Adrenocorticotropin Response and Nicotine-Induced Norepinephrine Secretion in the Rat Paraventricular Nucleus Are Mediated through Brainstem Receptors*

Fu, Yongjian; Matta, Shannon G.; Valentine, James D.; Sharp, Burt M.

doi:10.1210/endo.138.5.5122

Cited by 25 publications

(4 citation statements)

References 42 publications

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“…Both nicotine-naïve and regular nicotine users show dose-dependent increases in cortisol, ACTH and prolactin have been reported (see Mello, 2010 for review). Studies of the mechanism in animal models suggest that the effect of nicotine on the HPA axis is primarily through the nicotine-induced release of norepinephrine and CRH in the paraventricular nucleus of the hypothalamus (Fu et al, 1997; Matta et al, 1990; Okada et al, 2003). These collective findings indicate nicotine activates the HPA axis via its direct effects on the catecholaminergic and cholinergic stimulation of the ANS.…”

Section: Acute and Chronic Psychoactive Drug Effects On Peripheral Stmentioning

confidence: 99%

Drug-induced stress responses and addiction risk and relapse

Wemm¹,

Sinha²

2019

Neurobiology of Stress

108

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A number of studies have assessed the effects of psychoactive drugs on stress biology, the neuroadaptations resulting from chronic drug use on stress biology, and their effects on addiction risk and relapse. This review mainly covers human research on the acute effects of different drugs of abuse (i.e., nicotine, cannabis, psychostimulants, alcohol, and opioids) on the hypothalamic-pituitary-adrenal (HPA) axis and the autonomic nervous system (ANS) responses. We review the literature on acute peripheral stress responses in naïve or light recreational users and binge/heavy or chronic drug users. We also discuss evidence of alterations in tonic levels, or tolerance, in the latter relative to the former and associated changes in the phasic stress responses. We discuss the impact of the stress system tolerance in heavy users on their response to drug- and stress-related cue responses and craving as compared to control subjects. A summary is provided of the effects of glucocorticoid responses and their adaptations on brain striatal and prefrontal cortices involved in the regulation of drug seeking and relapse risk. Finally, we summarize important considerations, including individual difference factors such as gender, co-occurring drug use, early trauma and adversity and drug use history and variation in methodologies, that may further influence the effects of these drugs on stress biology.

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Section: Acute and Chronic Psychoactive Drug Effects On Peripheral Stmentioning

confidence: 99%

Drug-induced stress responses and addiction risk and relapse

Wemm¹,

Sinha²

2019

Neurobiology of Stress

108

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“…Nicotine administration into the cerebral aqueduct leads to a dose-dependent increase in NE levels in the PVN, as measured by microdialysis, resulting in release of CRF and ACTH and subsequently affecting release of CORT from the adrenal gland [111,112]. NE is also increased in the PVN of mice self-administering nicotine following active bar presses and this response is desensitized with repeated bar presses [113].…”

Section: Neurochemical Mechanisms Underlying Nicotine's Effects On Emmentioning

confidence: 99%

Effect of nicotine and nicotinic receptors on anxiety and depression

Picciotto

Brunzell²,

Caldarone³

2002

Neuroreport

412

291

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Nicotine has been shown to have effects on anxiety and depression in both human and animal studies. These studies suggest that nicotinic acetylcholine receptors (nAChRs) can modulate the function of pathways involved in stress response, anxiety and depression in the normal brain, and that smoking can result in alterations of anxiety level and mood. The effects of nicotine are complex however, and nicotine treatment can be either anxiolytic or anxiogenic depending on the anxiety model tested, the route of nicotine administration and the time course of administration. The paradoxical effects of nicotine on emotionality are likely due to the broad expression of nAChRs throughout the brain, the large number of nAChR subtypes that have been identified and the ability of nicotine treatment to both activate and desensitize nAChRs. Activation of nAChRs has been shown to modulate many systems associated with stress response including stress hormone pathways, monoaminergic transmission and release of classical neurotransmitters throughout the brain. Local administration studies in animals have identified brain areas that may be involved in the anxiogenic and anxiolytic actions of nicotine including the lateral septum, the dorsal raphe nuclei, the mesolimbic dopamine system and the hippocampus. The ensemble of studies to date suggest that under certain conditions nicotine can act as an anxiolytic and an antidepressant, but that following chronic use, adaptations to nicotine can occur resulting in increased anxiety and depression following withdrawal.

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“…Interestingly, the systemic effects of nicotine on the HPA are blocked both by lesions of hindbrain CA neurons and by antagonism of adrenoreceptors in the hypothalamus (59), suggesting hindbrain CA neurons to be important mediators of nicotine's actions. Consistent with this hypothesis, injections of nicotine directly into the NTS increases norepinephrine (NE) release in the paraventricular hypothalamus (PVH) and amygdala (103), and the effect of systemic nicotine to release NE is blocked by nAChR antagonists applied to the fourth ventricle (34). However, the underlying mechanisms by which nicotine controls the activity of NTS-CA neurons are unknown.…”

Section: Introductionmentioning

confidence: 97%

“…It acts at nicotinic acetylcholine receptors (nAChRs), ligand-gated ion channels whose endogenous neurotransmitter is acetylcholine (ACh). In addition to modulating reward, nicotine also stimulates a stress response, modulates cardiovascular and gastric reflexes, inhibits food intake, and reduces body weight (3,12,30,34,40,49,81,92), all behaviors and reflexes influenced by neurons in the nucleus of the solitary tract (NTS) in the hindbrain (1,10,38,60,63,77,79,84,91,95). The peripheral effects of nicotine on the hypothalamic-pituitary-adrenal (HPA) axis are blocked by nAChR antagonists injected into the hindbrain (59).…”

Section: Introductionmentioning

confidence: 99%

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

Page

Zhu

Appleyard

2019

American Journal of Physiology-Regulatory, Integrative and Comp

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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.

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Adrenocorticotropin Response and Nicotine-Induced Norepinephrine Secretion in the Rat Paraventricular Nucleus Are Mediated through Brainstem Receptors*

Cited by 25 publications

References 42 publications

Drug-induced stress responses and addiction risk and relapse

Drug-induced stress responses and addiction risk and relapse

Effect of nicotine and nicotinic receptors on anxiety and depression

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

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