Accelerated neural network formation in rat cerebral cortex cultures chronically disinhibited with picrotoxin
Our aim was to determine if chronic blockade of GABAergic inhibitory synaptic activity, monitored electrophysiologically at the neuronal level, would affect synapse formation and ultrastructure in dissociated fetal rat cerebral cortex cultures. This was achieved by adding picrotoxin to the serum-fre...
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Published in | Experimental neurology Vol. 97; no. 2; pp. 280 - 288 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Amsterdam
Elsevier Inc
01.08.1987
Elsevier |
Subjects | |
Online Access | Get full text |
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Summary: | Our aim was to determine if chronic blockade of GABAergic inhibitory synaptic activity, monitored electrophysiologically at the neuronal level, would affect synapse formation and ultrastructure in dissociated fetal rat cerebral cortex cultures. This was achieved by adding picrotoxin to the serum-free growth medium in a dose that induced continuous epileptiform discharges throughout the culture period. Light and electron microscopic analysis suggested an accelerated synaptic network formation in the experimental cultures during the first 2 weeks
in vitro. The elimination of excess synapses (mainly on spines), which normally takes place during the fourth week
in vitro, occurred 1 week earlier in the presence of picrotoxin. Finally, the experimental cultures showed smaller spine synapses throughout the entire culture period. Because these effects were opposite those induced by chronic tetrodotoxin-blockade of spontaneous bioelectric activity in a previous study, the underlying causal factor could be the respective intensification and suppression of neuronal activity in the two experiments. An appropriate balance between excitatory and inhibitory synaptic drive seems therefore to be important for normal maturation of neocortical circuitry. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 0014-4886 1090-2430 |
DOI: | 10.1016/0014-4886(87)90089-6 |