Ltp Outside Of The Hippocampus

BOX 7 Pairing LTP in the amygdala. This figure shows "pairing"-induced LTP in neurons of the basolateral nucleus of the amygdala. The plot shows mean ± SE percent EPSP slope (relative to baseline) in cells treated with 0.1% DMSO vehicle (black squares) before and after LTP induction. Traces from an individual experiment before and 40 minutes after induction are shown in the inset. Traces are averages of five responses. Adapted from Schafe et al. (37).

BOX 7 Pairing LTP in the amygdala. This figure shows "pairing"-induced LTP in neurons of the basolateral nucleus of the amygdala. The plot shows mean ± SE percent EPSP slope (relative to baseline) in cells treated with 0.1% DMSO vehicle (black squares) before and after LTP induction. Traces from an individual experiment before and 40 minutes after induction are shown in the inset. Traces are averages of five responses. Adapted from Schafe et al. (37).

The abundance of literature dedicated to studying LTP in the hippocampus might lead a newcomer to the field to suppose that LTP is somehow restricted to these synapses. However, plasticity of synaptic function, including phenomena such as LTP and LTD, is the rule rather than the exception for most forebrain synapses. LTP outside the hippocampus has been mostly studied in the cerebral cortex and the amygdala (see figure). The likely functional roles for LTP at these other sites are quite diverse, but two specific examples are worth highlighting. LTP-like processes in the cerebral cortex play a role in activity-dependent development of the visual system and other sensory systems. LTP in the amygdala has received prominent attention as a mechanism contributing to cued fear conditioning. The role of LTP in amygdala-dependent fear conditioning in fact is the area for which the strongest case can be made for a direct demonstration of a behavioral role for LTP. It is important to bear in mind through the rest of the book, the next three chapters in particular, that cortical LTP and amygdalar LTP probably exhibit some mechanistic differences from the NMDA receptor-dependent LTP that we will be focusing on. However, in my opinion, the molecular similarities are likely to greatly outweigh the differences.

region. Nevertheless, on short time scales, the spine compartment may serve to localize signaling molecules effectively to a specific synapse. Moreover, molecules tethered to the PSD by scaffolding proteins and the like probably have fairly limited diffusion because the spine compartment will make them tend to rebind at the same PSD as they unbind and rebind. Thus, this spine morphology is likely to be an important component for achieving synaptic specificity in LTP and other forms of synaptic plasticity.

The compartmentalization of molecules by the dendritic spine is not paralleled by an electrical compartmentalization, by and large. At one point, a popular line of thinking was that the shape and properties of the spine neck might regulate the capacity of electrical signals to get to and from the spine head compartment. This idea is no longer considered tenable, and as a first approximation we can assume that the spine membrane potential reflects the local dendritic shaft membrane potential. However, it is likely that electrical compart-mentalization does occur in dendrites, but this is at the level of the various dendritic branches as well as a component contributed by their overall distance from the soma (see reference 25). This introduces the fascinating possibility that local generation and restricted propagation of action potentials within a specific dendritic subregion might be used as a mechanism for generating dendritic branch-specific plasticity.

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