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 micro g) 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.