Glutamic Acid Decarboxylase in Kitten Striate Cortex.
Abstract
Degeneration of the thalamic fibers in the visual cortex of turtles leads to an increase in the numerical density of cortical synapses with flattened vesicles and symmetrical membrane differentiations (Smith and Ebner, 1980). This change correlates with an increase in the cortical activity of glumatic acid decarboxylase (GAD), the synthetic enzyme for GABA. These data are consistent with the hypothesis that removal of thalamic input activity is the stimulus for cortical GABAergic neurons to form new synapses. Pharmacological evidence suggests that even simple environmental deprivation may induce a similar increase in the numerical density of GABAergic synapses in kitten striate cortex (Duffy et al., 1976). We have examined this possibility in monocularly deprived kittens using methods to localize and measure GAD. GAD in kitten striate cortex was localized using immunocytochemistry. These data suggest two conclusions: first, that the numerical density of GABAergic synapses in visual cortex is not regulated directly by thalamic activity; second, that changes in GABAergic synapse density do not account for the ocular dominance shift observed in kitten striate cortex after monocular deprivation (MD).
Document Details
- Document Type
- Technical Report
- Publication Date
- Mar 22, 1985
- Accession Number
- ADA152326
Entities
People
- D. E. Schmechel
- F. F. Ebner
- M. F. Bear
Organizations
- Brown University