Electrical brain stimulation

Electrical brain stimulation (EBS), also referred to as focal brain stimulation

(FBS), is a form of electrotherapy used as a technique in research and clinical
neurobiology to stimulate a neuron or neural network in the brain through
the direct or indirect excitation of its cell membrane by using an electric
current. It is used for research or for therapeutic purposes.

Electrical brain stimulation (EBS) is a routine clinical practice during

surgical evaluation of patients with epilepsy and resection of special cases of
brain tumor. During EBS, a volley of electrical discharges is delivered directly
to several brain regions of interest in awake human subjects to map their
functional involvement in sensation and movement, or cognitive functions
such as language and memory. On the basis of functional mapping of the
brain, the clinician draws a plan for the resection of the involved brain tissue
without causing major sensorimotor or cognitive impairments. Electrical
brain stimulation can be considered a useful tool for functional mapping in
the human brain. Contrary to most neuroimaging studies, which do not
probe directly the necessity of a given brain region in a particular cognitive
function, EBS can provide direct observations about the necessity of the
stimulated region for the perceptual or behavioral function that is being
studied. In fact, prior to neuroimaging era, the EBS was the only source of
observations about the human mind when conscious patients described
various experiential phenomena during the electrical stimulation of their
brain. The classical EBS studies provided the most direct evidence about the
localization of functions in the human brain. The map of somatosensory
homunculus in the primary sensory cortex is a prime example of this
(Penfield and Boldrey, 1937; Penfield, 1958, 1972). The classical EBS studies
(Penfield and Jasper, 1954) also revealed a wealth of information about the
potential involvement of each cortical region in a facet of human conscious
experience. Many of these early reports are no longer easily accessible, and
to our knowledge, an overview of those classical or most recent EBS reports
is missing from the current neuroscience literature. Such an overview would
be helpful for various reasons. For instance, it would provide additional layer
of information about the functional involvement of a given brain region in
perceptual or behavioral functions. For example, the observations about
laughter induced by stimulation of a given brain structure could help the
interested scientist sketch a plausible neuroanatomical map of the brain
circuitry involved in emotional expression. Moreover, a comprehensive map
of old and new EBS studies could provide useful data about the possible
involvement of a brain region in the genesis of a particular set of illusions,
hallucinations, delusional ideations and automatic behavior experienced by
patients with psychiatric disorders. I
Chemical brain stimulation
chemical brain stimulation technique that proved to be helpful in cases in
which the behavior pattern to be studied electrophysiologically is difficult to
elicit repetitively by external stimuli, but is easily obtained by brain
stimulation. The advantage of this technique over electrical elicitation of the
behavior is the avoidance of periodic stimulation artefacts that make detailed
analyses of pattern-correlated neuronal activity often impracticable.

Chemical Brain
Neurotransmission- transmitting information across a chemical synapse
It has 4 steps:
1) Neurotransmitter synthesis and storage
2) Neurotransmitter release
3) Receptor binding
4) Neurotransmitter deactivation

In Deatails
1) Neurotransmitter synthesis and storage Neurotransmitters are synthesised in the
soma and are transported to the axon terminal along microtubules Other
neurotransmitters synthesised in the axon terminal
In the axon terminal, all neurotransmitters are stored in vesicles Vesicles are
phospholipid bilayer compartments

2) Neurotransmitter release
When action potential reaches axon terminal, voltage changes on the presynaptic
membrane set off a series of processes to release neurotransmitter held in vesicles
into the synaptic cleft. Presynaptic membrane has many voltage sensitive calcium
channels which open in response to the membrane voltage change

Opening of CA2+ channel causes an influx of CA2+ into the axon terminal

CA2+ binds to a protein calmodulin which causes vesicles to move into the presynaptic
membrane The vesicle fuse with the presynaptic membrane to release their contents
into the synaptic cleft= exocytosis

3) Receptor Binding
Released neurotransmitter diffuses across synaptic cleft, binds with specialised
receptors that are embedded in the postsynaptic membrane

Receptors only bind specific neurotransmitters (certain neurotransmitters fit certain

types of receptors like a lock and key)

The receptors can be ion channels (ionotropic receptors) or proteins that don’t have a
pore for ions but instead initiate a cascade of chemical reactions (metabotropic
receptors)

Receptor Binding- 3 effects receptor binding can have on the postsynaptic membrane
Depolarisation of postsynaptic membrane- excite the postsynaptic neuron
Hyperpolarisation of postsynaptic membrane- inhibits postsynaptic neuron Initiate
modulatory chemical reactions that will indirectly produce excitation or inhibition of the
postsynaptic neuron

4) Neurotransmitter deactivation
Neurotransmitter in the synaptic cleft must be removed to stop the occupation and
stimulation of receptions
Deactivation can happen in 5 ways:
Diffusion- some of the neurotransmitter diffuses away from the synaptic cleft
Degradation- Enzymes in the synaptic cleft break down neurotransmitters. The
components are then returned to the axon terminal to be recycled back into
neurotransmitter
Re-uptake- Transporters on the presynaptic membrane bind neurotransmitters and
return them to the presynaptic terminal for re-use
Autoreceptor binding- Receptors on the presynaptic membrane bind
neurotransmitters that inhibit their further release Glial Uptake- Neurotransmitters can
be taken up by nearby glial cells which can be returned to the axon termina