Corticotropin-releasing factor enhances inhibitory synaptic transmission to type III neurons in the bed nucleus of the stria terminalis. (23rd July 2015)

• Record Type: Journal Article
• Authors: Nagano, Yusuke; Kaneda, Katsuyuki; Maruyama, Chikashi; Ide, Soichiro; Kato, Fusao; Minami, Masabumi
• Is Part Of: Neuroscience letters. Volume 600(2015)
• Page Start: 56
• Page End: 61
• Publication Date: 2015-07-23
• Subjects: BNST bed nucleus of the stria terminalis -- vBNST ventral part of the bed nucleus of the stria terminalis -- dlBNST dorsolateral part of the bed nucleus of the stria terminalis -- CRF corticotropin-releasing factor -- NPY neuropeptide Y -- IPSC inhibitory postsynaptic current -- GABA gamma-aminobutyric acid -- KYN kynurenic acid -- TTX tetrodotoxin -- NMDG N-methyl-d-glucamine -- HEPES 2-[4-(2-hydroxyethyl)-1-piperazinyl]ethanesulfonic acid -- VTA ventral tegmental area; Bed nucleus of the stria terminalis -- Corticotropin-releasing factor -- Emotion -- Extended amygdala -- GABAergic -- IPSC; Neurology -- Periodicals; Neurology -- Periodicals; Research -- Periodicals; Neurologie -- Périodiques; Neuroanatomie -- Périodiques; Neuropharmacologie -- Périodiques; Neurophysiologie -- Périodiques; Neurology; Periodicals; Electronic journals; 617.48
• DOI: 10.1016/j.neulet.2015.05.059
• Languages: English
• ISSNs: 0304-3940

Abstract

Highlights: The effects of CRF on type III dlBNST neurons were examined. CRF increased the frequency and amplitude of sIPSC. CRF failed to increase the frequency and amplitude of mIPSC. CRF enhances inhibitory synaptic transmission to type III neurons in dlBNST. Abstract: We previously reported that corticotropin-releasing factor (CRF) increased neuronal excitability specifically in type II neurons of the dorsolateral part of the bed nucleus of the stria terminalis (dlBNST). Because the majority of type II dlBNST neurons are thought to be GABAergic interneurons, at least a portion of which are considered to regulate type III dlBNST neurons, it is possible that CRF increases inhibitory input to type III neurons through the activation of type II neurons in the dlBNST. To test this possibility, we examined the effect of CRF on type III dlBNST neurons using whole-cell voltage-clamp recordings of inhibitory postsynaptic currents (IPSCs) from rat BNST slices in the presence of kynurenic acid. Spontaneous IPSCs (sIPSCs) and miniature IPSCs (mIPSCs) were recorded in the absence and presence of tetrodotoxin, respectively. Bath application of CRF significantly increased the frequency of sIPSCs, indicating that CRF enhances the inhibitory input to type III neurons. CRF application failed to increase the frequency of mIPSCs, suggesting that CRF-induced increases in sIPSCs are dependent on action potentials. Combined with our previous finding that CRF specifically depolarizes type II dlBNST neurons, these results suggest that CRF may attenuate type III neuron excitation by augmenting the inhibitory influence of type II neurons in the dlBNST.