhinal lesion, the degenerated perforant path appeared as a black band in the
molecular layer of the dentate fascia. So intense was the degeneration that it could easily be
seen by the naked eye! In a moment, this slide of Blackstad’s set my entire scientific course.
Immediately, I saw that this would make a fabulous preparation for a neurophysiologist interested
in cortical physiology. By stimulating a proper selection of input fibres, I could engage a set of
synapses located to a restricted part of the dendritic tree of the target neurons.
From 1953 to 1955 Per published several papers in collaboration with Jan K. S. Jansen and
Birger Kaada, mainly on the behavioural effects of stimulating limbic structures in cats. He
then moved on to do independent work for his PhD, focusing on the responses that electrical
stimulation of hippocampal neurons on one side of the brain evoked in the corresponding
regions on the opposite side.
∗ Numbers in this form refer to the bibliography at the end of the text.
Per Andersen 5
Figure 1. Per and Kari Andersen and their children (Espen, Line, Hege and Kristin), outside their house
in Oslo, 1975. (Photograph from the family collection.)
Apart from the two momentous postdoctoral years in Canberra, and a sabbatical half year
at Oxford in 1970, Per was to remain at the University of Oslo for the rest of his career. In
1955 he married Kari Sletten, who survives him. The couple had four children, Hege (born
27 July 1956), Kristin (born 8 October 1958), Espen (born 8 March 1961) and Line (born
22 July 1967) (figure 1). Per took an active interest in the public understanding of science
in Norway, and in encouraging the development of links between national neuroscience
organizations within Europe. In 1999 he was elected President of the European Neuroscience
Association, the forerunner of the Federation of European Neuroscience Societies. Per
played an enthusiastic role over several decades in explaining the brain to lay audiences.
He participated in popular television programmes and talk shows, gave numerous invited
lectures to meetings of non-scientific organizations and was well known as Norway’s pre-
eminent brain scientist. His enthusiasm for science, broad knowledge and ability to explain
complicated issues made him popular also at scientific meetings, where the organizers could
rely on Per to raise lively points for discussion
Thesis work on field potentials in the hippocampus

Per’s thesis resulted in four single-author papers published in Acta Physiologica Scandinavica
and the award in 1960 of the degree of Doctor Medicinae, the Norwegian equivalent of the
PhD for medically qualified students. In the most significant of the four papers Per analysed
the responses that electrical stimulation of commissural fibres evoked along apical and basal
dendrites of contralateral CA1 and CA3 pyramidal cells (1). A similar analysis had already
been published by Cragg & Hamlyn (1957), but Per had the advantage of knowing from
Blackstad’s anatomical studies where the commissural fibres terminated along the apical and
basal dendrites. He found that activity evoked by stimulation of commissural fibres from
the opposite side was maximally negative precisely at these locations. He argued that the
early extracellular negative wave was generated by the synchronous activation of excitatory
synapses that followed the stimulation of afferent commissural axons. The amplitude of this
negative wave, which Per called the population EPSP (excitatory postsynaptic potential),
depended on the number of activated fibres and on the mean synaptic strength. Crucially,
for a given stimulus, activating a fixed population of commissural axons, the amplitude of
the population EPSP provided a measure of the average synaptic strength of the population
of activated synapses. At the time (and for many years after) the only alternative method of
measuring synaptically generated currents was to insert a microelectrode into a single neuron
to measure the depolarization, or reduction in membrane potential, generated by activation
of an excitatory synapse, or hyperpolarization if the synapse was inhibitory. Intracellular
recording is a much more demanding manoeuvre, which usually only allows recordings to be
successfully maintained for a few tens of minutes. The introduction of field potential recording
allowed the possibility of monitoring synaptic responses for extended periods of time—hours
in anaesthetized animals, and indefinitely in awake animals with implanted electrodes.
Per was also the first to explicitly characterize the graded extracellular population spike
which with stronger stimulation was superimposed on the population EPSP as representing
‘the synchronous discharge of the CA3 neurons’. Moreover, whereas Cragg & Hamlyn
attributed the responses evoked in CA1 pyramidal cells to indirect activation via the dentate
area, Per showed that it was direct, in keeping with Blackstad’s anatomical results. Finally,
active conduction along dendrites implied that parts of the dendritic membrane were excitable,
which led Per to write with a tentativeness that was not to characterize his later career: ‘it is
not unlikely that the theory of Purpura and Grundfest concerning the electrical inexcitability
of the entire dendritic membrane may have to be somewhat modified’.
The results published in Per’s thesis were new and clear and their interpretations carefully
argued. They have stood the test of time and represented a major advance on what was known
at the time. Thanks to Per’s work, a generation of hippocampal neuroscientists has been able to
use field potential analysis as a technically accessible tool for investigating synaptic function
and plasticity in the hippocampus. Our own and later experiments on long-term potentiation
(LTP) benefited in particular from the clear distinction that could be made between the synaptic
potential, or population EPSP, and the synchronous cell discharge of target cells signalled by
the population spike. These papers were not the first attempts to analyse population responses
in the hippocampus, but they unquestionably brought clarity to a confused literature. We note
also how close Per came in these experiments to the discovery of LTP. Following tetanic (high-
frequency) stimulation of commissural afferents to pyramidal cells in area CA1, he observed
post-tetanic potentiation, but for reasons that are not clear this never lasted for more than a
few minutes. An engaging photograph survives of Per in his lab at this period (figure 2).
Canberra
In November 1961 Per moved with his family to Canberra to work with Sir John Eccles
FRS at the Australian National University in Canberra. Per has described his two years with
Per Andersen 7
Figure 2. Per Andersen in his lab at the Institute of Neurophysiology in Oslo, ca 1960. (Photograph
from the Institute collection.)
Eccles in Canberra as ‘fantastic’ and ‘incredible’ (21), recalling an atmosphere of almost

constant excitement at the stream of new results, intense learning, friendship, hard work and
total commitment to science. The period was also extraordinarily productive, resulting in 23
publications, eight of them in Nature. Per and Eccles worked closely together in the lab. When
not travelling, Eccles participated in experiments, often doing parts of the dissections himself,
and would frequently sit in front of the oscilloscope controlling the Grass camera.
Presynaptic inhibition
When Per arrived in Canberra, the phenomenon of presynaptic inhibition had over the
preceding years attracted much interest in many laboratories, including Eccles’s. Inhibitory
synapses are conventionally made by axons of inhibitory interneurons terminating on
postsynaptic target cells. By contrast, in presynaptic inhibition the inhibitory axons project
to the presynaptic terminals of excitatory axons to reduce the efficacy of transmitter release.
On the basis of indirect evidence, Eccles had predicted the existence of presynaptic inhibition
at the synapses made by somato-sensory axon terminals on relay cells in the spinal dorsal horn
(Eccles 1961). He then went on to prove it by showing that the depression of mono-synaptic
EPSPs in the relay cells and the appearance of so-called dorsal root reflexes were caused by
depolarization of the presynaptic terminals and the accompanying reduction in the release of
excitatory neurotransmitter from these terminals.
Per then suggested they studied presynaptic inhibition in the cuneate nucleus, where
primary somato-sensory afferents in the dorsal columns make synapses with relay cells that
send their axons to the ventro-basal nucleus of the thalamus on the opposite side. He knew
the structure and saw that it was more suited for detailed studies of presynaptic inhibition than
the dorsal horn. This initiative of Per led to five original papers, one in Nature in 1962 (2) and
four more in 1964 in the Journal of Neurophysiology. These papers are impressive for their
analytical approach and clarity of results.
Thalamo-cortical interactions and the genesis of barbiturate

spindle activity
After they had completed their studies of synaptic transmission in the dorsal column nuclei,
Eccles, according to Per in his autobiographical memoir (21), was ‘eager to proceed up to the
next station of the somatosensory system, the ventrobasal nucleus of the thalamus’.
Recording from thalamic relay cells, they first noted the unexpectedly large amplitude
and long duration of intracellularly recorded inhibitory postsynaptic potentials (IPSPs). They
were surprised by the large depolarizing responses that followed the IPSPs after orthodromic
stimulation, antidromic stimulation, or artificial hyperpolarization by intracellularly injected
currents. Equally surprising were the bursts of action potentials that arose on the crest of
such rebound depolarizations and the observation that the relay cells responded to single
orthodromic or antidromic stimuli by repetitive burst discharges at alpha frequencies (ca
10 Hz), corresponding to the duration (ca 100 ms) of the intracellularly recorded IPSPs.
These repetitive bursts resembled thalamic spindle activity (repetitive brief oscillations
in extracellular voltage that can be recorded in the thalamus during sleep or barbiturate
anaesthesia). They concluded that this pattern of activity, characterized as a ‘post-inhibitory
rebound’, was controlled by a recurrent inhibitory pathway because the IPSPs started
immediately after the action potentials evoked by single orthodromic or antidromic
stimuli.
Per and Eccles published their conclusions in a brief paper in Nature (3) with a single
figure showing the main results, and a drawing of a set of relay cells, whose axons branched
into many collaterals that contacted local inhibitory interneurons, which, in turn, sent their
axons to inhibit a much larger number of relay cells. Consequently, an initial spontaneous
burst discharge in one or a few relay cells would generate a synchronous post-IPSP rebound
in a much larger number of relay cells, which, in turn, would generate another synchronous
burst, and so on until the end of the spindle. Later, Per and Tom Sears, a PhD student from
England who established a life-long friendship with Per and was later to become Professor of
Neurophysiology at the Institute of Neurology in London, extended this work by showing that
spindle activity can arise from several major nuclei of the thalamus and went on to propose
a model of inhibitory phasing that explained how spindle activity could arise spontaneously
from recurrent inhibitory pathways and post-inhibitory rebound and then fade away, a scheme
that is still central to current understanding of thalamo-cortical spindle activity (6).
As Eccles was always quick to acknowledge, it was Per who introduced him to
experimental electrophysiological work on the brain in anaesthetized cats and rabbits. ‘Per
Per Andersen 9
helped navigate me through the foramen magnum’ he told the American neuroscientist Roger
Nicoll. So, with Per’s anatomical knowledge and experience of exposing the hippocampus
and other cortical structures to allow introduction of electrodes under visual control, they
had a flying start. But Eccles was mentally prepared, given his interest in higher brain
functions, as discussed in his publications from the early 1950s (Eccles 1951, 1953), where
he also dealt with sleep and sleep spindle activity from a theoretical viewpoint. While
Eccles was the driving force, it is also clear that Per’s comprehensive knowledge of cortical
anatomy was critical to the Canberra lab’s extraordinarily successful expansion into cortical
neurophysiology. In his autobiographical memoir (21) Per gives a lively account of the regular
twice-weekly experiments. When not travelling, Eccles was a regular participant, dividing
his time between writing in his office and active participation in the experiment—everyone
working long into the night, with a break at 11 p.m. for tea and discussions, as Tom Sears
remembers.
Identification of inhibitory synapses

Per has described the identification of inhibitory interneurons and their synapses in the
hippocampus as the most dramatic of his Canberra findings (21). After nearly a year’s work on
presynaptic inhibition and the somatosensory system, Eccles, to Per’s delight, proposed that
they should start investigating hippocampal pathways. Progress was initially slow and difficult
because intracellular recordings were hard to obtain. After exposure, the hippocampus moved
in time with respiratory movements and blood pulsations and the structure was much more
difficult to stabilize mechanically than the spinal cord. In addition, the cells were smaller
than motoneurons and required finer and higher-impedance glass electrodes for successful
penetrations. But they eventually succeeded, and found, first, that all excitatory inputs to CA1
pyramidal cells also produced an inhibitory postsynaptic potential (IPSP) and, second, that
the IPSP evoked by antidromic stimulation of the pyramidal cell started 1–2 ms after the
antidromically evoked action potential, which strongly suggested the existence of recurrent
inhibition via inhibitory interneurons with widely dispersed axonal branches. They also
showed that chloride injection into the pyramidal cell bodies reversed the IPSP, indicating
that the IPSP was caused by a chloride current flowing into the cells at the site of inhibitory
synapses on the cell bodies. As Per relates (21): ‘we were discussing our data in his [Eccles’s]
office at the end of an experiment, the famous 11pm tea break’. Eccles was explaining
how inward chloride flow would generate an outward positive current and hyperpolarize
the membrane, when Per realized the implications of the amplitude distribution of the field
potentials, which was maximally positive in the pyramidal layer. Per continues:
I nearly yelled, because I both saw the light and beamed with delight: ‘Sir, given the conclusion
that the inhibitory current flows across the soma membrane, I can tell you the cell type and
synapses that do it!’ He stared at me, but I went on: ‘Cajal has drawn both the cell, its synapses and
how it connects to the pyramidal cells.’ ‘Where?’ he said, surprised about my boyish excitement,
but clearly starting to think I had a point. He had never heard about such interneurons before.
I nearly shouted. ‘Let me show you!’ We ran down the corridor. A super thing about the JCSMR
was that the well-equipped library was open round the clock. We rushed in, and since I had so
often searched Ramon y Cajal’s two-volume (1911) masterpiece, The Histology of the Nervous
System of Man and Vertebrates [(Ramon y Cajal, 1911)], I found Figs. 473 and 474 straight away,
showing the beautiful basket cells and their elaborate relation to the many pyramidal cells they
innervate. Prof was elated, started to laugh, and exclaimed: ‘Here it is, here it is!’
This striking and fundamental work, a collaboration between Eccles, Per and Yngve Løyning,
also from Norway, was published in 1963 in Nature (4), and in two papers in the Journal of
Neurophysiology in 1964.
Feed-forward inhibition in the cerebellum

Eccles was elated at their discovery of the inhibitory basket cells in the hippocampus, and the
next day he came into Per’s ‘little 60-square foot office cubicle’ to discuss it further. As Per
relates in his memoir:
After some time, I ventured: ‘Prof, maybe we should check whether the basket cell arrangement is
a general organization or only something peculiar to the hippocampus.’ He did not understand at
first. I went on: ‘There is an additional structure with basket cells with a very similar termination
on their target neurons—the cerebellum.’ His answer was very disappointing: ‘Oh no, when
Raggen [Ragnar Granit ForMemRS] and Charles [Phillips] could not make head and tail of it,
we will not manage either.’ But a long fortnight later, he came into my cubicle and mused: ‘I
wonder whether we should test the basket cell idea in the cerebellum.’ He continued ‘It is a good
idea, you see’, leaving Per with the distinct impression that by now he had adopted the idea as his
own.
Per knew the cerebellum well. In Oslo, just before leaving for Canberra, he and Jan K. S.
Jansen had stimulated the surface of a cerebellar folium and studied the evoked field
potential and its reversal with depth. They also applied strychnine in doses that completely
blocked spinal glycine-mediated inhibition without observing any effect on inhibition in the
cerebellum (or the hippocampus), which was explained later when postsynaptic inhibition
in the cerebellum and the hippocampus was shown, by Masao Ito (ForMemRS 1992) and
David Curtis (FRS 1974) respectively, to be mediated not by glycine but by gamma-
aminobutyric acid (GABA). Per and Jansen submitted a paper on this work to the Journal
of Neurophysiology, and although it was rejected, it added an important dimension to the
expertise that Per brought to Canberra.
With this background and the identification of inhibitory basket cells in the hippocampus
behind them, the initial studies on the cerebellum must have appeared relatively
straightforward. Stimulating the parallel fibres along a narrow ‘beam’, they found the evoked
field potential to be maximally positive in the Purkinje cell body layer, which corresponded
to intracellularly recorded disynaptic IPSPs and occurred together with high-frequency burst
discharges during the rise time of the IPSPs, bursts that could be attributed to inhibitory
basket cells with their axonal terminals on the Purkinje cell bodies. Moreover, the positive
field potential evoked by the narrow beam of excited parallel fibres extended far beyond the
beam on either side, corresponding to the basket cell axons running transversely to the beam.
Interestingly, the mode of inhibition in the cerebellum differed from that in the hippocampus in
one important respect. Whereas basket cells in the hippocampus provide feed-back inhibition
to pyramidal cells, the inhibition provided by cerebellar basket cells is feed-forward onto
Purkinje cells, basket cells receiving excitation from the massive parallel fibre innervation
that also excites Purkinje cells (5).
Per Andersen 11
(a)
(b)
Figure 3. (a) Exposed view of the dorsal (septal) surface of the rabbit hippocampus. (b) The trisynaptic
circuit. Drawings by Per Andersen (10) which have been reproduced many times in the hippocampal
literature. Used with permission from Springer Nature. ento = entorhinal cortex, pp = perforant path
axons, mf = mossy fibres (axons of granule cells, not labelled), CA3 = pyramidal neurons of area CA3,
Sch = Schaffer collateral axons of CA3 neurons projecting to CA1 pyramidal neurons, fim = fimbria,
alv = alveus.
The trisynaptic circuit in the hippocampus

The trisynaptic circuit is a central feature of hippocampal circuitry (figure 3b). It encompasses
the perforant path input from entorhinal cortex (ento) to dentate granule cells (synapse 1), the
mossy fibre (mf) input from granule cells to CA3 pyramidal cells (synapse 2), and the Schaffer
collateral input from CA3 to CA1 pyramidal cells (synapse 3). It is central to phenomena such
as pattern separation in the DG and pattern completion in CA3, and is the structure where
engram cells, neurons that are part of a neural network encapsulating a particular memory,
were first directly demonstrated (Liu et al. 2012). The essential circuitry is contained within
each narrow transverse section of the hippocampus, which explains why in vitro studies using
transverse hippocampal slices have been so immensely popular and productive.
In his autobiographical memoir (21), Per devotes a separate section to the trisynaptic
circuit, the last of the projects he carried out in Canberra. At that time, Eccles was travelling,
and before leaving he had asked Per if he had an interesting problem that would occupy Per,
Birgitta Holmqvist from Sweden and Paul Voorhoeve from The Netherlands while he was
away. The answer to that, as Per tells it, ‘was a big yes’. He had long suspected that Ramon
y Cajal (ForMemRS 1909) was wrong in drawing the CA1 pyramidal axons as ‘traveling
towards the CA3 neurons and into the fimbria’ rather than towards the subiculum. With Eccles
away, Per was in command and could choose his favourite preparation, rabbits anaesthetized
with urethane and chloralose, to test his thesis.
This work resulted in two papers published in Acta Physiologica Scandinavica in 1966. In
the first paper (8), Per and his two colleagues stimulated the perforant path and showed that
dentate granule cells responded with monosynaptic EPSPs, and corresponding field EPSPs of
maximum amplitude precisely in the field of termination of the perforant path fibres. Thus, the
first synapse in the trisynaptic circuit was shown to be excitatory. In addition, they recorded
large, long-lasting (‘some 100 ms’) disynaptic IPSPs that could be attributed to inhibition
mediated by local basket cells, as drawn by Cajal and comparable to Per’s earlier findings
of feed-back inhibition in area CA1 and in the ventro-thalamic nucleus, and feed-forward
inhibition in the cerebellar cortex.
In the second paper (9), they likewise stimulated the perforant path and showed that
CA1 pyramidal cells responded with large field EPSPs precisely in the region along the
apical dendrite where the Schaffer collaterals terminate and at a time much later than
the simultaneously recorded monosynaptic responses in the dentate. These results provided
convincing evidence that the trisynaptic circuit consisted of three excitatory synapses in series.
But the study did not reveal whether CA1 pyramidal axons run back towards area CA3 and
into the fimbria, as depicted by Cajal, or in the opposite direction, towards the subiculum,
or both. Ten years later, Per, with Brian Bland and John Dudar, returned to the issue, and
concluded that CA1 neurons, at least in the septal two-thirds of the hippocampus, all project
in a caudal direction and terminate in the subiculum (12).
Back to Oslo
Per returned from Canberra at the end of 1963. He moved into laboratory space made available
in Domus Bibliotheca, one of three nineteenth-century buildings set around the courtyard of
the old University of Oslo on the city’s main street, Karl Johans Gate. A large room in that
building had just been vacated and converted into a lab with a mezzanine floor supporting
three different desks at which Per, his first secretary, Solveig Grinde, and, about a half year
later, one of us (Terje Lømo, Per’s first PhD student) had their desks. The screened lab for
electrophysiological recordings was located underneath.
To begin with, Per continued the work he had begun in Canberra on spindle activity in cats
anaesthetized with barbiturates, and his studies on the hippocampus in rabbits anaesthetized
with urethane and chloralose.
The work on spindle activity resulted in several papers, two in Nature, three in Journal of
Physiology, one in Acta Physiologica Scandinavica, and a book, Physiological basis of the
alpha rhythm (10), written in collaboration with Svend Andersson, from the University of
Gothenburg. Two of these papers, one in Nature, the other in the Journal of Physiology, were
studies of rhythmic activity in a simulated neuronal network. But as new research appeared
in the 1980s and 1990s, the picture became more complicated. The inhibitory interneurons
mainly responsible for the IPSPs and subsequent hyper-excitability in thalamic relay cells
turned out not to be local interneurons in the vicinity of the relay cells, but neurons in a separate
reticular nucleus with longer GABAergic axons targeting the relay cells. Interestingly, in one
Per Andersen 13
of their papers, Per, Eccles and Tom Sears anticipated this (7). Finding fewer than expected
postsynaptic inhibitory cells in the ventro-basal complex (VBC), they write: ‘maybe they are
concentrated in more peripheral zones of the VBC or even just beyond its confines, and so
have eluded our micro-electrode explorations’, which seems precisely to have been the case.
Long-term potentiation and the transverse hippocampal slice

Per had begun work in his new lab in Oslo in early 1964 and in August of that year he invited
one of us (Terje Lømo) to join him as his first graduate student. After working closely with
Per on his projects until the end of 1965, both felt that Lømo should start his own PhD project,
which at that time in Norway was supposed to be essentially independent work. This project,
it was agreed, should focus on the mechanisms underlying the striking potentiation of dentate
granule cell firing that occurred during high-frequency stimulation of the perforant path input
to the granule cells and that Per had already observed and published (8). In the early months
of 1966, Lømo confirmed Per’s finding but in addition saw that the potentiation could last
for hours after the last train of high-frequency stimulation (Lømo 1966), in contrast to the
experiments by Per, in which the potentiation outlasted the high-frequency potentiation by
only a few minutes. Then, the focus of the experiments changed, to cover the more basic
questions of the organization of the perforant path input and the mossy fibre output of the
dentate gyrus and the longitudinal distribution of the facilitation and inhibition evoked by
perforant path stimulation. As a result, neither frequency potentiation nor LTP was included
in the PhD thesis that Lømo defended in 1969.
In the autumn of 1968, one of us Tim Bliss (FRS 1994) arrived in Oslo on a year’s
sabbatical from the National Institute for Medical Research in Mill Hill, London, to learn
about field potential analysis, with a view to applying the technique to a study of synaptic
plasticity at monosynaptic cortical pathways. Bliss was immediately swept up in the creative
energy of the Oslo laboratory, and not long after his arrival he summarized his impressions of
Per in a letter to a friend in England:
It isn’t possible to be more up and coming than Per. He’s in his late 30’s, well established on the
international circuit, travels abroad mainly to the States for conferences 2–3 times a year, is on the
editorial board of the right journal, knows which of the important problems can be productively
tackled, is well connected and well read. Hard working but not ridiculously so, confident, a direct
and powerful mind . . . .
Per had told Bliss before he came to Oslo that ‘Terje has found something that will interest
you’. Now, on his arrival, Bliss discovered to his amazement that Lømo had already observed
long-lasting activity-dependent changes at perforant path–granule cell synapses, and had
published an abstract in the proceedings of a meeting of the Scandinavian Physiological
Society (Lømo 1966), but had not followed it up. Bliss persuaded him to devote a day (and
much of a night) each week to a systematic study of synaptic plasticity at the perforant path–
granule cell synapse, and during that year we gathered the data for the paper that was later
published in the Journal of Physiology (Bliss & Lømo 1973). LTP continues to be intensively
studied as the probable synaptic basis of learning and memory.
The next major advance, the development of the transverse hippocampal slice, was due
to Knut Skrede, a medical student in Per’s lab. In 1968–9 he had worked with Per and Bliss
on field potential analysis of hippocampal function. In the summer of 1970, Skrede spent
some weeks in Bliss’s lab at the National Institute for Medical Research in Mill Hill, London.
There, he observed the experiments on hippocampal slices that Bliss was doing with Chris
Richards. Richards had worked in Henry McIlwain’s laboratory at the Institute of Psychiatry
in London, where McIlwain had pioneered the technique of maintaining cortical tissue alive
in vitro. Bliss and Richards set about seeing whether LTP could be obtained in slices of the
dentate gyrus. To get the best access to granule cells they cut their slices parallel to the long
axis of the hippocampus, so that the slice contained the entire extent of the lower blade of the
dentate gyrus. With this preparation they demonstrated many of the properties displayed by
the dentate gyrus in vivo. However, they were not able to obtain LTP. (It later transpired that
LTP in vitro in the dentate gyrus, though not in other hippocampal subfields, requires the slice
to be treated with a GABA antagonist to block inhibition.)
Back in Oslo, Skrede built his own slice chamber, consisting of a metal cooking pot
containing the perfusion fluid, an aquarium heater bought from a local hardware shop, a silk
mesh floating on the surface to support hippocampal slices, with the crucial difference that
these were now cut transversely so that the whole trisynaptic circuit was made available. A
humid gas mixture of O2 + CO2 was streamed over the slices. Using this set-up, Skrede and a
fellow student, Rolf Westgaard, then carried out the experiments and wrote up the paper that
appeared as Skrede & Westgaard (1971).
Per’s custom of giving his students and postdoctoral visitors relatively free rein to pursue
their own ideas and to publish papers without his name on them deserves comment. We
ourselves were beneficiaries of this generosity. Three papers stand out in this respect, namely
Skrede & Westgaard (1971), Bliss & Lømo (1973), and Schwartzkroin & Wester (1975).
The transverse slice was developed by Skrede and Westgaard in 1970. As Per recalled in
his memoir (22): ‘I abstained from the authorship because these two colleagues had worked
so hard, in part in my absence, while I spent half a year on sabbatical leave to work with
Charles Garrett Phillips (1916 - 1994) FRS in Oxford.’ It is also likely that Skrede saw this
work as his own and that he and Westgaard, who had done the experiments and written up the
work, assumed authorship according to common practice at the time. Later, after Skrede had
left the lab, Per made improvements to the design of the bath and had the Institute’s workshop
produce the first ‘Oslo chamber’ for use by all members of his group, many of whom would
take with them a copy or have similar ones produced when they returned to their own labs.
Both Per and Lømo recognized the importance of the early results on LTP (Lømo 1966) and
their potential implications for the physiological basis of memory. And yet neither followed
up those findings at the time. Lømo turned to other experiments (see above) and Per evidently
also preferred to continue with his other projects. In any case, it now seems that neither
realized how those early findings stood out from their other results and, therefore, in 1966,
failed to turn their attention to one of the big questions in neuroscience, namely how we learn
and remember. With regard to the experiments that Bliss and Lømo did together in 1968–
9, Per left those entirely to us. Nor did he participate in writing the paper. It was not the
tradition at that time in Norway for laboratory heads to be co-authors of work that they did
not directly participate in, and papers resulting from PhD theses were usually single-author
publications, as was the case with both Per’s and Lømo’s theses. Hence, the question of
Per’s co-authorship never came up. A similar situation arose in 1973 to 1974 when Phillip
Schwartzkroin spent 10 months in Per’s lab and with Knut Wester first demonstrated LTP in
slices from the hippocampus (Schwartzkroin & Wester 1975). Again, as Philip Schwartzkroin
Per Andersen 15
recalls (personal communication), Per did not participate in their experiments. He read and
commented on their manuscript but did not expect to be a co-author. The upshot was that the
three most significant papers from Per’s lab in Oslo during this period appeared without his
name on them. Of course, all three carried the address of Per’s Laboratory of Neurophysiology
at the University of Oslo, and thus contributed to the high esteem in which Per and his lab were
held. Nick Rawlins, from the Department of Psychology at Oxford, collaborated with Per in
the 1970s, and remembers Per’s refusal to add his own name to a study of axonal projections
in the hippocampus of the anaesthetized rat carried out in the Oslo laboratory (Rawlins &
Green 1977). ‘Per was happy with the draft’, Rawlins wrote to one of us, ‘but said his name
should not appear—we should get the credit, and we wouldn’t if his name was on it as well.
Since we couldn’t have done it without him that was very generous of him’.
Per had made an initial foray into LTP in experiments with Tim Teyler and Knut Wester,
publishing an abstract in 1973 confirming the existence of the phenomenon in anaesthetized
animals. From the mid-1970s onwards a significant part of his lab’s activities was devoted to
the study of LTP in transverse hippocampal slices. In his first major contribution, Per, with
Haakan Sundberg, Ola Sveen and Holger Wigström (13), exploited the hippocampal slice
to demonstrate the property of input specificity of LTP (plastic changes are confined to the
synapses receiving high-frequency trains). By placing a pair of stimulating electrodes on either
side of the CA1 cell body layer, Per and his colleagues were able to activate two independent
groups of axons and demonstrate that a high-frequency train produced LTP in the pathway
receiving the train but not in the other pathway. This important result established that LTP was
not a cell-wide change, but was, as suspected, confined to the input in which the induction
conditions had been satisfied.
By the mid-1980s work by a number of investigators was suggesting that the criterion
for the induction of LTP was simply that a pathway should be active at a time when the
cell was strongly depolarized. Several laboratories set out to establish the truth or otherwise
of this prediction, including Per and his team in Oslo, and the group of Holger Wigström
and Bengt Gustafsson in Gothenburg. The experimental approach of the two Scandinavian
groups was similar: arrange to record intracellular synaptic responses (EPSPs) alternately
from two independent pathways and follow the stable responses obtained in the two pathways
for an initial control period; then, during the conditioning period, briefly depolarize the cell
each time one but not the other of the two pathways was stimulated, and then return to
control stimulation without depolarization. The expectation was that the pathway that had
been activated when the cell was depolarized would be potentiated while the control pathway
would remain unchanged. The two groups used different approaches to achieve the required
brief periods of depolarization. The Gothenburg group delivered depolarizing pulses via
an intracellular electrode, while the Oslo group used an extracellular electrode containing
glutamate to electrophorese brief pulses of glutamate onto the cell. The Gothenburg approach
led to lasting potentiation of the EPSP in the pathway experiencing coincident depolarization
and afferent stimulation, while the Oslo approach led to an increase in the probability of the
postsynaptic cell firing but no change in the EPSP. The two papers were sent to Nature—
and both were rejected, the referees requesting further control experiments. Wigström and
Gustafsson considered these demands unreasonable and published their results elsewhere the
same year (Wigström et al. 1986), while Per and his team spent several months performing
further experiments, only for their paper to be rejected by Nature a second time. The Oslo
paper was published in Experientia the following year (14). Per refers ruefully to this episode
in his memoir (21), concluding ‘they (Wigström and Gustafsson) deserved their win, but
slightly bitter it was’.
Theta activity in the hippocampus

Per started experiments on hippocampal theta activity when Brian Bland arrived in Oslo
in 1971. Bland came with a PhD from Cornelius (‘Case’) Vanderwolf’s lab in Canada
and an interest in the brain’s theta activity. With John Dudar, they made a detailed
electrophysiological topographical analysis of the outputs of CA3 and CA1 pyramidal cells
(12). With Trond Myhrer and Phillip Schwartzkroin, Per studied the mechanisms underlying
theta activity in the hippocampus, and confirmed the importance of the septum by showing
that a relatively small lesion that interrupted septal efferents to the hippocampus could abolish
hippocampal theta activity. In a review of these findings (15) Per emphasized the presence of
two generators of gross theta activity, one in CA1 (basal dendritic component) and one in the
dentate (molecular layer).
Today, after much further research, the overall picture has changed without becoming
any less complicated. It now appears that fast-spiking interneurons play an essential role
in generating hippocampal theta activity and that spike activity previously attributed to
granule or pyramidal cells probably represents the activity of interneurons. Nevertheless,
Per’s recognition that more than one dipole underlies hippocampus theta activity has remained
‘definitive’ (Gyorgy Buzsaki, personal communication).
For Bland, as for so many other postdocs from all over the world, coming to Per’s lab was
important not only for training and inspiration but also for the forming of lasting scientific
friendships. Per made every effort to make visiting scientists feel at ease in Norway, inviting
them to his home, to his cottage in the mountains, or for a voyage in his sailing boat. In
Bland’s case, he learnt not only Per’s ways of doing field potential analysis in combination
with intracellular recording from intact animals, but also, like other postdocs of Per’s, the
in vitro slice technique, which he would take with him when he returned to Canada. He worked
closely with Per and remembers ‘his hands on approach to science and his active involvement
in all stages of the work’.
Confocal and electron microscopy

In the early 1990s Per acquired a confocal microscope and with his PhD students Marie
Trommald and Vidar Jensen embarked on a quantitative assessment of dendritic spines on CA1
pyramidal cells filled with the fluorophore Lucifer Yellow (18). A pyramidal cell glowing with
thousands of fluorescent spines is an irresistible sight, and Per, who was a gifted draftsman,1
responded with enthusiasm to the challenges involved in accurately drawing dendritic arbours
and counting spine numbers. His laboratory extended this quantitative histological approach
1 A favourite conference trick of Per’s was to approach a blackboard with a piece of chalk in each hand, and with
two seamless sweeps of his arms draw the outline of a transverse section of the hippocampus. His drawings (see
figure 3) of the exposed rabbit hippocampus, and of the trisynaptic circuit, which he made for a paper on the
generation of population spikes (11), have been reproduced many times in textbooks and research papers, usually
without attribution, so engrained are they in the hippocampal zeitgeist).
Per Andersen 17
using electron microscopy to ask whether LTP in granule cells of the dentate gyrus is
associated with changes in spine dimensions or number (19). Their conclusion that there is
an increase in spine number but no change in spine dimensions in LTP remains one option
available from an inconsistent literature.
Long-term potentiation: international collaborations

Towards the end of his active career, Per’s work on LTP continued in collaboration with two
leading laboratories outside Norway, those of Paul Greengard at the Rockefeller Institute in
New York, and of Bert Sakmann (ForMemRS 1994) at Heidelberg University. In the second
half of the 1980s the role of protein kinases in sustaining LTP came under intense scrutiny.
Per collaborated with Paul Greengard on two projects. From the Greengard laboratory Per
obtained the activated form of protein kinase C, and he and his group injected it directly
into single pyramidal cells in hippocampal slices. They found it produced an increase in the
reliability of synaptic transmission, as judged by an enhanced probability that the impaled
cell would respond with an action potential to a threshold stimulus, similar to that seen after
the induction of LTP (16). A decade later Per’s lab collaborated again with the Greengard
group, to examine LTP in knock-out mice lacking inhibitor-1, a broad-spectrum protein kinase
inhibitor (20). Their results supported the conclusion that in some, though not all, hippocampal
pathways the suppression of protein kinases reduced the amplitude of synaptic potentiation.
A sustained collaboration was established towards the end of Per’s career with the
Heidelberg group of neuroscientists under Peter Seeburg, a leading expert on glutamate
receptor subtypes, and Bert Sakmann. Through this collaboration, in which the molecular
engineering was done in Heidelberg and the electrophysiology by Øivind Hvalby and Vidar
Jensen in Per’s laboratory in Oslo, emerged an unexpected and dramatic result (17). Mice in
which the GluA1 subunit of the tetrameric glutamate receptor had been deleted exhibited an
apparent complete absence of LTP in area CA1 of hippocampal slices. What was startling
about this finding was that the performance of the mutant mice was unaffected in the water
maze, a hippocampus-dependent learning task. The link between LTP and hippocampus-
dependent learning appeared to have been broken. Later it transpired that LTP in area CA1
could be obtained with different induction procedures and that LTP in the dentate gyrus was
unaffected. Relative calm was restored.
Per’s last experimental paper, a study of the variability of conduction velocity in the axons
of CA3 pyramidal cells, was published in 2004. In 2007 The hippocampus book, a multi-author
volume covering all aspects of hippocampal anatomy and physiology, was finally published
after a gestation period of many years. Per had proposed this project to the other editors, Tim
Bliss, Richard Morris, David Amaral and John O’Keefe, at a meeting in Palermo in the early
1990s, and writing had progresssed fitfully over the intervening years, during which the editors
enjoyed many convivial gatherings at a variety of locations in Norway, the UK and the USA,
to discuss the project, and listen to Per’s vivid accounts of colleagues and projects past and
present. This, however, was not getting the book written, and in the end the editors realized
that they lacked the time and expertise to cover all the vast hippocampal literature themselves,
and other leading experts were invited to contribute many of the chapters. It is a measure of
Per’s standing in the neuroscience community that not a single invitation to contribute to the
book was declined. The hippocampus book, of which he was the chief editor, and to which he
contributed much of the history chapter, was the last of his more than 150 publications (22).
Figure 4. Per near his hytta in Hemsedal. (Photograph from the Institute collection.)
Family life, sailing and last years

Per’s family recall his long hours in the lab and the many foreign conferences, but they
also remember that he was always with them in school holidays and on vacations, which
invariably took place in Norway. They had a large cottage, originally an old log farmhouse, in
the mountains bordering Hemsedal, between Oslo and Bergen. He had bought the farmhouse
in 1965 and then had it transported and re-erected on a plot of land lying at an altitude of
about 1000 m above Hemsdal. All the subsequent fitting out, as well as later extensions, he
carried out himself, with occasional help from visiting friends and lab members, including
Terje Lømo, who remembers filling up his station wagon in Oslo with LECA blocks for Per to
build a new chimney through the two storeys of the house. And there the family would go on
ski trips in the Christmas and Easter holidays and long walks in summertime (figure 4). They
also spent part of their summers on Langøy, an island near Mandal and the most southern point
of Norway, bathing, fishing and sailing. The place belonged to Kari’s parents but Per built an
extra cottage to make room for them all. His daughter Hege remembers ‘a lovely childhood,
one in which we learnt so much from our parents by participating in all their activities and
feeling we belonged to a team’.
Sailing remained a lifelong passion. He often sailed the length of the fjord, Oslo to Langøy,
with his family or visitors. He bought the hull of a sailboat and fitted out the rest himself. Jean
Claude Lacaille, who was a postdoc with Per in the mid-1980s, remembers being conscripted
as a crew member in the 24-hour handicap race that took place annually along the length of
the Oslo fjord. He had no previous sailing experience and recalls that this was no pleasure
trip—competing was what mattered. Per was never less than competitive in whatever activity
he was involved in. And we, Terje Lømo and Tim Bliss, remember an early spring day in 1969
when we were recruited in the afternoon with others in Per’s lab to help launch his sailboat
at a marina near his house in Oslo. Afterwards everyone repaired to Terje Lømo’s house in
Nesodden on the other side of the fjord to celebrate. That evening, after the party, Per passed
the marina on his way home, and saw no sign of his boat. It had sunk, never to be recovered.
Per lost no time in fitting out another boat.
Per Andersen 19
By the early 2000s, Per’s active engagement in hippocampal research was coming to an
end, but he maintained an office at the Institute of Neurophysiology’s new home on the
Gaustad campus for a few more years. In 2007, he spoke at the opening of the Kavli Institute
for Systems Neuroscience headed by his ex-students Edvard and Mai-Britt Moser at the
Norwegian University of Science and Technology in Trondheim. A notable event was the
award of the 2014 Nobel Prize in Physiology or Medicine to the Mosers for their discovery of
grid cells in the entorhinal cortex. Per’s 80th birthday in January 2010 brought many friends
from across the world to Oslo to celebrate the occasion. In retirement he lived quietly with
Kari in Blummenholm, a suburb to the west of Oslo in the house they had bought shortly after
returning from Canberra. He died on 17 February 2020 at the age of 90.
Honours
1968 Fridtjof Nansen Prize, Norwegian Academy of Sciences
1975 Member of the Norwegian Academy of Sciences
1988 Member of the Royal Norwegian Society of Sciences and Letters
1990 President of the European Neuroscience Association
1991 Member of the Royal Swedish Academy of Sciences
1993 Ipsen Prize for Neuronal Plasticity
1994 Member of the National Academy of Sciences of the USA
1995 Fernström Prize
1996 Lundbeck Prize
1997 Commander of the Order of St Olav
1998 Honorary doctorate, Karolinska Institute
2002 Foreign Member of the Royal Society
Acknowledgements
The frontispiece portrait photograph was taken in 2002 by Prudence Cuming Associates and is copyright © The Royal
Society.
References to other authors

Bliss, T. V. P. & Lømo, T. 1973 Long-lasting potentiation of synaptic transmission in the dentate area of the
anaesthetised rabbit following stimulation of the perforant path. J. Physiol. 232, 331–356. (doi:10.1113/
jphysiol.1973.sp010273)
Cragg, B. G. & Hamlyn, L. H. 1957 Some commissural and septal connexions of the hippoocampus in the rabbit; a
combined histological and electrical study. J. Physiol. 135, 460–485. (doi:10.1113/jphysiol.1957.sp005724)
Eccles, J. C. 1951 Interpretation of action potentials evoked in the cerebral cortex. Electroenceph. Clin. Neurophysiol.
3, 449–464. (doi:10.1016/0013-4694(51)90033-8)
Eccles, J. C. 1953 The neurophysiological basis of mind: the principles of neurophysiology. Oxford, UK: Clarendon
Press.
Eccles, J. C. 1961 The mechanism of synaptic transmission. Ergebn. Physiol. 51, 299–430. (doi:10.1007/BF02269100)
Liu, X., Ramirez, S., Pang, P. T., Puryear, C. B., Govindarajan, A., Deisseroth, K. & Tonegawa, S. 2012 Optogenetic
stimulation of a hippocampal engram activates fear memory recall. Nature 484, 381–385. (doi:10.1038/
nature11028)
Lømo, T. 1966 Frequency potentiation of excitatory synaptic activity in the dentate area of the hippocampal formation.
Acta Physiol. Scand. 68(Suppl. 277), 128. (doi:10.1038/nature/11028)
Rawlins, J. N. & Green, K. F. 1977 Lamellar organisation in the rat hippocampus. Exp. Brain Res. 28, 335–344.
(doi:10.1007/BF00235715)
Schwartzkroin, P. A. & Wester, K. 1975 Long-lasting facilitation of a synaptic potential following tetanization in the
in vitro hippocampal slice. Brain Res. 89, 107–119. (doi:10.1016/0006-8993(75)90138-9)
Skrede, K. K. & Westgaard, R. H. 1971 The transverse hippocampal slice: a well-defined cortical structure maintained
in vitro. Brain Res. 35, 589–593. (doi:10.1016/0006-8993(71)90508-7)
Wigström, H., Gustafsson, B., Huang, Y. Y. & Abraham, W. C. 1986 Hippocampal long-term potentiation is induced
by pairing single afferent volleys with intracellularly injected depolarizing current pulses. Acta Physiol. Scand.
126, 317–319. (doi:10.1111/j.1748-1716.1986.tb07822.x)

Ramon y Cajal, S. 1911 Histologie du système nerveux de l’homme et des vertébrés. Édition française, revue et mise
à jour par l’auteur, traduite de l’espagnol par le Dr. L. Azoulay. Tome 2 1911.
Bibliography
The following publications are those referred to directly in the text. A full bibliography is available at https://doi.org/
10.6084/m9.figshare.c.7064877.
(1) 1960 Interhippocampal impulses. II. Apical dendritic activation of CA1 neurons. Acta Physiol. Scand. 48,
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(2) 1962 (With J. C. Eccles & R. F. Schmidt) Presynaptic inhibition in the cuneate nucleus. Nature 194,
741–743. (doi:10.1038/194741a0)
(3) (With J. C. Eccles) Inhibitory phasing of neuronal discharge. Nature 196, 645–647. (doi:10.1038/
196645a0)
(4) 1963 (With J. C. Eccles & Y. Løyning) Recurrent inhibition in the hippocampus with identification of the
inhibitory cell and its synapses. Nature 198, 540–542. (doi:10.1038/198540a0)
(5) (With J. C. Eccles, Y. Løyning & P. E. Voorhoeve) Inhibitory synapses on somas of Purkinje cells in
the cerebellum. Nature 199, 655–656. (doi:10.1038/199655a0)
(6) 1964 (With T. A. Sears) The role of inhibition in the phasing of spontaneous thalamo-cortical discharge.
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(7) (With J. C. Eccles & T. A. Sears) The ventro-basal complex of the thalamus: types of cells,
their responses and their functional organization. J. Physiol. 174, 370–399. (doi:10.1113/jphysiol.
1964.sp007493)
(8) 1966 (With B. Holmqvist & P. E.Voorhoeve) Entorhinal activation of dentate granule cells. Acta Physiol.
Scand. 66, 448–460. (doi:10.1111/j.1748-1716.1966.tb03223.x)
(9) (With B. Holmqvist & P. E. Voorhoeve) Excitatory synapses on hippocampal apical dendrites
activated by entorhinal stimulation. Acta Physiol. Scand. 66, 461–472. (doi:10.1111/j.
1748-1716.1966.tb03224.x)
(10) 1968 (With S. A. Andersson) Physiological basis of the alpha rhythm. New York, NY: Appleton-Century-
Crofts.
(11) 1971 (With T. V. P. Bliss & K. K. Skrede) Unit analysis of hippocampal population spikes. Exp. Brain Res.
13, 208–221. (doi:10.1007/BF00234086)
(12) 1973 (With B. H. Bland & J. D. Dudar) Organization of the hippocampal output. Exp. Brain Res. 17,
152–168. (doi:10.1007/BF00235025)
(13) 1977 (With S. H. Sundberg, O. Sveen & H. Wigström) Specific long-lasting potentiation of synaptic
transmission in hippocampal slices. Nature 266, 736–737. (doi:10.1038/266736a0)
(14) 1987 (With O. Hvalby, J. C. Lacaille, G. Y. Hu) Postsynaptic long-term potentiation follows coupling
of dendritic glutamate application and synaptic activation. Experientia 43, 599–601. (doi:10.1007/
BF02126343)
Per Andersen 21
(15) 1980 Participating neurones and mechanisms underlying theta activity in unanaesthetized rabbits. Prog.
Brain Res. 54, 371–380. (doi:10.1016/S0079-6123(08)61649-0)
(16) 1987 (With G. Y. Hu, O. Hvalby, S. I. Walaas, K. A. Albert, P. Skjeflo & P. Greengard) Protein kinase
injection into hippocampal pyramidal cells elicits features of long-term potentiation. Nature 328, 426–
429. (doi:10.1038/328426a0)
(17) 1990 (With others) Importance of AMPA receptors for hippocampal synaptic plasticity but not for spatial
learning. Science 284, 1805–1811. (doi:10.1126/science.284.5421.1805)
(18) 1995 (With M. Trommald & V. Jensen) Analysis of dendritic spines in rat CA1 pyramidal intracellularly
filled with a fluorescent dye. J. Comp. Neurol. 353, 260–274. (doi:10.1002/cne.903530208)
(19) 1996 (With M. Trommald & G. Hulleberg) Long-term potentiation is associated with new excitatory spine
synapses on rat dentate granule cells. Learn. Mem. 3, 218–228. (doi:10.1101/lm.3.2-3.218)

(20) 2000 (With others) Protein phosphatase-1 regulation in the induction of long-term potentiation:
heterogeneous molecular mechanisms. J. Neurosci. 20, 3537–3543. (doi:10.1523/jneurosci.20-10-
03537.2000)
(21) 2004 The history of neuroscience in autobiography, 4, pp. 2–38. Amsterdam, The Netherlands: Elsevier.
(22) 2007 The hippocampus book. New York, NY: OUP.

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org/ on 03 March 2024

Biogr. Mems Fell. R. Soc.

12 January 1930 — 17 February 2020

Elected ForMemRS 1987

By Tim Bliss FRS1, * and Terje Lømo2,†

2024 The Author(s)

Early life and education

Thesis work on field potentials in the hippocampus

Eccles in Canberra as ‘fantastic’ and ‘incredible’ (21), recalling an atmosphere of almost

Thalamo-cortical interactions and the genesis of barbiturate

Identification of inhibitory synapses

Feed-forward inhibition in the cerebellum

The trisynaptic circuit in the hippocampus

Long-term potentiation and the transverse hippocampal slice

Theta activity in the hippocampus

Confocal and electron microscopy

Long-term potentiation: international collaborations

Family life, sailing and last years

returning from Canberra. He died on 17 February 2020 at the age of 90.

References to other authors

126, 317–319. (doi:10.1111/j.1748-1716.1986.tb07822.x)

synapses on rat dentate granule cells. Learn. Mem. 3, 218–228. (doi:10.1101/lm.3.2-3.218)

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