Effect of chronic administration of nicotine on acetylcholinesterase activity in the hypothalamus and medulla oblongata of the rat brain. An ultrastructural study

Chang, Ping-Lung; Bhagat, B.

doi:10.1016/0006-8993(73)90035-8

Cited by 16 publications

(5 citation statements)

References 13 publications

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“…2). The present findings are correlated with the study demonstrating a significant decrease in AChE activity in the rat brain after chronic exposure to Nic [37]. Neither in the frontal cortex nor in the hippocampus there was a significant difference in ChAT levels at both time points in the Nic group.…”

Section: Discussionsupporting

confidence: 91%

Effects of Systemic Nicotine, Alcohol or Their Combination on Cholinergic Markers in the Frontal Cortex and Hippocampus of Rat

et al. 2010

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Acute alcohol (Alc) intoxication has been shown to decrease choline acetyltransferase (ChAT) in the rat brain. The present study extends that finding by examining the effects of nicotine (Nic), Alc, and their combination on ChAT and acetylcholinesterase (AChE) in the frontal cortex and hippocampus of rat. The samples were collected at 30 and 120 min after intraperitoneal administration of saline (0.9%, control), Nic (1 mg/kg), Alc (1 g/kg), and Nic + Alc and analyzed by RT-PCR, Western blot and colorimetry. Alc alone considerably reduced ChAT mRNA expression, whereas Nic alone decreased AChE mRNA expression. In contrast, Nic + Alc exposure had resulted in no significant change in the parameters. These findings are consistent with the results of the Western blot and AChE activity analysis. The results, therefore, indicate that Nic and Alc alone may interact with the central cholinergic system. This interactive effect may contribute to a frequent association of tobacco and Alc consumption.

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Section: Discussionsupporting

confidence: 91%

Effects of Systemic Nicotine, Alcohol or Their Combination on Cholinergic Markers in the Frontal Cortex and Hippocampus of Rat

et al. 2010

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“…Increased nicotinic receptor activation during sleep may provide the only excitatory mechanism capable of counteracting or attenuating the numerous factors that combine to reduce XII motoneuron excitability and airway tone during sleep. Attenuation of the excitatory nicotinic effect by prenatal nicotine exposure, through upregulation (Pauly et al 1991) of desensitized nicotine receptors (Peng et al 1994), reduced ACh synthesis (Zahalka et al 1992) and increased acetylcholinesterase activity (Chang et al 1973; Mizobe & Livett, 1983), may increase vulnerability of the airway to occlusion and contribute to the increased apnoea observed in nicotine‐exposed animals in vivo .…”

Section: Discussionmentioning

confidence: 99%

Prenatal nicotine exposure increases apnoea and reduces nicotinic potentiation of hypoglossal inspiratory output in mice

Robinson

Peebles

Kwok

et al. 2002

The Journal of Physiology

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We examined the effects of in utero nicotine exposure on postnatal development of breathing pattern and ventilatory responses to hypoxia (7.4 % O2) using whole‐body plethysmography in mice at postnatal day 0 (P0), P3, P9, P19 and P42. Nicotine delayed early postnatal changes in breathing pattern. During normoxia, control and nicotine‐exposed P0 mice exhibited a high frequency of apnoea (fA) which declined by P3 in control animals (from 6.7 ± 0.7 to 2.2 ± 0.7 min−1) but persisted in P3 nicotine‐exposed animals (5.4 ± 1.3 min−1). Hypoxia induced a rapid and sustained reduction in fA except in P0 nicotine‐exposed animals where it fell initially and then increased throughout the hypoxic period. During recovery, fA increased above control levels in both groups at P0. By P3 this increase was reduced in control but persisted in nicotine‐exposed animals. To examine the origin of differences in respiratory behaviour, we compared the activity of hypoglossal (XII) nerves and motoneurons in medullary slice preparations. The frequency and variability of the respiratory rhythm and the envelope of inspiratory activity in XII nerves and motoneurons were indistinguishable between control and nicotine‐exposed animals. Activation of postsynaptic nicotine receptors caused an inward current in XII motoneurons that potentiated XII nerve burst amplitude by 25 ± 5 % in control but only 14 ± 3 % in nicotine‐exposed animals. Increased apnoea following nicotine exposure does not appear to reflect changes in basal activity of rhythm or pattern‐generating networks, but may result, in part, from reduced nicotinic modulation of XII motoneurons.

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“…Here, we present data showing N + OC exposure causes accumulation of FFA, PC, and acetylcholine in female rat brains (Figure 7). Since nicotine is a neuronal nicotinic acetylcholine receptor (nAChR) agonist and is also known to decrease acetylcholinesterase activity, the metabolomic data furthermore confirm this well-established fact by showing that N alone or in combination with OC significantly increases the levels of acetylcholine in the brain of female rats [33].…”

mentioning

confidence: 61%

The Impact of Nicotine along with Oral Contraceptive Exposure on Brain Fatty Acid Metabolism in Female Rats

Patel

Timón‐Gómez

Pradhyumnan

et al. 2022

IJMS

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Smoking-derived nicotine (N) and oral contraceptive (OC) synergistically exacerbate ischemic brain damage in females, and the underlying mechanisms remain elusive. In a previous study, we showed that N + OC exposure altered brain glucose metabolism in females. Since lipid metabolism complements glycolysis, the current study aims to examine the metabolic fingerprint of fatty acids in the brain of female rats exposed to N+/−OC. Adolescent and adult Sprague–Dawley female rats were randomly (n = 8 per group) exposed to either saline or N (4.5 mg/kg) +/−OC (combined OC or placebo delivered via oral gavage) for 16–21 days. Following exposure, brain tissue was harvested for unbiased metabolomic analysis (performed by Metabolon Inc., Morrisville, NC, USA) and the metabolomic profile changes were complemented with Western blot analysis of key enzymes in the lipid pathway. Metabolomic data showed significant accumulation of fatty acids and phosphatidylcholine (PC) metabolites in the brain. Adolescent, more so than adult females, exposed to N + OC showed significant increases in carnitine-conjugated fatty acid metabolites compared to saline control animals. These changes in fatty acyl carnitines were accompanied by an increase in a subset of free fatty acids, suggesting elevated fatty acid β-oxidation in the mitochondria to meet energy demand. In support, β-hydroxybutyrate was significantly lower in N + OC exposure groups in adolescent animals, implying a complete shunting of acetyl CoA for energy production via the TCA cycle. The reported changes in fatty acids and PC metabolism due to N + OC could inhibit post-translational palmitoylation of membrane proteins and synaptic vesicle formation, respectively, thus exacerbating ischemic brain damage in female rats.

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Effect of chronic administration of nicotine on acetylcholinesterase activity in the hypothalamus and medulla oblongata of the rat brain. An ultrastructural study

Cited by 16 publications

References 13 publications

Effects of Systemic Nicotine, Alcohol or Their Combination on Cholinergic Markers in the Frontal Cortex and Hippocampus of Rat

Effects of Systemic Nicotine, Alcohol or Their Combination on Cholinergic Markers in the Frontal Cortex and Hippocampus of Rat

Prenatal nicotine exposure increases apnoea and reduces nicotinic potentiation of hypoglossal inspiratory output in mice

The Impact of Nicotine along with Oral Contraceptive Exposure on Brain Fatty Acid Metabolism in Female Rats

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