Sentences with phrase «nicotinic receptors in»

First off, it contains Dinotefuran which is a lot similar in pharmacologic action to Imidacloprid especially in the inhibition of nicotinic receptors in the flea nervous system.

Although this study was looking at the role of nicotinic receptors in disordered mood and the self - medication of mood by smoking, we may be able to extrapolate this for our purposes because it was this one subset of smokers who were more depressed after tryptophan depletion.

Varenicline stimulates the nicotinic receptors in the brain to help reduce withdrawal symptoms, and also helps reduce the pleasure of smoking if the quitter sneaks a cigarette.

Precisely where these findings will lead drug treatment strategies is unclear, but this work provides insight into the role of nicotinic receptors in the vulnerability to multiple classes of addictive drugs.»

Functional distribution of nicotinic receptors in CA3 region of the hippocampus.

PDZ - containing proteins provide a functional postsynaptic scaffold for nicotinic receptors in neurons.

This illustration shows how the rabies virus inhibits nicotinic receptors in the brain, which interferes with communication and induces frenzied behavior.

The development of nicotinic receptors in the human medulla oblongata: inter-relationship with the serotonergic system

To some extent, all of these medications, which are approved by the FDA, all target the nicotinic receptor in the brain, and this might not be the optimal strategy for women.

Not exact matches

In animal models, exposure to cigarette smoke or nicotine during fetal development alters the expression of the nicotinic acetylcholine receptor in areas of the brainstem important for autonomic function, 28 alters the neuronal excitability of neurons in the nucleus tractus solitarius (a brainstem region important for sensory integration), 29 and alters fetal autonomic activity and medullary neurotransmitter receptors.30 In human infants, there are strong associations between nicotinic acetylcholine receptor and serotonin receptors in the brainstem during development.31 Prenatal exposure to tobacco smoke attenuates recovery from hypoxia in preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDIn animal models, exposure to cigarette smoke or nicotine during fetal development alters the expression of the nicotinic acetylcholine receptor in areas of the brainstem important for autonomic function, 28 alters the neuronal excitability of neurons in the nucleus tractus solitarius (a brainstem region important for sensory integration), 29 and alters fetal autonomic activity and medullary neurotransmitter receptors.30 In human infants, there are strong associations between nicotinic acetylcholine receptor and serotonin receptors in the brainstem during development.31 Prenatal exposure to tobacco smoke attenuates recovery from hypoxia in preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin areas of the brainstem important for autonomic function, 28 alters the neuronal excitability of neurons in the nucleus tractus solitarius (a brainstem region important for sensory integration), 29 and alters fetal autonomic activity and medullary neurotransmitter receptors.30 In human infants, there are strong associations between nicotinic acetylcholine receptor and serotonin receptors in the brainstem during development.31 Prenatal exposure to tobacco smoke attenuates recovery from hypoxia in preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin the nucleus tractus solitarius (a brainstem region important for sensory integration), 29 and alters fetal autonomic activity and medullary neurotransmitter receptors.30 In human infants, there are strong associations between nicotinic acetylcholine receptor and serotonin receptors in the brainstem during development.31 Prenatal exposure to tobacco smoke attenuates recovery from hypoxia in preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDIn human infants, there are strong associations between nicotinic acetylcholine receptor and serotonin receptors in the brainstem during development.31 Prenatal exposure to tobacco smoke attenuates recovery from hypoxia in preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin the brainstem during development.31 Prenatal exposure to tobacco smoke attenuates recovery from hypoxia in preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDS.

Other companies, including Pfizer, based in New York, have invested in nicotinic - receptor modulators to treat Alzheimer's disease and attention - deficit hyperactivity disorder (see Aiming at the brain's nicotine receptors).

The research revealed that a molecule called a glycoprotein on the surface of the rabies virus can bind to nicotinic acetylcholine receptors in the muscles.

«We knew that nicotinic acetylcholine receptors, which bind to the virus in muscles, are also found in the brain, and we presumed that virus could also bind to such receptors.

Lindstrom and his colleagues inserted genes for human nicotinic receptors into frog eggs and incubated them with levels of nicotine similar to those found in the blood of a human smoker.

A polymorphism (rs1051730) in proximity to the cholinergic receptor, nicotinic, alpha 3 (CHRNA3) gene is associated with higher tobacco consumption among smokers and can therefore be used as a genetic proxy for high tobacco consumption.

Poison frogs have evolved mutations in nicotinic acetylcholine receptor genes that confer toxin resistance.

A Gain - of - Function Mutation in the α9 Nicotinic Acetylcholine Receptor Alters Medial Olivocochlear Efferent Short - Term Synaptic Plasticity

Chronic nicotine cell specifically upregulates functional α4 * nicotinic receptors: basis for both tolerance in midbrain and enhanced long - term potentiation in perforant path.

Novel seizure phenotype and sleep disruptions in knock - in mice with hypersensitive α4 * nicotinic receptors.

Distribution and synaptic localization of nicotinic acetylcholine receptors containing a novel α7 subunit isoform in embryonic rat cortical neurons.

Abstract Pentameric channel - receptors, including nicotinic acetylcholine, glycine and GABAA receptors, play a key role in fast excitatory and inhibitory transmission in the nervous system and are the target of numerous therapeutic and addictive drugs.

Neonicotinoids target nicotinic acetylcholine receptors (nAChRs) in the insect central nervous system.

This receptor, known as the nicotinic acetylcholine receptor (nAChR), increases excitability within in the brain's reward centers.

Yakel's research is directed toward understanding the role of the nicotinic acetylcholine receptor and brain function, as well as how dysfunction in this receptor leads to various neurodegenerative diseases and addiction.

Localized expression of Beta2 - containing nicotinic acetylcholine receptors in dopaminergic neurons in mice supports locomotor activating, but not rewarding effects of nicotine Yann Mineur, Yale University, New Haven, Connecticut USA

Perisynaptic surface distribution of multiple classes of nicotinic acetylcholine receptors on neurons in the chicken ciliary ganglion.

Objective: To study, at high spatial and temporal resolution, the conformational dynamics of the nicotinic receptors enabling neuronal communication in the brain, which are major therapeutic targets linked to cognition and tobacco dependence.

Synaptic and extrasynaptic distribution of two distinct populations of nicotinic acetylcholine receptor clusters in the frog cardiac ganglion.

To understand how nicotine affects nAChR localization, Ashley M. Fox — Loe and colleagues at the University of Kentucky developed sensitive, organelle - specific single - molecule imaging methods to quantify precisely changes in the stoichiometry of nicotinic receptors.

Antidepressant - like Activity of AMOP - H - OH («SAZETIDINE - A») in the Forced Swim TSest is Mediated by High Affinity Nicotinic Acetylcholine Receptors.

These latter compounds are neuroactive metabolites that act on N - methyl - D - aspartate (NMDA) and alpha 7 nicotinic acetylcholine receptors (nAChR) in the CNS and enteric nervous system (ENS).

The CHRNA5 - CHRNA3 - CHRNB4 nicotinic receptor subunit gene cluster affects risk for nicotine dependence in African — Americans and in European — Americans