Exposure to nicotine enhances the behavioral stimulant effect of nicotine and increases binding of [3H]acetylcholine to nicotinic receptors

Ksir, Charles; Hakan, Robert L.; Hall, David P.; Kellar, Kenneth J.

doi:10.1016/0028-3908(85)90058-9

Cited by 195 publications

(90 citation statements)

References 6 publications

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“…Nicotine pretreatment in rodents does not affect the disposition of a challenge injection of NIC (Pekonen et al 1993), a finding that argues against an altered metabolic rate of nicotine as a mechanism by which the effect of the drug is enhanced. Repeated administration of nicotine is associated with an increase in brain nicotinic binding (Ksir et al 1985;Lapchak et al 1989), a phenomenon that could be of importance for the sensitization to both behavioral and biochemical effects of nicotine. However, Lapchak et al (1989) demonstrated an increased binding of nicotine both in mPFC and in the striatum.…”

Section: Discussionmentioning

confidence: 99%

Chronic Nicotine Enhances Basal and Nicotine-Induced Fos Immunoreactivity Preferentially in the Medial Prefrontal Cortex of the Rat

Nisell

Nomikos

Chergui

et al. 1997

Neuropsychopharmacology

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In the present study, expression of the immediate early gene protein products Fos and Jun-B within the dorsolateral striatum, the core and shell of the nucleus accumbens (NAC), the medial prefrontal cortex (mPFC), and the ventrolateral orbital cortex was examined. Rats were injected SC with either saline or nicotine (0.5 mg/kg) once daily for 12 days. On day 13, animals received a challenge injection of either saline or nicotine (0.5 or 1.0 mg/kg, SC) and 2 h later their brains were examined for Fos-like (FLI) and Jun-B-like (JLI) immunoreactivity. Chronic nicotine significantly increased basal expression of FLI selectively in the mPFC. Nicotine challenge significantly increased FLI in the mPFC of saline-treated animals and even further increased FLI in the mPFC of nicotine-treated animals. In the shell of the NAC, nicotine challenge also increased FLI in nicotine-treated animals, whereas it increased JLI only in saline-treated animals. After chronic nicotine treatment, injection of D 1 receptor antagonist SCH 23390 (0.1 mg/kg, IP) 10 min before a nicotine challenge (0.5 mg/kg, SC), significantly attenuated the nicotine-induced FLI in theThe rewarding and dependence-producing actions of nicotine appear to be due, at least in part, to stimulation of the mesolimbic dopamine (DA) system (see Grenhoff and Svensson 1989; Clark 1990;Svensson et al. 1990;Corrigall 1991;Nisell et al. 1995). Thus, nicotinic receptors have been found to be located on both the cell bodies and the terminals of mesolimbic DA neurons Schwartz et al. 1984), and lesions of the mesolimbic DA system attenuate nicotine selfadministration and nicotine-induced locomotor stimulation in rats (Clarke et al. 1988; Corrigall et al. 1992). Furthermore, nicotine has been shown to increase neuronal activity, particularly burst activity, of midbrain DA cells Grenhoff et al. 1986;Lichtensteiger et al. 1982;Mereu et al. 1987. Systemically administered nicotine also increases release (Imperato et al. 1986;Nisell et al. 1994), synthesis, and metabolism of DA (Andersson et al. 1981;Grenhoff and Svensson 1988) The nicotine-induced locomotion is significantly enhanced with chronic pretreatment with the drug (Morrison and Stephenson 1972;Clarke and Kumar 1983;Benwell and Balfour 1992;Nisell et al. 1996). Although this behavioral activation is to a considerable extent dependent on mesolimbic dopaminergic transmission (see above), previous reports utilizing in vivo microdialysis have demonstrated not only increased (Benwell and Balfour 1992) but also unchanged (Damsma et al. 1989;Nisell et al. 1996) nicotine-induced DA release in the NAC after chronic nicotine treatment. Moreover, the behavioral sensitization observed after chronic, intermittent nicotine treatment for 12 days has been shown to be parallelled by an increase in nicotine-induced DA release in the medial prefrontal cortex (mPFC), whereas the response in the NAC was unaffected . Recently, by means of in vivo voltammetry, systemic administration of nicotine was shown to increase DA release to a greater ext...

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Section: Discussionmentioning

confidence: 99%

Chronic Nicotine Enhances Basal and Nicotine-Induced Fos Immunoreactivity Preferentially in the Medial Prefrontal Cortex of the Rat

Nisell

Nomikos

Chergui

et al. 1997

Neuropsychopharmacology

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“…However, chronic treatment of rats with nicotine increases the density of nicotinic receptors (Ksir et al, 1985;Hillard and Pound, 1993). Thus, caffeine might be increasing nicotinic receptors by enhancing acetylcholine release, rather than by decreasing release.…”

Section: Discussionmentioning

confidence: 99%

“…Chronic caffeine has been reported to reduce the excitatory effects of acetylcholine on rat cerebral cortical neurons (Lin and Phillis, 1990). Chronic nicotine results in tolerance to depressant effects of nicotine in spite of regulation of nicotinic receptors (Ksir et at., 1985).…”

Section: Discussionmentioning

confidence: 99%

Chronic caffeine alters the density of adenosine, adrenergic, cholinergic, GABA, and serotonin receptors and calcium channels in mouse brain

et al. 1993

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SUMMARY1. Chronic ingestion of caffeine by male NIH strain mice alters the density of a variety of central receptors.2. The density of cortical A 1 adenosine receptors is increased by 20%, while the density of striatal A 2A adenosine receptors is unaltered.3. The densities of cortical β 1 and cerebellar β 2 adrenergic receptors are reduced by ca. 25%, while the densities of cortical α 1 and α 2 adrenergic receptors are not significantly altered.Densities of striatal D 1 and D 2 dopaminergic receptors are unaltered. The densities of cortical 5 HT 1 and 5 HT 2 serotonergic receptors are increased by 26-30%. Densities of cortical muscarinic and nicotinic receptors are increased by 40-50%. The density of cortical benzodiazepine-binding sites associated with GABA A receptors is increased by 65%, and the affinity appears slightly decreased. The density of cortical MK-801 sites associated with NMDA-glutaminergic receptors appear unaltered.4. The density of cortical nitrendipine-binding sites associated with calcium channels is increased by 18%.5. The results indicate that chronic ingestion of caffeine equivalent to about 100 mg/kg/day in mice causes a wide range of biochemical alterations in the central nervous system.

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“…This may reflect receptor in transit to or from the plasma membrane. Previous studies have shown that chronic nicotine administration produces an up-regulation of high affinity nicotine binding sites (Ksir et al, 1985, Schwartz and Kellar, 1985, Collins et al, 1989, and that this is mediated by post-translational mechanisms (Marks et al, 1992, Peng et al, 1994. This suggests the possibility that the immunolabeling present in the cytoplasm of dendrites in the DR has the capacity to transfer to the plasma membrane under the appropriate conditions, for example after exposure to chronic nicotine administration.…”

Section: Methodological Considerationsmentioning

confidence: 99%

Alpha4 containing nicotinic receptors are positioned to mediate postsynaptic effects on 5-HT neurons in the rat dorsal raphe nucleus

Commons

2008

Neuroscience

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Nicotinic acetylcholine receptors containing the alpha4 and beta2 subunits constitute the most abundant high-affinity binding site of nicotine in the brain and are critical for the addictive qualities of nicotine. Serotonin neurotransmission is thought to be an important contributor to nicotine addiction. Therefore in this study it was examined how alpha4-containing receptors are positioned to modulate the function of serotonin neurons using ultrastructural analysis of immunolabeling for the alpha4 receptor subunit in the dorsal raphe nucleus (DR), a primary source of forebrain serotonin in the rat. Of 150 profiles labeled for the alpha4 subunit, 140 or 93% consisted of either soma or dendrites, these were often small-caliber (distal) dendrites <1.5 um in diameter (63/150 or 42%). The majority (107/150 or 71%) of profiles containing labeling for alpha4 were dually labeled for the synthetic enzyme for serotonin, tryptophan hydroxylase (TPH). Within dendrites immunogold labeling for alpha4 was present on the plasma membrane or near postsynaptic densities. However, labeling for alpha4 was commonly localized to the cytoplasmic compartment often associated with smooth endoplasmic reticulum, plausibly representing receptors in transit to or from the plasma membrane. Previous studies have suggested that nicotine presynaptically regulates activity onto serotonin neurons, however alpha4 immunolabeling was detected in only 10 axons in the DR or 7% of profiles sampled. This finding suggest that alpha4 containing receptors are minor contributors to presynaptic regulation of synaptic activity onto serotonin neurons, but rather alpha4 containing receptors are positioned to influence serotonin neurons directly at postsynaptic sites. Keywordsacetylcholine; nicotine; anxiety; 5-HT-1A; addictionThe dorsal raphe nucleus (DR) is one of the primary sources of serotonin (5-HT) in the forebrain. Cholinergic modulation of the DR likely influences several physiological functions including sleep cycle (Portas et al., 2000), anxiety and pain sensitivity. In addition, the actions of nicotine in the DR may contribute to nicotine addiction. Acute nicotine administration modifies 5-HT release in the forebrain (Toth et al., 1992, Ribeiro et al., 1993, Summers et al., 1996. Chronic nicotine administration produces alterations in 5-HT receptors, transporters and brain metabolism of 5-HT in both humans and animal models (Benwell and Balfour, Correspondence to: Kathryn G. Commons, Ph.D., Children's Hospital, 300 Longwood Ave., Enders 1206e, Boston, MA 02115, Telephone: 617-919-2220, Fax: 617-730-0235, Email: Kathryn.Commons@Childrens.Harvard.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discove...

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Exposure to nicotine enhances the behavioral stimulant effect of nicotine and increases binding of [3H]acetylcholine to nicotinic receptors

Cited by 195 publications

References 6 publications

Chronic Nicotine Enhances Basal and Nicotine-Induced Fos Immunoreactivity Preferentially in the Medial Prefrontal Cortex of the Rat

Chronic Nicotine Enhances Basal and Nicotine-Induced Fos Immunoreactivity Preferentially in the Medial Prefrontal Cortex of the Rat

Chronic caffeine alters the density of adenosine, adrenergic, cholinergic, GABA, and serotonin receptors and calcium channels in mouse brain

Alpha4 containing nicotinic receptors are positioned to mediate postsynaptic effects on 5-HT neurons in the rat dorsal raphe nucleus

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