Abstract:
:Brain functions are based on the dynamic interaction of excitatory and inhibitory inputs. Spillover of glutamate from excitatory synapses may diffuse to and modulate nearby inhibitory synapses. By recording unitary inhibitory postsynaptic currents (uIPSCs) from cell pairs in CA1 of the hippocampus, we demonstrated that low concentrations of Kainate receptor (KAR) agonists increased the success rate (P(s)) of uIPSCs, whereas high concentrations of KAR agonists depressed GABAergic synapses. Ambient glutamate released by basal activities or stimulation of the stratum radiatum increases the efficacy of GABAergic synapses by activating presynaptic KARs, which facilitate Ca(2+)-dependent GABA release. The results suggest that glutamate released from excitatory synapses may also function as an intermediary between excitatory and inhibitory synapses to protect overexcitation of local circuits.
journal_name
Neuronjournal_title
Neuronauthors
Jiang L,Xu J,Nedergaard M,Kang Jdoi
10.1016/s0896-6273(01)00298-7subject
Has Abstractpub_date
2001-05-01 00:00:00pages
503-13issue
2eissn
0896-6273issn
1097-4199pii
S0896-6273(01)00298-7journal_volume
30pub_type
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