Nicotine potentiates sulpiride-induced catalepsy in mice

Zarrindast, Mohammad Reza; Haeri-Zadeh, F.; Zarghi, Afshin; Lahiji, P.

doi:10.1177/026988119801200308

Cited by 10 publications

(3 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In rodents, nicotine stimulated dopamine release from striatal cells in vitro [32,33] and in vivo [34]. However, acute administration of nicotine potentiated rather than inhibited catalepsy induced in rats by haloperidol [35][36][37] and a few other cataleptogenic drugs [38,39]. To date, the influence of nicotine on somatostatin-mediated brain mechanisms has not been studied.…”

Section: Introductionmentioning

confidence: 99%

Cyclosomatostatin-induced catalepsy in the aged rat: a response to levodopa, diphenhydramine and nicotine

Ionov¹,

Gorev²,

Pushinskaya³

2018

Current Topics in Pharmacology

View full text Add to dashboard Cite

A decrease in somatostatin level is observed in parkinsonian brain. We recently reported that rats given an intracerebroventricular injection of a somatostatin antagonist, cyclosomatostatin, fall into catalepsy; the effect was observed in aged but not young animals. To evaluate the predictive validity of the cyclosomatostatin-induced catalepsy as a model of extrapyramidal disorders, the sensitivity of this catalepsy to clinically effective antiparkinsonian agents was determined. We examined the effects of levodopa and histamine antagonists; also, given an inverse association between Parkinson's disease and tobacco smoking, nicotine was tested. The experiments were conducted using 27-28month-old male Wistar rats. Catalepsy was measured using the bar test. Cyclosomatostatin-induced catalepsy was strongly antagonized by levodopa, which indicates a role for central dopaminergic deficiency in this model. Similarly, histamine H 1receptor antagonist, diphenhydramine, exhibited anticataleptic activity; in contrast, antagonists at H 2and H 3-receptors were without effect. Cataleptic response was inhibited by nicotine; the nicotine sensitivity distinguishes this catalepsy from other models, in particular, from haloperidol-induced catalepsy. Diphenhydramine and nicotine alone only partly suppressed catalepsy; however, coadministration of these drugs almost totally reversed the cataleptogenic effect of cyclosomatostatin. Thus, a similarity between the cyclosomatostatininduced catalepsy and Parkinson's disease with regard to the sensitivity to anti-parkinsonian agents was found. This supports the validity of the model as well as the role of somatostatinergic deficiency in the mechanism of parkinsonian symptoms. Coadministration of diphenhydramine and nicotine appears to be a promising treatment for extrapyramidal disorders in Parkinson's disease.

show abstract

Section: Introductionmentioning

confidence: 99%

Cyclosomatostatin-induced catalepsy in the aged rat: a response to levodopa, diphenhydramine and nicotine

Ionov¹,

Gorev²,

Pushinskaya³

2018

Current Topics in Pharmacology

View full text Add to dashboard Cite

show abstract

Section: Introductionmentioning

confidence: 99%

Cyclosomatostatin-induced catalepsy in the aged rat: a response to levodopa, diphenhydramine and nicotine

Ionov¹,

Pushinskaya²,

Gorev³

2018

View full text Add to dashboard Cite

A decrease in somatostatin level is observed in parkinsonian brain. We recently reported that rats given an intracerebroventricular injection of a somatostatin antagonist, cyclosomatostatin, fall into catalepsy; the effect was observed in aged but not young animals. To evaluate the predictive validity of the cyclosomatostatin-induced catalepsy as a model of extrapyramidal disorders, the sensitivity of this catalepsy to clinically effective antiparkinsonian agents was determined. We examined the effects of levodopa and histamine antagonists; also, given an inverse association between Parkinson's disease and tobacco smoking, nicotine was tested. The experiments were conducted using 27-28month-old male Wistar rats. Catalepsy was measured using the bar test. Cyclosomatostatin-induced catalepsy was strongly antagonized by levodopa, which indicates a role for central dopaminergic deficiency in this model. Similarly, histamine H 1receptor antagonist, diphenhydramine, exhibited anticataleptic activity; in contrast, antagonists at H 2and H 3 -receptors were without effect. Cataleptic response was inhibited by nicotine; the nicotine sensitivity distinguishes this catalepsy from other models, in particular, from haloperidol-induced catalepsy. Diphenhydramine and nicotine alone only partly suppressed catalepsy; however, coadministration of these drugs almost totally reversed the cataleptogenic effect of cyclosomatostatin.Thus, a similarity between the cyclosomatostatininduced catalepsy and Parkinson's disease with regard to the sensitivity to anti-parkinsonian agents was found. This supports the validity of the model as well as the role of somatostatinergic deficiency in the mechanism of parkinsonian symptoms. Coadministration of diphenhydramine and nicotine appears to be a promising treatment for extrapyramidal disorders in Parkinson's disease.

show abstract

“…The influence of nicotine on dopaminergic neurotransmission and catalepsy has been previously examined. Nicotine increased dopamine release from neurons in vitro [18] and in vivo [19]; however, acute administration of nicotine potentiated rather than inhibited catalepsy induced by haloperidol [20] and some other neuroleptics [21,22]. Nicotine in vitro protected dopaminergic neurons against a range of toxic insults [23]; however, in vivo this drug can increase the susceptibility of nigral neurons to toxic injury [24].…”

Section: Introductionmentioning

confidence: 99%

Cyclosomatostatin-Induced Catalepsy in the Aged Wistar Rats: Inhibition by Nicotine

Ionova

Pushinskaya²

2017

Avicenna. J. Neuro. Psycho. Physio.

View full text Add to dashboard Cite

Background: Recently, it has been found that Cyclosomatostatin (CSST) induces Catalepsy, a State Similar to extrapyramidal dysfunctions in Parkinson disease. The sensitivity of CSST-induced catalepsy to clinically effective antiparkinsonian agents is unknown. Epidemiological studies have documented an inverse association between parkinsonism and tobacco smoking that suggests an antiparkinsonian activity of nicotine. To evaluate the similarity between human illness and CSSTinduced catalepsy, we studied the sensitivity of this model to nicotine. Materials and Methods: The experiments were conducted on 27-to 28-month-old male Wistar rats. To determine the cataleptogenic doses of CSST, this drug (0.5, 2, and 10 µg) was injected intracerebroventricularly. Nicotine (0.1, 0.4, and 1 mg/kg) was given subcutaneously. Catalepsy was defined as an increased period of immobility in the bar test. All groups consisted of 8 animals. Results: CSST (10 µg) increased period of immobility compared with the controls (P<0.01). Nicotine (0.4 and 1 mg/kg) inhibited this effect (P<0.05). Conclusion: CSST-induced catalepsy in Wistar rats can be reduced by nicotine. These data support the validity of this behavioral response as a model of human extrapyramidal dysfunctions.

show abstract

Nicotine potentiates sulpiride-induced catalepsy in mice

Cited by 10 publications

References 26 publications

Cyclosomatostatin-induced catalepsy in the aged rat: a response to levodopa, diphenhydramine and nicotine

Cyclosomatostatin-induced catalepsy in the aged rat: a response to levodopa, diphenhydramine and nicotine

Cyclosomatostatin-induced catalepsy in the aged rat: a response to levodopa, diphenhydramine and nicotine

Cyclosomatostatin-Induced Catalepsy in the Aged Wistar Rats: Inhibition by Nicotine

Contact Info

Product

Resources

About