Figure 8: Mechanistic model of increased anxiety during nicotine withdrawal. | Nature Communications

Figure 8: Mechanistic model of increased anxiety during nicotine withdrawal.

From: Increased CRF signalling in a ventral tegmental area-interpeduncular nucleus-medial habenula circuit induces anxiety during nicotine withdrawal

Figure 8

(a) The IPN receives glutamatergic input (Glu) from the MHb. Chronic nicotine induces CRF synthesis in a population of VTA DAergic neurons41 that innervate the ventral IPN including the IPI. In addition, chronic nicotine increases expression of the CRF1 receptor in type II neurons of the IPI. (b) During nicotine withdrawal, CRF from the VTA is released and activates the upregulated CRF1 receptors on Type II IPI neurons, increasing signalling (speaker icon) and amplitude of sEPSCs (presumably through NMDA/AMPA receptors). CRF also increases sEPSC frequency indicating increased glutamate release, which stems from MHb inputs. We speculate that MHb terminals may also express the CRF1 receptor, which would underlie increased glutamate release during withdrawal.

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