A variety of experiments suggest that glutamate receptors are important in sensory-dependent plasticity in the visual cortex. The signals for sensory-dependent plasticity are carried to the cortex by electrical activity, which releases glutamate in the cortex. Glutamate activates NMDA, AMPA/kainate and metabotropic glutamate receptors. The importance of NMDA receptors is suggested by evidence that (i) antagonists to NMDA receptors reduce plasticity; (ii) NMDA receptors are most abundant at the peak of the critical period for sensory-dependent plasticity; (iii) the functional contribution of NMDA receptors to the visual response is reduced during the critical period; and (iv) rearing in the dark postpones the change in the NMDA contribution to the visual response, just as it postpones other events in sensory-dependent plasticity. This proposal will evaluate the mechanisms by which the function of NMDA receptors changes during the critical period for sensory-dependent plasticity. Less is known about metabotropic glutamate receptors, and how their influence changes during the critical period. This proposal will evaluate the contribution that metabotropic glutamate receptors make to the visual response, and how this is altered during development. Metabotropic glutamate receptors affect K+ channels, Ca++ channels, and second messengers. The proposal will also test the action of metabotropic glutamate receptors on the second messenger cAMP: which metabotropic receptor activates it, whether the activation follows the time course of the critical period, and how the activation is affected by rearing in the dark.
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