Sentences with phrase «nicotine receptors»

«We do suspect kids exposed to secondhand tobacco smoke, their nicotine receptors are primed to make them more susceptible to cigarette smoking,» Wilson said.

More research is needed to fully understand how BCX slows lung cell production of nicotine receptors, Chellappan said.

The genes linked with smoking were ones that regulated nicotine receptors in the brain.

For instance, the skin toxins of poison - dart frogs drew attention 20 years ago as a potential painkiller that worked by targeting nicotine receptors.

Now researchers report that they have sorted out how the drug toys with nicotine receptors in the brain.

Schulte, an expert on nicotine receptors, is a former UAF professor now at the University of the Sciences in Philadelphia.

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).

Nicotine receptors in the striatum, the comma - shaped structure near the center of the brain where movements are planned and controlled, are located near the terminals that regulate and emit dopamine.

«While it's clear that sex differences in varenicline efficacy exist, we don't yet know why varenicline is particularly effective for women,» McKee said, adding that sex differences in the nicotine receptor system in the brain may be a key factor.

In the parents» generation, for example, the researchers saw a correlation between early death in men and the presence in their children (and therefore presumably in the parents) of a nicotine receptor allele that makes it harder to quit smoking.

Cell autonomy, receptor autonomy, and thermodynamics in nicotine receptor up - regulation.

Not exact matches

The most recent study report described in these same regions decreased tissue levels of 5 - HT and tryptophan hydroxylase, the synthesizing enzyme for serotonin, and no evidence of excessive serotonin degradation as assessed by levels of 5 - hydroxyindoleacetic acid (the main metabolite of serotonin) or ratios of 5 - hydroxyindoleacetic acid to serotonin.30 A recent article described a significant association between a decrease in medullary 5 - HT1A receptor immunoreactivity and specific SIDS risk factors, including tobacco smoking.40 These data confirm results from earlier studies in humans39, 41 and are also consistent with studies in piglets that revealed that postnatal exposure to nicotine decreases medullary 5 - HT1A receptor immunoreactivity.42 Animal studies have revealed that serotonergic neurons located in the medullary raphe and adjacent paragigantocellularis lateralis play important roles in many autonomic functions including the control of respiration, blood pressure, heart rate, thermoregulation, sleep and arousal, and upper airway patency.

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 SIDS.

Changes in serotoninergic receptors 1A and 2A in the piglet brainstem after intermittent hypercapnic hypoxia (IHH) and nicotine

Previous research had shown that nicotine seems to have conflicting effects on different types of nicotinic acetylcholine receptors, proteins on the surface of brain cells that respond to nicotine and the naturally occurring neurotransmitter acetylcholine.

Lindstrom says the deadening of the a-4 and a-7 receptors might explain why longtime smokers can handle amounts of nicotine that would make a first - time smoker very ill.

Neuroscientist Jon Lindstrom of the University of Pennsylvania Medical Center in Philadelphia and his colleagues set out to determine more precisely how extended exposure to nicotine affected three different types of 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.

The work «nails to the wall» the theory that different receptors respond very differently to nicotine, says pharmacologist Allan Collins of the University of Colorado, Boulder.

By using pharmacological small molecule inhibitors as well as neutrophils from genetically modified mouse strains the team could identify essential receptor and signaling pathways involved in the nicotine - mediated activation of neutrophils.

The drug stimulates a brain protein called the serotonin 2C receptor, which reduces the desire to consume nicotine in lab rats.

This study further investigated the impact of nicotine use / smoking status and variation in the mu opioid receptor gene (OPRM1), specifically, an A118G single nucleotide polymorphism (SNP, or DNA sequence variation), on the effects of naltrexone on a range of drinking outcomes.

The results provide strong evidence that the a4 * receptors are sufficient to create nicotine addiction.

Once in the brain, nicotine hijacks neurons» receptors for acetylcholine, causing them to fire even in the absence of the real thing.

That meant that the scientists could activate the a4 * - containing receptors with doses of nicotine too small to affect other types of acetylcholine receptors.

«It could be that as your brain is maturing, you become less susceptible to the addictive effects of nicotine because the genetic component that is influencing the way nicotine interacts with these receptors may have less effect,» says Chris Amos, a genetic epidemiologist at the University of Texas M. D. Anderson Cancer Center in Houston, who wasn't involved in the study.

Specifically, substance abusers (cocaine, methamphetamine, alcohol, heroin, and nicotine), but not marijuana abusers (14 ⇓ — 16), show reduced baseline availability of DA D2 receptors in striatum (reviewed ref.

Gestational nicotine exposure regulates expression of AMPA and NMDA receptors and their signaling apparatus in developing and adult rat hippocampus.

Nicotine also boosts the cells» production of this specific receptor.

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

«After the neurobiological studies pointed out the important role of the GABAB receptor in nicotine reward, and we had positive data in a variety of animal models of nicotine dependence, it was time to focus our efforts on discovery of new molecules that could become therapeutics to assist people to quit smoking.»

The grant from the National Institutes of Health (NIH) will fund research focused on finding novel positive modulators for GABAB receptors that have the potential to become treatments for nicotine addiction.

Subsequently, work in the Markou laboratory showed that these compounds had desirable effects on nicotine dependence in animal models, while offering a better side - effect profile than other alternatives under study (full agonists at the same receptors).

Acetylcholine receptor, which is the target of drugs (nicotine, ethanol) and current therapeutics (anaesthetics, anxiolytics, anti-smoking and anti-Alzheimer's).

«It raises the possibility that nicotinic receptors may be important targets for the treatment of multiple addictions, not just nicotine.

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

Observations suggest that nicotine exposure affects the ratio of these receptors on the surface versus those in the endoplasmic reticulum of the cell and thus the cells» sensitivity to these receptors» natural ligands.

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.

Publishing the research in the Journal of Biological Chemistry, the team concluded that nicotine exposure affects receptor distribution through combined effects on both receptor assembly and trafficking, which eventually could help explain the effects of drugs like nicotine on neuromuscular functioning.

Blocking either of these receptors during nicotine exposure eliminated the drug's ability to cause persistent changes in excitability.

Mao discovered that nicotine - induced synaptic plasticity in the VTA is dependent upon one of the drug's usual targets, a receptor for the neurotransmitter acetylcholine located on the dopamine neurons.

For the rest, the quick onset of withdrawal symptoms — craving, irritability, hunger, and headache — is too much; the brain begins to raise hell and demand a fresh dose of nicotine, which binds to certain receptors and causes the pleasurable release of dopamine.

CB receptor antagonists are also under investigation for medical use in nicotine addiction and obesity.

Adding to the problem, certain substances (i.e. caffeine, alcohol, nicotine) and many medications can contribute to neurotransmitter depletion and resulting symptoms by suppressing or artificially stimulating neurotransmitter receptor function.

Nicotine may also act as an anti-estrogenic compound, inhibiting aromatase and one of the two estrogen receptors directly; this may underlie some of the side - effects associated with chronic usage of nicotine / cigarettes, particularly iNicotine may also act as an anti-estrogenic compound, inhibiting aromatase and one of the two estrogen receptors directly; this may underlie some of the side - effects associated with chronic usage of nicotine / cigarettes, particularly inicotine / cigarettes, particularly in women.

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

Effects of prenatal nicotine exposure on primate brain development and attempted amelioration with supplemental choline or vitamin C: Neurotransmitter receptors, cell signaling and cell development biomarkers in fetal brain regions of rhesus monkeys