scholarly journals Fetal and Postnatal Nicotine Exposure Modifies Maturation of Gonocytes to Spermatogonia in Mice

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Rosa María Vigueras-Villaseñor ◽  
Martín Alejandro Fuentes-Cano ◽  
Margarita Chávez Saldaña ◽  
Liliana Rivera Espinosa ◽  
Rafael Reynoso-Robles ◽  
...  
Keyword(s):  
Germ Cells ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Testicular Tissue ◽  
Male Offspring ◽  
Laboratory Animals ◽  
Nicotine Exposure ◽  
Tissue Samples ◽  
Nicotine Administration ◽  
Immunohistochemical Studies

Studies in laboratory animals have shown that male offspring from dams, exposed to nicotine during pregnancy and postnatal periods, show alterations in fertility, although the origin of this is still uncertain. In this study, we examined in a mouse model if the process of gonocyte maturation to spermatogonia was affected in male offspring from dams with nicotine administration during pregnancy and postnatal periods. BALB/C mice, with and without nicotine administrations in pregnancy and postnatal periods, were studied. The animals were euthanized at 3, 7, 10, 16, and 35 days postpartum (dpp). Testicular tissue samples were processed for histological, ultrastructural, and immunohistochemical studies; and testicular lipoperoxidation was determined. It was observed that in the nicotine-exposed animals, there was increased apoptosis and a reduction in the number of gonocytes that matured to spermatogonia. This gonocyte-spermatogonia maturation reduction was associated with a greater immunoreactivity to nicotinic acetylcholine receptors in the germ cells. Lipoperoxidation was similar in both groups until 16 dpp, with significant reduction at 35 dpp. Our findings suggest that nicotine intake during pregnancy and postnatal periods can affect the process of maturation of gonocytes to spermatogonia and the pool of available spermatogonia for spermatogenesis.

scholarly journals Interactions of Glutamatergic Neurotransmission and Brain-Derived Neurotrophic Factor in the Regulation of Behaviors after Nicotine Administration

2019 ◽  
Vol 20 (12) ◽  
pp. 2943 ◽  
Author(s):  
Jieun Kim ◽  
Ju Hwan Yang ◽  
In Soo Ryu ◽  
Sumin Sohn ◽  
Sunghyun Kim ◽  
...  
Keyword(s):  
Nicotine Dependence ◽  
Nicotinic Acetylcholine Receptors ◽  
Neurotrophic Factor ◽  
Acetylcholine Receptors ◽  
Glutamate Release ◽  
Brain Derived Neurotrophic Factor ◽  
Nicotine Exposure ◽  
Glutamatergic Neurotransmission ◽  
Basal Nuclei ◽  
Nicotine Administration

Nicotine causes tobacco dependence, which may result in fatal respiratory diseases. The striatum is a key structure of forebrain basal nuclei associated with nicotine dependence. In the striatum, glutamate release is increased when α7 nicotinic acetylcholine receptors expressed in the glutamatergic terminals are exposed to nicotine, and over-stimulates glutamate receptors in gamma amino-butyric acid (GABA)ergic neurons. These receptor over-stimulations in turn potentiate GABAergic outputs to forebrain basal nuclei and contribute to the increase in psychomotor behaviors associated with nicotine dependence. In parallel with glutamate increases, nicotine exposure elevates brain-derived neurotrophic factor (BDNF) release through anterograde and retrograde targeting of the synapses of glutamatergic terminals and GABAergic neurons. This article reviews nicotine-exposure induced elevations of glutamatergic neurotransmission, the bidirectional targeting of BDNF in the striatum, and the potential regulatory role played by BDNF in behavioral responses to nicotine exposure.

Toxic effects of subchronic oral acetamiprid exposure in rats

2019 ◽  
Vol 35 (11-12) ◽  
pp. 679-687 ◽  
Author(s):  
Bahar Ulus Karaca ◽  
Yağmur Emre Arican ◽  
Tugce Boran ◽  
Sevgi Binay ◽  
Alper Okyar ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Male Rats ◽  
Sprague Dawley ◽  
Tissue Samples ◽  
Plasma Urea ◽  
Sprague Dawley Rats ◽  
Organ Systems ◽  
Liver And Kidney

Acetamiprid, a selective agonist of type-2 nicotinic acetylcholine receptors, is one of the most widely used neonicotinoids. The hepato- and nephrotoxic potential of acetamiprid has not been clarified although it is known to be toxic to other several organ systems, including the nervous, respiratory and immune systems. The present study aimed to investigate acetamiprid liver and kidney toxicity in male rats after a 90-day subchronic exposure to 12.5, 25 and 35 mg/kg. The biochemical and oxidative damage parameters were determined in the plasma and tissue samples as well as histopathological evaluation in the liver and kidney tissues. Acetamiprid caused oxidative damage and affected the liver, denoted by injury markers including the levels of cholesterol, and alanine aminotransferase and aspartate aminotransferase enzymes. There was also a decrease in plasma urea, uric acid and creatinine levels, all of which might result from liver injury. Additionally, acetamiprid was more toxic to the liver than the kidney according to the histopathological examinations. In conclusion, acetamiprid exhibited hepatotoxic potential at all treatment doses on male Sprague Dawley rats.

scholarly journals α6β2*-subtype nicotinic acetylcholine receptors are more sensitive than α4β2*-subtype receptors to regulation by chronic nicotine administration

2014 ◽  
Vol 130 (2) ◽  
pp. 185-198 ◽  
Author(s):  
Michael J. Marks ◽  
Sharon R. Grady ◽  
Outi Salminen ◽  
Miranda A. Paley ◽  
Charles R. Wageman ◽  
...  
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Nicotinic Acetylcholine ◽  
Chronic Nicotine ◽  
Nicotine Administration

Nicotinic Acetylcholine Receptors in Glucose Homeostasis: The Acute Hyperglycemic and Chronic Insulin-Sensitive Effects of Nicotine Suggest Dual Opposing Roles of the Receptors in Male Mice

Endocrinology ◽  
2014 ◽  
Vol 155 (10) ◽  
pp. 3793-3805 ◽  
Author(s):  
Christine U. Vu ◽  
Jawed A. Siddiqui ◽  
Paul Wadensweiler ◽  
Jiaur R. Gayen ◽  
Ennio Avolio ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Nicotine Exposure ◽  
Dependent Manner ◽  
Nicotinic Acetylcholine ◽  
Nicotine Treatment ◽  
Chronic Nicotine ◽  
Chronic Nicotine Treatment

Abstract Cigarette smoking causes insulin resistance. However, nicotine induces anti-inflammation and improves glucose tolerance in insulin-resistant animal models. Here, we determined the effects of nicotine on glucose metabolism in insulin-sensitive C57BL/J6 mice. Acute nicotine administration (30 min) caused fasting hyperglycemia and lowered insulin sensitivity acutely, which depended on the activation of nicotinic-acetylcholine receptors (nAChRs) and correlated with increased catecholamine secretion, nitric oxide (NO) production, and glycogenolysis. Chlorisondamine, an inhibitor of nAChRs, reduced acute nicotine-induced hyperglycemia. qRT-PCR analysis revealed that the liver and muscle express predominantly β4 > α10 > α3 > α7 and β4 > α10 > β1 > α1 mRNA for nAChR subunits respectively, whereas the adrenal gland expresses β4 > α3 > α7 > α10 mRNA. Chronic nicotine treatment significantly suppressed expression of α3-nAChR (predominant peripheral α-subunit) in liver. Whereas acute nicotine treatment raised plasma norepinephrine (NE) and epinephrine (Epi) levels, chronic nicotine exposure raised only Epi. Acute nicotine treatment raised both basal and glucose-stimulated insulin secretion (GSIS). After chronic nicotine treatment, basal insulin level was elevated, but GSIS after acute saline or nicotine treatment was blunted. Chronic nicotine exposure caused an increased buildup of NO in plasma and liver, leading to decreased glycogen storage, along with a concomitant suppression of Pepck and G6Pase mRNA, thus preventing hyperglycemia. The insulin-sensitizing effect of chronic nicotine was independent of weight loss. Chronic nicotine treatment enhanced PI-3-kinase activities and increased Akt and glycogen synthase kinase (GSK)-3β phosphorylation in an nAChR-dependent manner coupled with decreased cAMP response element–binding protein (CREB) phosphorylation. The latter effects caused suppression of Pepck and G6Pase gene expression. Thus, nicotine causes both insulin resistance and insulin sensitivity depending on the duration of the treatment.

Localization of Nicotinic Acetylcholine Receptors on Somatic Spines of Chick Ciliary Ganglion Neurons

1999 ◽  
Vol 5 (S2) ◽  
pp. 1028-1029
Author(s):  
R. Shoop ◽  
M. Martone ◽  
N. Yamada ◽  
M. Ellisman ◽  
D. Berg
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Transmitter Release ◽  
Acetylcholine Receptors ◽  
Ciliary Ganglion ◽  
Nicotinic Acetylcholine ◽  
Selective Ligand ◽  
Somatic Spines ◽  
Ciliary Ganglion Neurons ◽  
Ganglion Neurons ◽  
Immunohistochemical Studies

Nicotinic acetylcholine receptors (nAChRs) are pentameric membrane proteins that function as cation selective, ligand-gated ion channels and are widely distributed throughout the vertebrate nervous system. One of the most abundant nAChRs is a species that contains the α7 gene product (α7-AChRs), binds the snake venom oc-bungarotoxin, and rapidly desensitizes. These receptors have been shown to function at presynaptic sites to modulate transmitter release, as well as on postsynaptic cells where they mediate transmission. Interestingly, these receptors have an exceptionally high relative permeability to calcium.In the chick ciliary ganglion, the α 7-AChRs play a prominent role, by generating large synaptic currents, but the receptors appear to be excluded from postysnaptic densities on the cell. Immunohistochemical studies have shown that the receptors form large clusters on the surface of the ciliary ganglion neurons. We have recently shown that the α 7-containing receptors are concentrated on mats of somatic spines in close proximity to putative sites of presynaptic transmitter release.

scholarly journals Exploration of the role of CHRNA5-A3-B4 genotype in smoking behaviours

2019 ◽  
Author(s):  
Glenda Lassi ◽  
Vanessa Tan ◽  
Liam Mahedy ◽  
Ana Sofia F. Oliveira ◽  
Maddy L. Dyer ◽  
...  
Keyword(s):  
Gene Cluster ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Association Studies ◽  
Strong Association ◽  
Genome Wide Association Studies ◽  
Nicotine Exposure ◽  
Tobacco Exposure ◽  
Smoking Topography ◽  
Never Smokers

AbstractGenome-wide association studies have identified associations between variation at rs16969968/rs1051730 in the CHRNA5–A3–B4 gene cluster and smoking related outcomes. Experiments in rodents have described the nicotinic acetylcholine receptors (nAChRs) subunits encoded by this gene cluster and showed a lack of nicotine aversion in nAChRs deficient animal models. We conducted a nicotine challenge and a smoking topography study in humans, hypothesising that: 1. responses to a nicotine challenge would differ according to the rs16969968/rs1051730 genotype and 2. genotype may influence nicotine intake via smoking topography.We used linear regressions to examine associations between rs16969968/rs1051730 genotype and subjective (questionnaires) and objective (physiological parameters) responses following acute nicotine exposure in never smokers (hypothesis 1) or cigarette smoking in current smokers (hypothesis 2). There was evidence to suggest nicotine exposure increases blood pressure and heart rate, and negatively affects mood, but insufficient evidence that these effects differ by genotype. Carriers of the minor allele following smoking one cigarette, exhibited reduced cravings (b=-2.46, 95% CI -4.87 to - 0.06, p=0.04) and inhaled less smoke per cigarette (b=-0.24, 95% CI - 0.43 to - 0.06, p=0.01) and per puff (b=-0.18, 95% CI -0.32 to -0.01, p=0.02). These results suggest that we need to carefully consider the translational value of the findings of aversion behaviour in nAChRs rodent models, and that deeper inhalation does not explain the strong association between rs16969968/rs1051730 genotype and objective biomarkers of tobacco exposure.

scholarly journals Increased nicotinic receptor desensitization in hypoglossal motor neurons following chronic developmental nicotine exposure

2012 ◽  
Vol 107 (1) ◽  
pp. 257-264 ◽  
Author(s):  
Jason Q. Pilarski ◽  
Hilary E. Wakefield ◽  
Andrew J. Fuglevand ◽  
Richard B. Levine ◽  
Ralph F. Fregosi
Keyword(s):  
Motor Neurons ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Upper Airway ◽  
Motor Nucleus ◽  
Nicotine Exposure ◽  
Neuronal Nicotinic Acetylcholine Receptors ◽  
Whole Cell Patch Clamp ◽  
Nachr Subtype ◽  
Inward Currents

Neuronal nicotinic acetylcholine receptors (nAChRs) are expressed on hypoglossal motor neurons (XII MNs) that innervate muscles of the tongue. Activation of XII MN nAChRs evokes depolarizing currents, which are important for regulating the size and stiffness of the upper airway. Although data show that chronic developmental nicotine exposure (DNE) blunts cholinergic neurotransmission in the XII motor nucleus, it is unclear how nAChRs are involved. Therefore, XII MN nAChR desensitization and recovery were examined in tissues from DNE or control pups using a medullary slice preparation and tight-seal whole cell patch-clamp recordings. nAChR-mediated inward currents were evoked by brief pressure pulses of nicotine or the α4β2 nAChR agonist RJR-2403. We found that, regardless of treatment, activatable nAChRs underwent desensitization, but, following DNE, nAChRs exhibited increased desensitization and delayed recovery. Similar results were produced using RJR-2403, showing that DNE influences primarily the α4β2 nAChR subtype. These results show that while some nAChRs preserve their responsiveness to acute nicotine following DNE, they more readily desensitize and recover more slowly from the desensitized state. These data provide new evidence that chronic DNE modulates XII MN nAChR function, and suggests an explanation for the association between DNE and the incidence of central and obstructive apneas.

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