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SECTION III
Central & Peripheral Neurophysiology
CONDITIONED REFLEXES
A classic example of associative learning is a
conditioned re-
flex.
A conditioned reflex is a reflex response to a stimulus that
previously elicited little or no response, acquired by repeatedly
pairing the stimulus with another stimulus that normally does
produce the response. In Pavlov’s classic experiments, the sali-
vation normally induced by placing meat in the mouth of a dog
was studied. A bell was rung just before the meat was placed in
the dog’s mouth, and this was repeated a number of times until
the animal would salivate when the bell was rung even though
no meat was placed in its mouth. In this experiment, the meat
placed in the mouth was the
unconditioned stimulus (US),
the
stimulus that normally produces a particular innate response.
The
conditioned stimulus (CS)
was the bell ringing. After the
CS and US had been paired a sufficient number of times, the CS
produced the response originally evoked only by the US. The CS
had to precede the US. An immense number of somatic, viscer-
al, and other neural changes can be made to occur as condi-
tioned reflex responses.
Conditioning of visceral responses is often called
biofeed-
back.
The changes that can be produced include alterations in
heart rate and blood pressure. Conditioned decreases in blood
pressure have been advocated for the treatment of hyperten-
sion; however, the depressor response produced in this fashion
is small.INTERCORTICAL TRANSFER OF MEMORY
If a cat or monkey is conditioned to respond to a visual stim-
ulus with one eye covered and then tested with the blindfold
transferred to the other eye, it performs the conditioned re-
sponse. This is true even if the optic chiasm has been cut, mak-
ing the visual input from each eye go only to the ipsilateral
cortex. If, in addition to the optic chiasm, the anterior and
posterior commissures and the corpus callosum are sectioned
(“split-brain animal”), no memory transfer occurs. Partial cal-
losal section experiments indicate that the memory transfer
occurs in the anterior portion of the corpus callosum. Similar
results have been obtained in humans in whom the corpus cal-
losum is congenitally absent or in whom it has been sectioned
surgically in an effort to control epileptic seizures. This dem-
onstrates that the neural coding necessary for “remembering
with one eye what has been learned with the other” has been
transferred to the opposite cortex via the commissures. Evi-
dence suggests that similar transfer of information is acquired
through other sensory pathways.WORKING MEMORY
As noted above, working memory keeps incoming informa-
tion available for a short time while deciding what to do with
it. It is that form of memory which permits us, for example, to
look up a telephone number, then remember the number
while we pick up the telephone and dial the number. It con-
sists of what has been called a
central executive
located in the
prefrontal cortex, and two “rehearsal systems:” a
verbal sys-
tem
for retaining verbal memories and a parallel
visuospatial
system
for retaining visual and spatial aspects of objects. The
executive steers information into these rehearsal systems.HIPPOCAMPUS & MEDIAL
TEMPORAL LOBEWorking memory areas are connected to the hippocampus
and the adjacent parahippocampal portions of the medial
temporal cortex (Figure 19–4). In humans, bilateral destruc-
tion of the ventral hippocampus, or Alzheimer disease and
similar disease processes that destroy its CA1 neurons, cause
striking defects in short-term memory, as do bilateral lesions
of the same area in monkeys. Humans with such destruction
have intact working memory and remote memory. TheirFIGURE 19–3
Production of LTP in Schaffer collaterals in the
hippocampus.
Glutamate (Glu) released from the presynaptic neuron
binds to AMPA and NMDA receptors in the membrane of the postsyn-
aptic neuron. The depolarization triggered by activation of the AMPA
receptors relieves the Mg
2+
block in the NMDA receptor channel, and
Ca
2+
enters the neuron with Na
. The increase in cytoplasmic Ca
2+
ac-
tivates calmodulin (CaM), which in turn activates Ca
2+
/calmodulin ki-
nase II (CaM kII). The kinase phosphorylates the AMPA receptors (P),
increasing their conductance, and moves more AMPA receptors into
the synaptic cell membrane from cytoplasmic storage sites. In addi-
tion, a chemical signal (PS) may pass to the presynaptic neuron, pro-
ducing a long-term increase in the quantal release of glutamate.
(Courtesy of R Nicoll.)
Ca2+ Na+Ca2+Mg2+NMDA AMPAGluPSAMPACaM CaM kIIP