RESUMO
Classical conditioning of the nictitating membrane response in rabbits is a well defined model of cerebellar-dependent motor memory. This memory undergoes a period of consolidation after the training session, when it is sensitive to reversible inactivations of the cerebellar cortex, but not of the cerebellar nuclei, with the GABA(A) receptor agonist muscimol. Here, the temporal properties of this cerebellar cortex-dependent consolidation were examined using delayed infusions of muscimol in cortical lobule HVI. Cortical infusions delayed by 5 or 45 min after a conditioning session produced significant and very similar impairments of consolidation, but infusions delayed by 90 min produced little or no impairment. Behavioral measures indicate that the muscimol infusions produced significant effects after approximately 30 min and they lasted for a few hours. So, over a time window beginning approximately 1 hr after the end of the training session and closing 1 hr after that, intracortical activity is critical for consolidation of this motor memory.
Assuntos
Cerebelo/fisiologia , Memória/fisiologia , Animais , Autorradiografia , Comportamento Animal/efeitos dos fármacos , Comportamento Animal/fisiologia , Cateterismo , Cerebelo/efeitos dos fármacos , Condicionamento Clássico/efeitos dos fármacos , Condicionamento Clássico/fisiologia , Condicionamento Palpebral/efeitos dos fármacos , Condicionamento Palpebral/fisiologia , Infusões Parenterais , Aprendizagem/efeitos dos fármacos , Masculino , Memória/efeitos dos fármacos , Muscimol/farmacocinética , Muscimol/farmacologia , Membrana Nictitante/fisiologia , Coelhos , Tempo de Reação/fisiologia , Fatores de TempoRESUMO
Several forms of motor learning, including classical conditioning of the eyeblink and nictitating membrane response (NMR), are dependent upon the cerebellum, but it is not known how motor memories are stored within the cerebellar circuitry. Localized infusions of the GABA(A) agonist muscimol were used to target putative consolidation processes by producing reversible inactivations after NMR conditioning sessions. Posttraining inactivations of eyeblink control regions in cerebellar cortical lobule HVI completely prevented conditioning from developing over four sessions. In contrast, similar inactivations of eyeblink control regions in the cerebellar nuclei allowed conditioning to develop normally. These findings provide evidence that there are critical posttraining memory consolidation processes for eyeblink conditioning mediated by the cerebellar cortex.