Amygdala beta-noradrenergic influence on hippocampal long-term potentiation in vivo.
We have previously shown that hippocampal long-term potentiation (LTP), one form of synaptic plasticity that may underlie learning and memory, is attenuated by blocking neuron activity of the basolateral amygdala (BLA). In the present study we investigated the amygdala noradrenergic or cholinergic contribution to hippocampal LTP formation. When propranolol, a beta-adrenoceptor antagonist, was injected into the BLA 10 min before tetanus, the formation of LTP in the perforant path-dentate granule cell synapses was significantly impaired. Scopolamine, a muscarinic cholinergic receptor antagonist, did not affect the formation of LTP. These results suggest that amygdala beta-noradrenergic activity plays a critical role in modulation of hippocampal LTP.
Ikegaya
Y
Y
Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, University of Tokyo, Japan.
Nakanishi
K
K
Saito
H
H
Abe
K
K
D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D000679:Amygdala / Q000502:physiology*; D000818:Animals; D006624:Hippocampus / Q000502:physiology*; D017774:Long-Term Potentiation; D008297:Male; D018727:Muscarinic Antagonists / Q000494:pharmacology*; D011433:Propranolol / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D012601:Scopolamine / Q000494:pharmacology
D000319:Adrenergic beta-Antagonists; D018727:Muscarinic Antagonists; D011433:Propranolol; D012601:Scopolamine