Effect of nicotine on levels of extracellular amino acids in regions of the rat brain in vivo

Tóth, Eugene; Vízi, E. S.; Lajtha, Ábel

doi:10.1016/0028-3908(93)90192-6

Cited by 100 publications

(68 citation statements)

References 28 publications

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“…Intracerebral administration of nicotine at a dose of 50 mM increases glycine in the hippocampus of anesthetized rats but s.c. administration does not [107]. Similarly perfusion of 1 mM of nicotine does not alter glycine levels but 5 mM increases glycine in the striatum and prefrontal cortex [108]. In the present study, pretreatment with NT69L significantly increased glycine levels in the alcohol and nicotine treated animals and lowered it in the alcohol/nicotine group indicating that in addition to its effect on DA and glutamate NT69L might affect alcohol and nicotine-dependence through modulating glycinergic neurotransmission.…”

Section: Effect Of Nt69l On Nicotine-and Alcohol-induced Biochemical contrasting

confidence: 43%

Novel Therapy for Nicotine Addiction in Alcohol Dependent Rats

Boules¹,

Stennett²,

Muhktar³

et al. 2013

J Addict Res Ther

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IntroductionNicotine and alcohol addiction are frequently co-morbid problems [1]. The co-dependence of nicotine and alcohol addiction complicates treatment and is often associated with significant morbidity and mortality. Prevalence of smoking in alcoholics is as high as 90% compared to 30% for the general population [2] and alcohol consumption is associated with high nicotine use [3,4]. Co-morbid cigarette smoking and alcoholism has been associated with higher rates of depression in comparison with non-alcoholic smokers [5] and increased cravings for nicotine in comparison with non alcohol dependent smokers [6]. Additionally, smoker alcoholics are more likely to die from smoking related diseases rather than directly from an alcohol related medical condition [7]. Pharmacotherapeutic options for the treatment of alcohol and tobacco co-dependence are limited. Thus, there is a critical need for the development of novel drugs implementing new therapeutic targets.Neurotensin (NT) is a neuropeptide that is closely associated with, and modulates dopamine (DA) [8], acetylcholine (ACh), glutamate, and γ-aminobutyric acid (GABA) neurotransmission, all of which are involved in addiction and reward pathways. Local administration of NT in the prefrontal cortex (PFC) increases extracellular levels of ACh and GABA [9]. Similar data were obtained with the extracranial injection of the NT agonist NT69L [10], a compound that was developed in our laboratory. NT also enhances GABAergic activity in rat hippocampus [11] and reduces glutamatergic neurotransmission in dorsolateral striatum [12]. However, NT must be administered centrally to have an effect because it is easily degraded by peptidases. Our laboratory has developed many NT agonists that can be administered extracranially and mimic the central effects of NT. The most studied of these agonists is NT69L, which binds with equal affinity to the two well-characterized NT receptors, subtype 1 (NTS1) and subtype 2 (NTS2). Our work with NT69L shows that it blocks nicotine-induced sensitization and nicotine self-administration [13][14][15].In addition to its role in animal models for nicotine addiction, the NT system has been strongly implicated in the neurochemical and behavioral effects of alcohol use [16,17]. Chronic administration of NT69L reduces alcohol preference and consumption in mice through modulation of the NTS1 [18]. Biochemically, NT69L normalizes the nicotine-induced changes in DA [19], the neurotransmitter that promotes the motivational process for both nicotine and alcohol, and the alcohol-induced increase in DA and glutamate in the striatum [20]. Additionally, NT modulates other neurotransmitters implicated in alcohol use disorder (AUD). It causes neurochemical changes similar to acamprosate (the calcium salt of acetylhomotaurine), which is one of three FDA-approved drugs to treat AUD. Administration of acamprosate or NT69L increases extracellular concentration of DA in striatum [10,11] and both acamprosate and NT69L modulate glutamate [21,22].Considering the behav...

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Section: Effect Of Nt69l On Nicotine-and Alcohol-induced Biochemical contrasting

confidence: 43%

Novel Therapy for Nicotine Addiction in Alcohol Dependent Rats

Boules¹,

Stennett²,

Muhktar³

et al. 2013

J Addict Res Ther

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“…Nicotine administration also produces increased glutamate release throughout the striatum (McGehee et al, 1995, Schilström et al, 2000, Schilström et al, 2003and Toth et al, 1993, allowing for the potential of glutamatergic mediation of the conditional stimulus properties of nicotine. To our knowledge, only one study has examined the effects of MPEP, an mGluR5 antagonist, on the nicotine discriminative stimulus.…”

Section: Discussionmentioning

confidence: 99%

Behavioral and neuropharmacological characterization of nicotine as a conditional stimulus

Murray

Bevins

2007

European Journal of Pharmacology

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“…Nicotine receptors do not only exist on neuronal cell bodies and dendrites but are also located on axon terminals and are involved in modulation of multiple transmission release. Local application of nicotine to the striatum produced an increase in the extracellular level of glutamate (6). Nicotine increased the release of DA in the rat striatum in vivo and it has been reported that the N-type Ca 2+ channel and voltage dependent sodium channels are involved in the releasing effect of nAChR stimulation (7).…”

Section: Neuronal Nicotine Receptorsmentioning

confidence: 96%

Neuronal Nicotinic Receptor and Psychiatric Disorders: Functional and Behavioral Effects of Nicotine

Araki

Suemaru

Gomita

2002

Japanese Journal of Pharmacology

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ABSTRACT-Both retrospective and prospective clinical studies have demonstrated positive associations of smoking with psychiatric disorders such as schizophrenia, depression and anxiety. Neuronal nicotinic acetylcholine receptors (nAChR) belong to a family of ligand-gated ion channels that are widely distributed in the brain. The pre-synaptically located nAChR, which are composed of =3 or =4 subunits in combination with >2 subunit on axon terminals, modulate the multiple transmission release. Several studies indicated which individual nicotinic receptor subtype is responsible for mediating each of the behavioral effects of nicotine. A reduced number of =7 nicotinic receptor subtypes in the hippocampus were reported in schizophrenic patients. In addition, it was assumed that nicotine provided useful therapeutic treatment for a variety of cognitive impairments including those found in Alzheimer's disease, schizophrenia and attention deficit hyperactive disorder. Both =7 and =4>2 nicotinic receptors in the hippocampus are involved in these phenomena. In the genetic depressive rats, nicotine showed antidepressant-like effects in forced swim models of depression, suggesting the involvement of =4>2 nicotinic receptor in this phenomenon. Thus, it appears likely that pre-synaptic nAChR on monoaminergic fibers are composed of =3 or =4 subunits in combination with the >2 subunit, and these subunit compositions mediate dopaminergic and noradrenergic release, and glutamate is mainly controlled by the =7 subunit. All these findings suggest that nicotine and other nicotinic drugs warrant further study for possible clinical prescription to psychiatric disorders.

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Effect of nicotine on levels of extracellular amino acids in regions of the rat brain in vivo

Cited by 100 publications

References 28 publications

Novel Therapy for Nicotine Addiction in Alcohol Dependent Rats

Novel Therapy for Nicotine Addiction in Alcohol Dependent Rats

Behavioral and neuropharmacological characterization of nicotine as a conditional stimulus

Neuronal Nicotinic Receptor and Psychiatric Disorders: Functional and Behavioral Effects of Nicotine

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