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. 2018 Aug 17;175(19):3773–3783. doi: 10.1111/bph.14447

Figure 4.

Figure 4

Schematic representation illustrating the local mechanisms by which NO released from nNOS into the BNST modulates the cardiovascular responses to restraint stress. (Inhibitory mechanism) The red dotted arrows indicate the pathway related to the predominant inhibitory influence of BNST nitrergic neurotransmission in the control of cardiovascular responses to restraint. The NO synthesized by nNOS stimulates the release of noradrenaline which in turn facilitates local GABA release via activation of α1‐adrenoceptors in GABAergic terminals. The GABA evokes inhibitory postsynaptic currents (IPSCs) via activation of the GABAA receptor. (Facilitatory mechanism) The blue arrows indicate the facilitatory pathway of nitrergic neurotransmission in the BNST in controlling the cardiovascular responses to restraint stress. The NO synthesized by nNOS is a prominent signalling mechanism involved in the effects of NMDA receptor activation (yellow channel). The thickness of the arrows indicates the predominance of the pathways (i.e. inhibitory and facilitatory mechanism). See text for further details.