Stabilization of thalamo-cortical long-term potentiation by the amygdala: cholinergic and transcription-dependent mechanisms.
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.
Dringenberg
Hans C
HC
Department of Psychology and Centre for Neuroscience Studies, Queen's University, Kingston, Ont., K7L 3N6, Canada. dringenb@psyc.queensu.ca
Kuo
Min-Ching
MC
Tomaszek
Summer
S
D000679:Amygdala / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D000818:Animals; D000841:Anisomycin / Q000494:pharmacology; D004558:Electric Stimulation / Q000379:methods; D019706:Excitatory Postsynaptic Potentials / Q000502:physiology / Q000528:radiation effects; D007839:Functional Laterality; D005829:Geniculate Bodies / Q000502:physiology* / Q000528:radiation effects; D017774:Long-Term Potentiation / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D008297:Male; D018727:Muscarinic Antagonists / Q000494:pharmacology; D009434:Neural Pathways / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D011500:Protein Synthesis Inhibitors / Q000494:pharmacology; D051381:Rats; D020318:Rats, Long-Evans; D011976:Receptors, Muscarinic / Q000502:physiology*; D012601:Scopolamine / Q000494:pharmacology; D013569:Synapses / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D013997:Time Factors; D014158:Transcription, Genetic / Q000502:physiology*; D014793:Visual Cortex / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects
D018727:Muscarinic Antagonists; D011500:Protein Synthesis Inhibitors; D011976:Receptors, Muscarinic; D000841:Anisomycin; D012601:Scopolamine