Abstract
There are cholinergic inputs responsible for pressor responses in the rostral ventrolateral medulla (RVLM) and stimulation of midbrain central gray (CG) increases arterial pressure via activation of neurons in the RVLM. In this study, we examined whether the CG was involved in mediation of the cholinergic inputs to the RVLM. Male Wistar rats were anesthetized, paralyzed, and artificially ventilated. Unilateral microinjection of l-glutamate into the CG produced a pressor response. Microinjection of the muscarinic receptor antagonist scopolamine into the unilateral RVLM inhibited the pressor response to l-glutamate injected ipsilaterally into the CG, whereas microinjection of the cholinesterase inhibitor physostigmine into the RVLM enhanced it. CG stimulation also enhanced the firing rate of RVLM barosensitive neurons and the enhancement of the firing rate was inhibited by scopolamine iontophoretically applied on neurons. CG injection of l-glutamate produced a release of acetylcholine in the RVLM. Unilateral microinjection of l-glutamate into the pedunculopontine tegmental nucleus (PPT) also produced a pressor response, but the pressor response to l-glutamate was not affected by scopolamine injected ipsilaterally into the RVLM. These results provide evidence that the CG but not the PPT is involved in mediation of cholinergic inputs responsible for pressor responses in the RVLM.
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