Molecules that regulate synaptic plasticity in the hippocampus

Molecules that regulate synaptic plasticity in the hippocampus

S24 SlO-3 MOLECULES THAT REGULATE SYNAPTIC PLASTICITY IN THE HIPPOCAMPUS TOSHIYA MANABE Department of Neurophysiology, Faculty of Medicine, Univers...

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S24

SlO-3

MOLECULES THAT REGULATE SYNAPTIC PLASTICITY IN THE HIPPOCAMPUS

TOSHIYA MANABE Department of Neurophysiology, Faculty of Medicine, University of Tokyo, Bunkyo-ku, Tokyo 113-0033 Synaptic plasticity, represented by long-term potentiation (LTP) in the hippocampus, is thought to underlie some forms of learning and memory. Although the involvement of some molecules, such as NMDA receptors, in LTP induction and expression has been elucidated, it still remains to be shown what other molecules regulate synaptic plasticity in the brain. It had been technically difficult to manipulate the function of some molecules that might be involved in synaptic plasticity. However, the recent development of gene-targeting techniques has made it possible to eliminate specifically the function of a certain molecule of interest by disrupting its gene. Applying the technique to the research on synaptic plasticity, we have identified some unexpected links between synaptic plasticity and some molecules, including receptors, signal transduction molecules and adhesion molecules.

SlO-4

ACTIVITY-DEPENDENT

COOPERATION

AND COMPETITION

BETWEEN

DEVELOPING

RETINOTECTAL

SYNAPSES

MU-MING PO0 Department of Biology-0357.

University

of California

at San Diego.

La Jolla, CA 92093-0357

/II TWOwhole-cell recording from developing Xcrro/,r/.vtectal neurons revealed that convergent

retinotectal

persistent

activity

window

homoSynaptic

potentiated,

while

and heterosynaptic inputs

that

subthreshold

depression depend on activation activity critical tectum

of appropriate

patterns

for activity-dependent

modification

are repetitively inputs

activated

of NMDA-subtype

followin, (r correlated activated within

20 ms before

synaptic

and competition

depressed

receptors and can be readily strenyth

between

and the relative

convergent

synapses underyo

within

a narrow

the spikin g of the tectal

20 ms after the spikin g become

ofglutamate

Thus both the initial cooperation

within

pre- and posts\naptic

neuron

of synaptic

inputs

become

potentiatlon

reversed by subsequent

timing

retinotectal

Both

and

spiking

actl\,ation

in the developing

time

are optic