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.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Nagano Y,Kaneda K,Maruyama C,Ide S,Kato F,Minami Mdoi
10.1016/j.neulet.2015.05.059subject
Has Abstractpub_date
2015-07-23 00:00:00pages
56-61eissn
0304-3940issn
1872-7972pii
S0304-3940(15)00426-7journal_volume
600pub_type
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