Stabilization of thalamo‐cortical long‐term potentiation by the amygdala: cholinergic and transcription‐dependent mechanisms

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Abstract
Synaptic potentiation allows neurons to enhance excitability and store information for extended time periods. We examined the role of the amygdaloid complex, known to facilitate long‐term memory encoding, to influence synaptic strength at thalamo‐cortical synapses. In urethane‐anaesthetized rats, theta‐burst stimulation of the dorsal lateral geniculate nucleus of the thalamus induced early phase (1–2 h) long‐term potentiation (LTP) of the field postsynaptic potential (fPSP) recorded in the ipsilateral primary visual cortex. Electrical stimulation (100 Hz) of the amygdala 5 min after thalamic stimulation converted early phase LTP to stable late‐phase (> 4 h) LTP. This effect was not correlated with the degree of electrocorticographic activation of V1 induced by amygdala stimulation. Amygdala stimulation without thalamic theta‐burst stimulation did not change thalamo‐cortical fPSPs. The centrally acting cholinergic‐muscarinic receptor antagonist scopolamine (1 mg/kg, i.p.), but not peripherally acting methyl‐scopolamine, completely blocked the amygdala‐induced conversion of early to late‐phase thalamo‐cortical LTP. Further, ventricular application of the transcription inhibitor anisomycin (250 µg) reduced amygdala‐induced late‐phase LTP induction. These results demonstrate that the amygdaloid complex transforms time‐limited synaptic enhancement of thalamo‐cortical transmission into long lasting increases in synaptic strength. These processes are mediated, at least in part, by cholinergic and transcription‐dependent mechanisms. These amygdaloid‐induced effects provide a potential mechanism underlying long‐term enhancement of sensory transmission and information encoding in thalamo‐cortical networks.