Psyciwhikal Review

1973, Vol. 80, No. 1, 69-79

AMNESIA, CONSOLIDATION, AND RETRIEVAL 1

RALPH R. MILLER 2 AND ALAN D. SPRINGER
Brooklyn College of the City University of New York

A memory model is proposed in which information enters an initial structural-

chemical format within fractions of a second. Experimental amnesia is
viewed as a failure to retrieve information from long-term memory rather
than a failure of the information to be consolidated in long-term memory.
Consolidation and retrieval failure explanations of experimental amnesia
are found to differ primarily on the issue of recovery of memory. The
nature of experimental amnesia paradigms is such that the consolidation
position can never be supported; it may only be refuted by an occurrence
of recovery of memory or left as an unresolved issue by a lack of recovery.
The use of noncontingent stimuli to induce recovery from amnesia has been
successful in several instances, thereby supporting the retrieval failure hy-
pothesis. Success in producing amnesia for reactivated "old" memories
further corroborates the retrieval position. Arguments that effectively
delivered, high-intensity or high-dosage amnestic agents will disrupt consoli-
dation beg the question and are presently without any empirical support.
Two-process theories proposing both retrieval and consolidation failures are
presently neither necessary nor parsimonious.

Despite the numerous explanations of ex- of operations constituting memory. The

perimental amnesia proposed in recent years
(e.g., Lewis, 1969; McGaugh, 1966; Spe-
vack & Suboski, 1969), a few threads of
consensus are detectable. Although all of
the suggested hypotheses do not rely on the
same model of memory, each of the models
includes identifiable consolidation processes
(the establishment of an enduring neurologi-
cal memory trace, sometimes referred to as
storage), retention processes (the passive
maintenance of this trace, also sometimes
referred to as storage), and retrieval pro-
cesses (the events by which this trace comes
to influence subsequent behavior). All more
specifically defined processing functions can
be subsumed under these three aspects of
memory. Each of these three stages is essen-
tial for proper functioning of memory. A
memory failure could, in effect, be attributed
to a disruption of any stage in the sequence
1 Gaugh, 1966). The basic phenomenon cited
Preparation of this article and research re-
ported within were supported by United States
Public Health Service Grant MH 19497 and Re-
search Foundation of the City University of New
York Grant 1385.
Thanks are due Anthony Sclafani for his criti-
cism of an earlier version of this article.
2
Requests for reprints should be sent to Ralph
R. Miller, Department of Psychology, Brooklyn
College of the City University of New York,
Brooklyn, New York 11210.
69
following comments are concerned with those
behavioral deficits that stem explicitly from
memory failures as distinct from those defi-
cits caused by changes in performance vari-
ables often seen in (a) studies examining
long intervals between acquisition and ad-
ministration of amnestic agents, (b*) short
intervals between amnestic agent administra-
tion and retention test, or (c) certain select
behavioral tasks (e.g., Chorover & Schiller,
1966; Spevack & Suboski, 1969).
CONSOLIDATION
Experimental amnesia induced by electro-
convulsive shock, hypothermia, metabolic in-
hibitors (e.g., puromycin, cycloheximide)
and various other amnestic agents within a
retroactive interference paradigm tradition-
ally has been attributed to failures of the
consolidation process (Glickman, 1961; Mc-
in support of this view is the often reported
observation that the resultant amnesia is
retrograde, that is, memory failure increases
as the interval between information input
and administration of the amnestic agent
decreases.
The early models suggesting that a dis-
ruption of consolidation was the source of
retrograde amnesia held that recently re-
70 RALPH R. MILLER AND ALAN D. SPRINGER
ceived information was uniquely encoded in
short-term memory in the form of electro-
chemically active, neural reverbatory circuits
that were ultimately terminated by decay
and/or intereference processes (e.g., Hebb,
1949). The continued action of these cir-
cuits over hours (later minutes or seconds)
was believed to give rise to a more perma-
nent, long-term memory of an energetically
passive, chemical-structural format. Elec-
troconvulsive shock and hypothermia were
thought to terminate short-term memory
processes before long-term memory could be
established (McGaugh, 1966). Metabolic
inhibitors were believed to block the forma-
tion of long-term memory during the finite
duration of the relevant information in short-
term memory (Barondes & Cohen, 1968).
In both cases, the consolidation explanation
of experimental amnesia demands that the
induced amnesia be permanent.
Numerous recent experiments have placed
in question these explanations and their un-
derlying model of memory. For instance,
information received immediately prior to
electroconvulsive shock has been observed
to be available for tens of minutes after elec-
troconvulsive shock (Geller & Jarvik, 1968b;
McGaugh & Landfield, 1970; Miller &
Springer, 1971). This suggests that either
electroconvulsive shock fails to destroy all
information uniquely encoded in short-term
memory or, alternatively, information enters
long-term memory far more rapidly than is
ordinarily assumed. As difficulties with the
detailed consolidation explanation of the
19SO's and early 1960's became apparent,
many researchers turned to more general
models within the consolidation framework
(e.g., McGaugh, 1968) while others sought
explanations of experimental amnesia in dis-
ruption of the memory sequence subsequent
to consolidation (e.g., Lewis, 1969). The
latter set of explanations is a variation on
the retrieval failure theme. Few, if any,
researchers have suggested that retention
(passive storage) is subject to disruption.
Consolidation is ordinarily defined as the
formation of permanent storage of the rele-
vant information; hence, a prevention of
consolidation that is prolonged beyond the
duration of any temporary memory storage
requires that the information be irrevocably
lost. If retrieval is defined as all memory
processes necessary for the utilization of
information already in passive storage, then
a retrieval failure implies that the informa-
tion is present but unavailable on the test
trial. On the basis of these definitions, a
potential distinction between retrieval and
consolidation views of experimental amnesia
is whether or not the memory impairment
is permanent. Some specific models hypoth-
esize further distinctions (e.g., Hebb, 1949;
Weiskrantz, 1966), but the issue of perma-
nence remains primary. The retrieval ex-
planation of experimental amnesia would be
established by recovering the unavailable
memory in the absence of any subsequent
training. On the other hand, the consolida-
tion position could hardly be said to be
proven by a failure of recovery from amnesia.
The possibility of recovery under untried
circumstances always remains. Moreover,
a retrieval failure could theoretically be ir-
reversible. In the latter case, no behav-
ioral test would suffice to distinguish a re-
trieval failure from a consolidation failure,
and the issue could not be resolved until
future technology provided us with tests that
are other than behavioral (e.g., biochemical).
Clearly, behavioral studies of experimental
amnesia are, due to the nature of the para-
digm, poorly suited for establishing the
validity of consolidation theory.
Most studies have found amnesia to vary
inversely with the interval between acquisi-
tion and administration of the amnestic agent
and, given a fixed interval between training
and test trials, to be relatively independent of
the interval between administration of the
amnestic agent and the retention test (after
correcting for effects of the amnestic agent
on performance variables). These data indi-
cate that amnestic agents interfere with time-
dependent, memorial processes that are initi-
ated during or soon after acquisition and are
completed in relatively short order. This
constraint is consistent with the consolida-
tion failure explanation of experimental am-
nesia since all initial entry into long-term
storage must occur soon after training if
there is to be any retention displayed. How-
ever, the constraint is also consistent with a
retrieval failure explanation as some retrie-
val processes must occur during or soon after
 AMNESIA, CONSOLIDATION AND RETRIEVAL 71
acquisition periods to permit later access to poral distinction between consolidation and
the relevant information. As an analogy, retrieval is an operational definition inde-
consider the acquisition of a new book by pendent of any behavioral consequences of
a library. Placing the book on a shelf may the operation, such as the permanence of am-
be viewed as equivalent to consolidation and nesia. Inasmuch as focusing on the perma-
making the appropriate entry in the card nence rather than the temporal distinction
catalog could be considered a retrieval func- between consolidation and retrieval is both
tion, one that must be performed soon after more common and more fruitful, this article
acquisition. Without the appropriate entry will adhere to the former definitions.
in the card catalog, the book may be physi-
cally present in the library but not available RECOVERY FROM AMNESIA
on request. The logical difficulty with consolidation
Returning to memorial processes, the re- explanations of experimental amnesia has
trieval view of experimental amnesia is that always been present. However, the short-
the relevant information is successfully con- comings of the consolidation position were
solidated within the central nervous system far less evident in prior years since there
and that the amnestic agent has impaired were no clear instances on record of recovery
the establishment or future functioning of (of the most recently acquired information)
the cataloging system necessary for retriev- from experimental amnesia. Considerable
ing the information from long-term storage clinical literature reporting spontaneous re-
at some later time, that is, during the reten- covery from traumatic amnesia, oldest mem-
tion test. The retrograde gradient for de- ories returning first, was ignored on the
gree of amnesia as a function of the interval grounds that there was no evidence of re-
between training and administration of the covery for the last few seconds preceding
amnestic agent is, according to the retrieval the traumatic event. The fact that most
position, a measure of the temporally de- memories did return was overshadowed by
creasing vulnerability of some cataloging the less well documented supposition that a
mechanism to the amnestic agent. Clearly few memories did not return spontaneously.
the cataloging mechanism is in itself a mem- The issue of recovery from experimental
ory of some sort; however, it should not be amnesia was first raised by Zinkin and Miller
confused with the fully elaborated memory (1967) who observed partial spontaneous
of the training event, which may exist inde- recovery from electroconvulsive shock-in-
pendently of catalog-type memories. Cata- duced amnesia when retention intervals
log-type memories are assumed not to be greater than the traditional 24 hours were
sources of primary information, but rather used in a repeated-tests paradigm. Subse-
means to facilitate access to primary in- quent studies have frequently failed to repli-
formation. One hypothesis to explain why cate this phenomenon, particularly when the
amnestic agents act preferentially on cata- possibly confounding repeated-tests aspect
loging processes rather than on consolidation of the experiment was removed (Herz &
is to assume that consolidation of primary Peeke, 1968; Luttges & McGaugh, 1967).
information occurs extremely rapidly, per- While spontaneous recovery from electro-
haps in fractions of a second, while catalog- convulsive shock-induced amnesia seems a
ing occurs over seconds, minutes, or even doubtful phenomenon, several recent studies
hours. Data and arguments supporting this have reported extensive spontaneous re-
hypothesis comprise much of the remainder covery from amnesia induced by the protein
of this article. synthesis inhibitor cycloheximide (e.g.,
As an alternative to the above schema, a Quartermain & McEwen, 1970).
few investigators have defined all events Koppenaal, Jagoda, and Cruce (1967)
occurring during acquisition as uniquely part initiated a second approach to the problem
of the consolidation process and all events of the permanence of electroconvulsive
occurring during testing as retrieval (Cher- shock-induced experimental amnesia. After
kin, 1970; Weiskrantz, 1966). While one training and amnesia-producing treatment,
can not dispute a definition, such a tem- they subjected their animals to a second
72 RALPH R. MILLER AND ALAN D. SPRINGER
training trial (reminder) with reinforcement
intensity sufficiently reduced from initial
training such that animals receiving only
the second training trial learned little or
nothing. The amnestic animals, however,
displayed considerable recovery of memory.
Geller and Jarvik (1968a) successfully repli-
cated this phenomenon. The difficulty with
both of these examples of recovery is that
the initial training and amnesia-producing
treatment may have created an animal devoid
of the relevant memory but with a superior
learning potential during the second training
trial. Lewis, Misanin, and Miller (1968)
observed a significant return of memory
after correcting for this ambiguity by adding
control groups and administering the re-
minder stimuli under noncontingent circum-
stances (outside of the training-test environ-
ment) that prohibited learning during the
reminder trial. Miller and Springer (1972a)
replicated this phenomenon and further
demonstrated that the apparent recovery of
memory was truly memorial in nature rather
than a systemically induced phenomenon
such as an alteration in activity level.
Quartermain, McEwen, and Azmitia
(1970) reported studies corroborating the
effectiveness of a noncontingent presentation
of the training reinforcer in restoring mem-
ory after either cycloheximide or electro-
convulsive shock. They produced consider-
able recovery of memory only when the
reinforcer (footshock) was presented within
an hour after an initial retention test. How-
ever, Miller and Springer (1972a) observed
extensive recovery even when a retention
test was not given to the recovery group
prior to presentation of the noncontingent
reminder. The same study also observed
significant recovery from anmnesia over
electroconvulsive shock-reminder intervals of
up to 2 weeks (the longest interval ex-
amined). Consequently, we are inclined to
reject the notion of an absolute critical period
for recovery-inducing agents.
Numerous other studies have found a di-
verse group of stimuli and pharmaceutical
agents that induce partial or total recovery
from experimental amnesia. Typical of the
pharmacological studies are the experiments
of Davis, Thomas, and Adams (1971) that
indicate memory in rats rendered amnestic
with electroconvulsive shock can be largely
restored with scopolamine injected just prior
to testing. Unfortunately, the permanence
of the restored memory in this study was
not examined; however, even a temporary
return of memory indicates that the informa-
tion was previously present although un-
available. Another example is provided by
Flexner and Flexner (1967) who, under
select circumstances, produced significant re-
covery from puromycin-induced amnesia in
mice by intracerebral injection of saline.
The explanations of these studies are far
from clear. Davis, Thomas, and Adams
(1971) theorize about the importance of
appropriate cholinergic levels for retrieval
paralleling Deutsch's (1971) cholinergic
model of spontaneous forgetting. However,
all such recovery studies add weight to the
retrieval view of experimental amnesia which
postulates that the relevant information is
present but unavailable.
The stimulus used to induce recovery of
memory in most studies of facilitated re-
covery from electroconvulsive shock-induced
amnesia has been the same aversive rein-
forcer as was used in training. The question
of stimulus specificity of the recovery agent
with respect to the training reinforcer was
recently raised by Springer and Miller
(1972). They used a one-trial passive
avoidance task with ice water immersion as
the reinforcer. Rats receiving electrocon-
vulsive shock immediately after training dis-
played essentially complete amnesia, but
appreciable recovery of memory was ob-
served if they were subjected to a noncon-
tingent footshock between electroconvulsive
shock and the test trial. Control animals
indicated that the observed avoidance was
not due to changes in activity levels. Non-
specificity of the recovery agent for electro-
convulsive shock-induced amnesia is also
evident in the previously mentioned scopola-
mine-induced recovery of memory reported
by Davis, Thomas, and Adams (1971) and
is consistent with the prevention of cyclo-
heximide-induced amnesia achieved with
amphetamine and corticosteroids by Bar-
ondes and Cohen (1968), although in the
latter case these stimulants were effective
only when injected soon after training and
cycloheximide treatment.
 AMNESIA, CONSOLIDATION AND RETRIEVAL
The results of the Springer and Miller
(1972) study suggested that the word re-
minder may be a misnomer for many stimuli
that can induce recovery from amnesia.
What this study did not make clear is
whether any stressor can act as a recovery
agent regardless of the training task. Or
alternatively, is a stimulus similarity of the
internal physiological state produced by the
typically aversive training reinforcer and the
stressful recovery agent, thus permitting the
latter state to act as a generalized reminder ?
To resolve this issue, Miller, Springer, and
Vega (1972) used a one-trial appetitive task
and administered electroconvulsive shock im-
mediately after training. Several parametric
studies varying noncontingent recovery
shock level failed to restore memory con-
trary to the high effectiveness of noncon-
tingent shock in restoring memory of aver-
sive events. This suggested that the stress
of recovery shock in Springer and Miller
(1972) was specifically acting as a reminder
of earlier stressful events rather than as a
reverser of all potential amnesias. Further
experiments by Miller, Springer, and Vega
(1972) found that appetitive memories could
be largely restored after electroconvulsive
shock through either brief (1 minute) non-
contingent presentation of the appetitive re-
inforcer or somewhat longer exposure (three
exposures of 1 minute each) to the training
apparatus in the absence of the reinforcer.
Looking for apparatus cues that could
restore aversive memories after electrocon-
vulsive shock brought to light a study by
Adams (1966) in which amnesia for mul-
tiple-trial, aversive training in a shuttle box
was greatly attenuated through three ex-
posures of 5 minutes each to the start com-
partment. Adams used a classical condition-
ing explanation of electroconvulsive shock-
induced amnesia (US = electroconvulsive
shock, UR — convulsion, CS = apparatus
cues, CR = partial covert convulsion) and
explained his data as an instance of extinc-
tion. Due to other data, the classical con-
ditioning position has been discounted by
most researchers today (e.g., McGaugh &
Petrinovich, 1966) ; however, consolidation
theory offers no alternative explanation of
Adams' data. The retrieval position can
interpret the phenomenon by regarding ap-
73
propriately long exposure to the training
environment as an effective reminder.
The multitrial training used by Adams
(1966) differs significantly from the one-
trial training tasks that dominate the more
recent literature. Consequently, to examine
Adams' effect in a contemporary context,
Miller, Springer, and Vega (1972) gave
one-trial aversive training in a shuttle box
followed by immediate electroconvulsive
shock and found that memory could be
largely restored with brief exposure to the
punishment compartment or somewhat longer
exposure to the start compartment. How-
ever, the data suggested that overexposure
to either compartment not only did not
further improve retention but could actually
impair retention. Seemingly, after memory
has been restored, it is vulnerable to extinc-
tion like any normal memory. The potential
of apparatus cues to restore memories after
administration of an amnestic agent suggests
that memory could reappear over repetitive
test trials. In this light, the Zinkin and
Miller (1967) study, frequently ignored
exactly because of its multiple test trials,
becomes worthy of reexamination. Perhaps
these data are not an example of spontaneous
recovery but rather recovery facilitated by
intervening test trials that serve as re-
minders. Moreover, the shade of doubt
surrounding these data due to the failure
of others to replicate them (e.g., Luttges &
McGaugh, 1967) is eased by the recent suc-
cess of Quartermain, McEwen, and Azmitia
(1972) in restoring considerable memory
with repeated test trials after either cyclo-
heximide or electroconvulsive shock treat-
ment.
Collectively, these recovery of memory
studies indicate that at least some instances
of experimental amnesia are cases of re-
trieval failure and that many of the recovery
agents may reasonably be called reminder
stimuli. Until there is concrete evidence for
two different sources of experimental am-
nesia, it would seem reasonable to assume
the generality of the retrieval failure hypoth-
esis. However, an alternative to the unipro-
cess retrieval hypothesis has been proposed.
The hypothetical argument has frequently
been made that if the amnestic agent (e.g.,
electroconvulsive shock) were "effectively
74 RALPH R. MILLER AND ALAN D. SPRINGER
delivered" at sufficiently high intensities,
then the resultant amnesia would reflect dis-
rupted consolidation and would be perma-
nent (e.g., King & Glasser, 1970). The
basis for this belief apparently lies in the
greater degree of amnesia seen after (a)
high-intensity electroconvulsive shock and
( b ) transcorneal (as opposed to transpin-
nate) electroconvulsive shock electrode place-
ment (e.g., Ray & Barrett, 1969). The
former effect is typically explained through
a traditional intensity argument. The latter
effect is thought to stem from transcorneal
electrodes delivering a greater percentage
of the applied current to the central nervous
system than transpinnate electrodes and/or
the part of the brain receiving the greatest
current concentrations being more suscepti-
ble to the induction of amnesia. Insofar as
high- and low-electroconvulsive-shock cur-
rent intensity differ in degree rather than
kind, it appears to us more reasonable to
assume that differing depths of amnesia also
differ only in degree at least until evidence
to the contrary is found. As for differences
in amnesia resulting from variation in elec-
trode placement, no data currently exist
suggesting that this is other than a conse-
quence of diverse intensities reaching the
brain. Diverse electrode sites may actually
result in varying current intensities reaching
the brain or may affect different neuro-
anatomical loci. Nevertheless, the fact re-
mains that differing electrode placements
yield amnesias that, to date, do not appear
to differ in any fashion other than degree.
Consistent with this view, Miller and
Springer (1972b) demonstrated the effec-
tiveness of noncontingent reminder shock in
reversing amnesia induced by transcorneal
electroconvulsive shock. In summary, there
appears to be no basis for believing that
increased current intensity or appropriate
electrode placement would prove capable of
disrupting consolidation when lesser con-
vulsive currents and other convulsion-induc-
ing electrode placements apparently act on
retrieval processes. If "appropriate" means
those conditions that by definition disrupt
consolidation, then the question has been
begged and does not merit further discussion.
Gherkin (1972) has proposed another way
to save the consolidation explanation of ex-
perimental amnesia from the recovery of
memory data. Gherkin found that he could
use reminder stimuli to recover significant
amounts of memory after inducing amnesia
with moderate but not strong doses of
flurothyl. These data are complemented by
several other studies in which weaker train-
ing stimuli and/or stronger amnestic agents
failed to yield the recovery of memory seen
after stronger training stimuli and/or moder-
ate amnestic agents. Gherkin argues that a
"partial consolidation failure" could push
memory below an effective threshold and
that a reminder stimulus may bring the
memory into the suprathreshold range. The
problem with this explanation is that non-
contingent reminder trials have been found
to be effective in restoring memory. Inas-
much as a reminder trial cannot provide the
animal with any information by virtue of
it being noncontingent, any memory ex-
pressed on the retention test must reflect
information held within the animal since
initial training. Hence, this argument does
not counter the retrieval position. Further-
more, it should be noted that experiments
reporting a failure to obtain recovery from
amnesia in certain circumstances have to
date not clone any parametric study of the
intensity and duration of the hypothetical
recovery agent, and, consequently, the im-
plications of their null results are not com-
pelling. Moreover, as was previously noted,
even if there were instances of compelling
recovery failures, these would not distinguish
between consolidation impairments and ir-
reversible retrieval failures.
REACTIVATION
Reactivation within the experimental am-
nesia literature refers to paradigms in which
an animal is trained and then at a later time
is presented noncontingently with a memory
reactivator (ordinarily either the apparatus
cues or the reinforcer) followed immediately
with an amnestic agent. The time between
training and reactivation is usually 24 hours,
an interval sufficient to insure consolidation
by most any standard and inadequate to
permit appreciable forgetting. Amnesia that
depends on the amnestic agent following
soon after memory reactivation has been
observed in numerious instances with both
 AMNESIA, CONSOLIDATION AND RETRIEVAL
appetitive and aversive reinforcers (e.g.,
Davis & Hirtzel, 1970; Davis & Klinger,
1969; DeVietti & Larson, 1971; Howard
& Meyer, 1971; Lewis, Bregman, & Mahan,
1972; Misanin, Miller, & Lewis, 1968;
Schneider & Sherman, 1968). There have
also been failures to obtain the reactivation
phenomenon (Banker, Hunt, & Pagano,
1969; Dawson & McGaugh, 1969; Gold &
King, 1972; Jamieson & Albert, 1970);
however, none of the studies reporting null
results distinguish themselves by making
extensive parametric attempts to find the
optimal conditions for the phenomenon.
Clearly all of the variables controlling the
phenomenon are not understood; however,
the pervasiveness of the effect across tasks,
species, amnestic agents, and independent
laboratories argues for the validity of the
phenomenon.
Considering the long training-electrocon-
vulsive shock interval used in reactivation
studies, consolidation failure appears to be
a most unlikely explanation of the observed
memory deficit. However, the administra-
tion of an amnestic agent in conjunction
with select stimulus configurations at any
time prior to behavioral testing could, in
principle, prevent the normal functioning of
retrieval processes during the test trial. The
occurrence of experimental amnesia pro-
duced at the time of reactivation further
suggests that at least some experimental
amnesia is due to a retrieval failure, a con-
clusion in concurrence with the studies re-
porting recovery from amnesia. Again, if
some experimental amnesia is due to re-
trieval failure, parsimony compels us to ac-
cept all experimental amnesia as resulting
from retrieval failure until evidence to the
contrary is presented. Such evidence, due
to experimental design, cannot be provided
by any experimental amnesia paradigm used
to date.
DETENTION
Despite apparent discrepancies in the para-
digms used, the recent studies of posttraining
detention are closely related to both re-
covery and reactivation phenomena. Several
research groups have recently reported that
detaining an animal in the training apparatus
after acquisition can both produce amnesia
75
and potentiate the memory loss caused by
an amnestic agent administered immediately
after detention. To cite a few examples,
Rbbustelli and Jarvik (1968) found that
detention caused amnesia in mice and, if
followed immediately by electroconvulsive
shock, potentiated the amnestic effect of
electroconvulsive shock. Davis and Klinger
(1969) and Davis and Hirtzel (1970), using
goldfish, observed that detention potentiated
the amnesia produced by KC1, puromycin,
acetoxycycloheximide, and electroconvulsive
shock. And Geller, Robustelli, and Jarvik
(1971) found that posttraining detention
of mice produces a memory deficit that is
additive to one produced by cycloheximide.
Considering detention as a performance
attenuating treatment in its own right, the
question arises as to whether detention is
merely an example of extinction (cessation
of previous reinforcement contingencies as-
sociated with training cues) and/or retro-
active interference (due to irrelevant in-
formation input) or whether it is a new
phenomenon in and of itself. Two variables
that facilitate understanding of the detention
effect are the place of detention and the delay
between training and detention. Robustelli
and Jarvik (1968) presented data suggesting
that detention becomes less effective as an
amnestic agent as the stimuli during deten-
tion become increasingly divergent from
those of the training apparatus. This is
consistent with detention effects resulting
from extinction (to those conditioned stimu-
lus elements present during detention) and
retroactive interference (provided interfer-
ence is assumed greatest when the irrelevant
information concerns aspects of the context-
ual cues of the training situation). Calhoun
and Murphy (1966) presented data support-
ing this assumption for a passive avoidance
task similar to that used by Robustelli and
Jarvik (1968). Similarly, the memory deficit
produced by detention increases with dimin-
ishing intervals between training and deten-
tion (e.g., Robustelli & Jarvik, 1968). As
extinction and interference are most effective
soon after acquisition (Skinner, 1938), this
too is congruent with detention being re-
garded as a combination of these two factors.
Moreover, a spontaneous decrement in de-
tention-induced deficits over a 24-hour, post-
 76 RALPH R. MILLER AND ALAN D. SPRINGER
detention-retention interval (Robustelli, Gel-
ler, & Jarvik, 1969) is consistent with
spontaneous recovery from extinction. Fi-
nally, the poor memory displayed by animals
rendered amnestic with electroconvulsive
shock and subsequently exposed to apparatus
cues for extended periods of time may be
consistently viewed as a reminder-induced,
memory increment followed by a deten-
tion-induced, memory decrement (Miller,
Springer, & Vega, 1972).
The potentiation of memory deficits pro-
duced by amnestic agents administered im-
mediately after detention is thought by some
to be an interaction of detention and the
amnestic agent (e.g., Davis & Hirtzel, 1970;
Davis & Klinger, 1969) while others regard
the two decremental effects as merely addi-
tive (e.g., Geller, Robustelli, & Jarvik, 1971).
However, other studies by the latter investi-
gators have yielded data suggesting a strong
interaction (Robustelli, Geller, & Jarvik,
1968). Conceivably these discrepancies are
due to differences in species and amnestic
agents; however, it is possible that altera-
tion in temporal parameters is responsible
for determining whether the results of the
tandem treatments are merely additive or
reflect an interaction. Paradigms involving
detention followed by an amnestic agent are
essentially the same as the reactivation
studies analyzed previously; only the dura-
tion of detention is ordinarily greater than
that used in reactivation studies. Detention
can be viewed as serving to reactivate or
maintain the activity of the relevant memory
immediately prior to administering the am-
nestic agent. For the present time, it ap-
pears reasonable to regard interactions of
detention and amnestic agents as further
examples of reactivation rather than new
phenomena in their own right. This appears
consistent with detention serving as an ex-
tinction period, for reactivation of a memory
seems a likely prerequisite for extinction
of that memory to occur. A reactivation
interpretation of the interaction of detention
and amnestic agents offers an answer to
the question of why doesn't the postdetention
amnestic agent cause amnesia for the extinc-
tion that occurs during detention. Possibly
amnesia for part or all of the detention period
does, in fact, take place, but the reactivation
phenomenon produces sufficient amnesia to
mask this effect.
THE STATE-DEPENDENT HYPOTHESIS
The state-dependent hypothesis is one
particular form of the retrieval failure view
of experimental amnesia recently taken by
several researchers. There is little doubt
that treatments such as electroconvulsive
shock administered soon before acquisition
yield memories more readily expressed in the
post-electroconvulsive shock state than the
normal state (Gardner, Click, & Jarvik,
1972). However, the use of the state-
dependent model to explain retroactive am-
nesia requires careful consideration.
There are essentially two different state-
dependent models. The first hypothesis
(DeVietti & Larson, 1971; Nielson, 1968)
assumes the subject learns in the "normal"
physiological state, and the subsequent am-
nestic treatment creates an altered state that
lasts for several days. During this time,
retrieval of information concerning training
should be hampered. The basic problem
with this model is that it predicts spon-
taneous recovery from experimental am-
nesia, an event that is rarely observed (e.g.,
Luttges & McGaugh, 1967). Moreover, if
the altered state is induced prior to acquisi-
tion and amnesia-producing treatment, the
acquired information should be available
from the time of training until the normal
state is reestablished. Miller, Malinowski,
Puk, and Springer (1972) failed to observe
this predicted lack of amnesia on a 24-hour
retention test.
A second version of the state-dependent
hypothesis (Thompson & Grossman, 1972;
Thompson & Neely, 1970) assumes that
the physiological state that must be present
for effective retrieval is the state present
soon after acquisition, presumably the time
during which consolidation occurs according
to this model. Consequently, the memory
is stored in an altered state produced by the
electroconvulsive shock and/or aversive re-
inforcer and from which the animal is as-
sumed to quickly recover. Tests very soon
after electroconvulsive shock do, in fact,
yield evidence of retention consistent with
the model (e.g., McGaugh & Landfield,
1970; Miller & Springer, 1971). Moreover,
 AMNESIA, CONSOLIDATION AND RETRIEVAL
returning the subject to the altered state
shortly before a retention test has been seen
to restore the previously unavailable memory
(Thompson & Neely, 1970). However, the
restoration data supporting this seemingly
successful model have been generated by a
paradigm similar to the one used in the pre-
viously described reminder studies with the
stimuli affecting the return to the altered
state serving as the recovery agent. The
basic distinction between this state-depen-
dent model and the reminder model is
that the state-dependent position predicts
that if the retention test is delayed a day or
more after the animal has been returned to
the altered physiological state for the second
time, memory should once again be unavail-
able. Miller, Malinowski, Puk, and Springer
(1972) examined this prediction and found
that memories once recovered do not fade
again over several days. Moreover, Miller,
Springer, and Vega (1972) found some
effective recovery agents that do not subject
the amnestic animal to the drastic change
in physiological state that scopolamine, foot-
shock, and/or electroconvulsive shock pro-
duce. Consequently, this second version of
the state-dependent hypothesis is also found
to be inadequate. Experimental amnesia
appears to reflect a retrieval failure, but does
not seem to be a dissociated learning phe-
nomenon.
CONCLUSION
The preceding arguments in support of a
retrieval explanation of experimental am-
nesia are not meant to refute the concept of
consolidation but rather to question its appli-
cability to the amnesia data. Assuredly, in-
formation impinging on an organism is initi-
ally represented by electrochemical, neural
transmission. At much later periods of time,
this information is apparently stored in some
energetically passive, structural-chemical for-
mat (as, for example, evidenced by retention
of all but the most recently acquired informa-
tion over a period of extreme hypothermia
and consequent neural-electrical silence
(Lipp, 1964; Riccio, Hodges, & Randall,
1968)). Ignoring the possibility of more
than two states of memory (short-term mem-
ory and long-term memory), if the initial
establishment of the latter state is defined
77
as the time of consolidation, the only serious
question can be what are the temporal pa-
rameters ?
In addition to interfering with retrieval,
electroconvulsive shock may reasonably be
assumed to produce neural-electrical silence
during the subsequent comatose state, or, at
least, to inject sufficient noise into the neural
system to obliterate any information encoded
uniquely in electrochemical transmission
(unconsolidated memory). Therefore all in-
formation surviving electroconvulsive shock,
whether immediately available or observable
only after administration of a recovery agent,
must have already achieved a structural-
chemical format. In view of the recovery
data, this suggests extremely short consoli-
dation times. In fact, Lewis, Miller, and
Misanin (1969) report that under select
circumstances (noncontingent familiarization
with the training environment prior to train-
ing) even a 500-millisecond interval between
training onset and electroconvulsive shock
onset failed to yield amnesia. Lack of am-
nesia following pretraining environmental
familiarization has also been obtained with
hypothermia as the potential amnestic agent
(Jensen & Riccio, 1970). These data argue
for the occurrence of consolidation in inter-
vals of less than 500 milliseconds under these
select circumstances and perhaps more gen-
erally. Such consolidation intervals may
seem extremely short by traditional stan-
dards, but numerous metabolic reactions in
the nervous system are completed in equiva-
lent temporal spans.
One phenomenon not readily understood
in either a consolidation or a retrieval frame-
work is the short post-electroconvulsive
shock interval during which memories ac-
quired immediately prior to electroconvulsive
shock are available (e.g., McGaugh & Land-
field, 1970; Miller & Springer, 1971). Both
the consolidation and retrieval positions
would be satisfied by hypothesizing that elec-
troconvulsive shock either prevents consoli-
dation or future retrieval but does not de-
stroy short-term memory that is seen to be
increasingly attenuated over time due to
either decay or interference. This possi-
bility, however, seems most unlikely if short-
term memory is encoded in electrochemical
neural transmission, for such a format would
78 RALPH R. MILLER AND ALAN D. SPRINGER
be highly vulnerable to electroconvulsive
shock. The retrieval position can generate
at least two more hypotheses. Perhaps there
is an intermediate-term memory stage that
is passive, chemical-structural in format
(hence postconsolidation), and is subject to
decay or interference and consequently of
rather limited size and does not require an
operating catalog system to facilitate re-
trieval. This hypothesis explains the phe-
nomenon, but at the expense of generating
another stage of memory. An alternative
retrieval hypothesis is to assume that re-
trieval processing is established as rapidly
as is consolidation, but the cataloging system
remains vulnerable for some time after its
establishment. If electroconvulsive shock is
delivered during this vulnerable period, the
cataloging system is not immediately im-
paired but is subject to increasing dysfunc-
tion over time. This hypothesis does not
require a third memory stage but appears to
place some rather unlikely constraints on
the cataloging system. Further research is
required to resolve this issue.
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(Received September 11, 1972)