We sought to determine if body temperature and energy expenditure are influenced by a cholinergic input to neurons in the rostral raphe pallidus (rRPa), the site of sympathetic premotor neurons controlling brown adipose tissue (BAT) thermogenesis. Nanoinjections of the muscarinic acetylcholine receptor (mAChR) receptor agonist, oxotremorine, or the cholinesterase inhibitor, neostigmine (NEOS), in the rRPa of anaesthetized rats decreased cold‐evoked BAT sympathetic nerve activity (SNA, nadirs: −72%, and −95%), BAT temperature (TBAT, −0.5°C and −0.6°C), expired CO2 (Exp. CO2, −0.3% and −0.5%), and heart rate (HR, −22 bpm and −41 bpm). NEOS into rRPa reversed the increase in BAT SNA evoked by blockade of GABA receptors in rRPa. Nanoinjections of the mAChR antagonist, scopolamine (SCOP), in the rRPa of warm rats increased BAT SNA (peak: +1087%), TBAT (+1.8°C), Exp. CO2 (+0.7%), core temperature (TCORE, +0.5°C), and HR (+54 bpm). SCOP nanoinjections in rRPa produced similar activations of BAT during cold exposure, following a brain transection caudal to the hypothalamus, and during the blockade of glutamate receptors in rRPa. We conclude that a tonically‐active cholinergic input to the rRPa inhibits BAT SNA via activation of local mAChR. The inhibition of BAT SNA mediated by mAChR in rRPa does not depend on activation of GABA receptors in rRPa. The increase in BAT SNA following mAChR blockade in rRPa does not depend on the activity of neurons in the hypothalamus or on glutamate receptor activation in rRPa. This article is protected by copyright. All rights reserved