This talk focuses on the amygdaloid complex, a nucleated
structure of the temporal lobe. Much data suggests that
the amygdala plays a critical role in the expression and
learning of fear responses. Moreover, it is believed that
disturbances in amygdala excitability are responsible
for some human anxiety disorders, such as post-traumatic
stress disorder. The amygdale is comprised of many nuclei.
I will focus on two of them: the basolateral and central
nuclei. The basolateral group receives sensory afferents
and projects to the central nucleus, the main source of
amygdale projections to brainstem nuclei mediating fear
responses. Thus, the basolateral and central nuclei are
seen as the input and output stations of the amygdale,
respectively.
The work I present examines how transmission of sensory
inputs from the basolateral group to the central nucleus
is regulated by a group of inhibitory neurons, known as
the intercalated cell masses. Intercalated neurons receive
excitatory inputs from the basolateral group and in turn
inhibit neurons of the central nucleus. However, because
intercalated neurons are interconnected, the amount of
inhibition they generate in the central nucleus depends
on the timing and nature of sensory inputs. As a result,
the behavioral consequence of sensory events will vary.
I also describe experiments indicating that intercalated
neurons express a form of short-term memory inscribed
in their intrinsic membrane properties. I show that intercalated
neurons express an unusual potassium current that causes
them to modify their excitability as a function of their
recent activity.
The final section of my talk focuses on mechanisms of
synaptic plasticity that is how the brain stores information.
Memory is believed to depend on activity-dependent changes
in the strength of synapses. In part, this view is based
on evidence that the efficacy of synapses can be enhanced
or depressed depending on the timing of pre- and postsynaptic
activity. However, when such plastic synapses are incorporated
in neural network models, stability problems develop because
the potentiation or depression of synapses increases the
likelihood that they will be further strengthened or weakened.
I describe biological evidence for a homeostatic mechanism
that reconciles the apparently opposite requirements of
plasticity and stability. I show that in intercalated
neurons, activity-dependent potentiation or depression
of particular inputs leads to opposite changes in the
strength of inputs ending at other dendritic sites. As
a result, no net change in total synaptic weight occurs
even though the relative strength of inputs is modified.
Thus, in intercalated neurons at least, the total weight
of plastic synapses is conserved by inverse homo vs. heterosynaptic
modifications.
