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.

scholarly journals Nicotine-Induced Effects on Nicotinic Acetylcholine Receptors (nAChRs), Ca2+ and Brain-Derived Neurotrophic Factor (BDNF) in STC-1 Cells

PLoS ONE ◽  
2016 ◽  
Vol 11 (11) ◽  
pp. e0166565 ◽  
Author(s):  
Jie Qian ◽  
Shobha K. Mummalaneni ◽  
Reem M. Alkahtani ◽  
Sunila Mahavadi ◽  
Karnam S. Murthy ◽  
...  
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Neurotrophic Factor ◽  
Acetylcholine Receptors ◽  
Brain Derived Neurotrophic Factor ◽  
Nicotinic Acetylcholine

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.

BDNF and nicotine dependence: associations and potential mechanisms

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Zeyi Huang ◽  
Daichao Wu ◽  
Xilin Qu ◽  
Meixiang Li ◽  
Ju Zou ◽  
...  
Keyword(s):  
Nicotine Dependence ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Molecular Mechanisms ◽  
Public Health Problem ◽  
Nicotine Addiction ◽  
Tyrosine Kinase Receptor ◽  
Bdnf Expression ◽  
High Affinity Receptor ◽  
The Brain

AbstractSmoking is the leading preventable cause of death worldwide and tobacco addiction has become a serious public health problem. Nicotine is the main addictive component of tobacco, and the majority of people that smoke regularly develop nicotine dependence. Nicotine addiction is deemed to be a chronic mental disorder. Although it is well known that nicotine binds to the nicotinic acetylcholine receptors (nAChRs) and activates the mesolimbic dopaminergic system (MDS) to generate the pleasant and rewarding effects, the molecular mechanisms of nicotine addiction are not fully understood. Brain-derived neurotrophic factor (BDNF) is the most prevalent growth factor in the brain, which regulates neuron survival, differentiation, and synaptic plasticity, mainly through binding to the high affinity receptor tyrosine kinase receptor B (TrkB). BDNF gene polymorphisms are associated with nicotine dependence and blood BDNF levels are altered in smokers. In this review, we discussed the effects of nicotine on BDNF expression in the brain and summarized the underlying signaling pathways, which further indicated BDNF as a key regulator in nicotine dependence. Further studies that aim to understand the neurobiological mechanism of BDNF in nicotine addcition would provide a valuable reference for quitting smoking and developing the treatment of other addictive substances.

N-cholinergic facilitation of glutamate release from an individual retinotectal fiber in frog

2001 ◽  
Vol 18 (4) ◽  
pp. 549-558 ◽  
Author(s):  
A. KURAS ◽  
N. GUTMANIENĖ
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Action Potentials ◽  
Acetylcholine Receptors ◽  
Kynurenic Acid ◽  
Glutamate Release ◽  
Synaptic Potentials ◽  
Lower Vertebrates ◽  
Optic Fibers ◽  
Retinotectal Transmission

Nicotinic acetylcholine receptors are localized on retinotectal axons' terminals in lower vertebrates. The effects of activation of these receptors by endogenous acetylcholine were observed under stimulation of mass optic fibers. This study was designed to determine whether endogenous acetylcholine facilitates frog retinotectal transmission, provided only the synapses of an individual optic axon are activated, and to evaluate the feasible extent of nicotinic facilitation in these synapses by applied agonist. To this end, the effects of cholinergic drugs on the extracellular action and synaptic potentials recorded from the terminal arborization of a separate retinotectal fiber (in layer F of the tectum) were investigated in vivo. Glutamatergic nature of retinotectal synapses was reexamined by treatment with kynurenic acid. Both kynurenic acid (0.25–1 mM) and d-tubocurarine chloride (10–15 μM) significantly depressed the synaptic potentials. Carbamylcholine chloride (50–150 μM) evoked a large augmentation of the synaptic potentials and a slight but statistically significant decrease of the action potentials. D-tubocurarine reduced the effect of carbamylcholine. Pilocarpine hydrochloride (50 μM) had only a weak effect. The paired-pulse facilitation of the synaptic potentials changed significantly under the action of carbamylcholine and d-tubocurarine. The obtained results suggest that the glutamate release from activated synapses of individual retinotectal axons is facilitated by endogenous acetylcholine via presynaptic nicotinic receptors. Under used stimulation conditions, this modulation mechanism was employed only partially since its activation by applied carbamylcholine could enhance synaptic transmission up to 2.8 times.

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
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