Abstract:
: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.
journal_name
Neuroreportjournal_title
Neuroreportauthors
Ikegaya Y,Nakanishi K,Saito H,Abe Kdoi
10.1097/00001756-199709290-00027subject
Has Abstractpub_date
1997-09-29 00:00:00pages
3143-6issue
14eissn
0959-4965issn
1473-558Xjournal_volume
8pub_type
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