we found that 5-HT neurons co-release 5-HT and glutamate onto BA neurons in a cell-type-specific and frequency-dependent manner
First-pass extracted concept
5-HT/glutamate cotransmission
Candidate: concept label1 source documents6 linked claims
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Aliases
5-HT and glutamate co-release
Evidence Snippets
Supporting Sources
Linked Claims
Fast-spiking and non-fast-spiking basal amygdala interneurons display differential modulation by glutamate and 5-HT.
Quoted textsource-backed
Interestingly, fast-spiking and non-fast-spiking INs displayed differential modulation by glutamate and 5-HT.
5-HT neurons exert frequency-dependent, cell-type-specific control over basal amygdala circuitry via 5-HT and glutamate co-release to inhibit basal amygdala output.
Quoted textsource-backed
Collectively, these findings suggest that 5-HT neurons exert a frequency-dependent, cell-type-specific control over BA circuitry via 5-HT and glutamate co-release to inhibit the BA output.
5-HT neurons co-release 5-HT and glutamate onto basal amygdala neurons in a cell-type-specific and frequency-dependent manner.
Quoted textsource-backed
We found that 5-HT neurons co-release 5-HT and glutamate onto BA neurons in a cell-type-specific and frequency-dependent manner.
Higher-frequency optical stimulation of 5-HT terminals evokes slow excitation and slow inhibition of basal amygdala interneurons mediated by 5-HT through 5-HT2A and 5-HT1A receptors, respectively.
Quoted textsource-backed
Optical stimulation of 5-HT terminals at higher frequencies (10-20 Hz) evoked both slow excitation and slow inhibition of INs. These effects were mediated by 5-HT because they were blocked by antagonists of 5-HT2A and 5-HT1A receptors, respectively.
Low-frequency optical stimulation of 5-HT terminals evokes short-latency excitation of basal amygdala interneurons that is mediated by glutamate rather than 5-HT.
Quoted textsource-backed
Optical stimulation of 5-HT terminals at low frequencies (≤1 Hz) evoked a short-latency excitation of BA interneurons (INs) ... Pharmacological analysis revealed that this effect was mediated by glutamate and not 5-HT because it was abolished by ionotropic glutamate receptor antagonists.
Optical stimulation of 5-HT terminals does not evoke glutamate release onto basal amygdala principal neurons, but inhibits these cells directly via 5-HT1A receptors and indirectly via enhanced GABA release.
Quoted textsource-backed
optical stimulation of 5-HT terminals did not evoke glutamate release onto BA principal neurons, but inhibited these cells directly via activation of 5-HT1A receptors and indirectly via enhanced GABA release