Presynaptic α4β2 Nicotinic Acetylcholine Receptors Increase Glutamate Release and Serotonin Neuron Excitability in the Dorsal Raphe Nucleus
Dorsal raphe nucleus
Serotonergic cell groups
DOI:
10.1523/jneurosci.0941-12.2012
Publication Date:
2012-10-24T16:44:19Z
AUTHORS (7)
ABSTRACT
Several behavioral effects of nicotine are mediated by changes in serotonin (5-HT) release brain areas that receive serotonergic afferents from the dorsal raphe nucleus (DRN). In vitro experiments have demonstrated increases firing activity majority DRN 5-HT neurons and contains nicotinic acetylcholine receptors (nAChRs) located at both somata presynaptic elements. One most common is to increase glutamate release. Although receives profuse glutamatergic afferents, effect on has not been studied detail. Using whole-cell recording techniques, we investigated input rat midbrain slices. Low concentrations, presence bicuculline tetrodotoxin (TTX), increased frequency but did change amplitude glutamate-induced EPSCs, recorded identified neurons. Nicotine-induced EPSC persisted 10–20 min after drug withdrawal. This was mimicked exogenous administration (ACh) or inhibition ACh metabolism. addition, nicotine-induced abolished blockade α4β2 nAChRs, voltage-gated calcium channels, intracellular signaling α7 nAChR antagonists. These data suggest endogenous can through activation nAChRs DRN. The involves long-term synaptic function, it dependent channels stores.
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