Effects of acute and chronic nicotine on catecholamine neurons of the nucleus of the solitary tract

Abstract

Nicotine is an addictive drug that has broad effects throughout the brain. One site of action is the nucleus of the solitary tract (NTS), where nicotine initiates a stress response and modulates cardiovascular and gastric function through nicotinic acetylcholine receptors (nAChRs). Catecholamine (CA) neurons in the NTS influence stress and gastric and cardiovascular reflexes, making them potential mediators of nicotine’s effects; however nicotine’s effect on these neurons is unknown. Here, we determined nicotine’s actions on NTS-CA neurons by use of patch-clamp techniques in brain slices from transgenic mice expressing enhanced green fluorescent protein driven by the tyrosine hydroxylase promoter (TH-EGFP). Picospritzing nicotine both induced a direct inward current and increased the frequency of spontaneous excitatory postsynaptic currents (sEPSCs) in NTS-CA neurons, effects blocked by nonselective nAChR antagonists TMPH and MLA. The increase in sEPSC frequency was mimicked by nAChRα7 agonist AR-R17779 and blocked by nAChRα7 antagonist MG624. AR-R17779 also increased the firing of TH-EGFP neurons, an effect dependent on glutamate inputs, as it was blocked by the glutamate antagonist NBQX. In contrast, the nicotine-induced current was mimicked by nAChRα4β2 agonist RJR2403 and blocked by nAChRα4β2 antagonist DHβE. RJR2403 also increased the firing rate of TH-EGFP neurons independently of glutamate. Finally, both somatodendritic and sEPSC nicotine responses from NTS-CA neurons were larger in nicotine-dependent mice that had under gone spontaneous nicotine withdrawal. These results demonstrate that 1) nicotine activates NTS-CA neurons both directly, by inducing a direct current, and indirectly, by increasing glutamate inputs, and 2) NTS-CA nicotine responsiveness is altered during nicotine withdrawal.

Differences in Hemodynamic Status in Users of Tobacco Cigarettes and E-Cigarettes

“…It acts on nicotinic acetylcholine receptors (nAChRs), ligandgated ion channels whose endogenous neurotransmitter is acetylcholine (ACh). The influence of nicotine reaches the Nucleus Tractus Solitary (NTS) which works as the center of the human cardiovascular system located in the hindbrain [24]. Initially nicotine will be absorbed through the mouth and throat and will enter the pulmonary venous circulation, then enter the arterial circulation and travel to the brain through the blood-brain barrier.…”

Evaluation of c-reactive protein level, antioxidant and acetylcholinesterase enzyme activities among snuff users

“…Nicotine can act as an adrenergic agonist by mediating the release of catecholamine, angiotensinogen (and angiotensin in its active form) and vasopressin (and aldosterone) leading to vasoconstriction and thus increase blood pressure (Page et al, 2019). 5 As a consequence, an increase in catecholamine may lead to cardiac dysfunction (Page et al, 2019). 5 This result tallies with the research conducted by Hergens et al, (2008) 6 who discovered that there is an increased risk of hypertension among Swedish male snuff users (Hergens et al, 2008).…”

Prevalence and factors associated with electrocardiographic abnormalities among adults attending Methadone Assisted Therapy in Dodoma, central Tanzania

“…Another factor that predicted sinus bradycardia was cigarette smoking, an observation that could be attributed to nicotine which is the main constituent of cigarettes and is a potent blocker of the cardiac A-Type K + channels, which causeeffect on cardiac physiology (59). While nicotine is thought to stimulate catecholamine release by activating nicotine acetylcholine receptors in peripheral postganglionic sympathetic nerve ending and adrenal medulla leading to cardiac tachycardia (60,61), a paradoxical effect of nicotine through its effect on A-type K + leading to bradycardia has also been observed (59).…”