Evidence for a cholinergic role in haloperidol-induced catalepsy

Klemm, W. R.

doi:10.1007/bf00428402

Cited by 59 publications

(17 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Postsynaptic striatal dopamine D1 and D2 receptors are blocked in case of a typical neuroleptic induced catalepsy (Sanberg, 1980;Farde et al, 1992). Despite the above evidence, role of several other neurotransmitters such as acetylcholine, GABA and serotonin, have also been phenomenon (Klemm, 1985;Somani et al, 1999). Along with dysfunction of various neurotransmitters in haloperidol induced catalepsy, involvement of reactive oxygen species has also been suggested by many clinical and preclinical studies (Polydoro et al, 2004;Sagara, 1998).…”

Section: Discussionmentioning

confidence: 99%

Effect of various extracts of Tabernaemontana divaricata on haloperidol induced catalepsy in rats

Raj

Balasubramaniam²,

Nadeem³

2014

Int Curr Pharm J

View full text Add to dashboard Cite

Parkinsons disease (PD) is one of the neurodegenerative diseases with selective loss of dopamine neurons of the substantia nigra pars compacta. In the present study, anti-cataleptic activity of Tabernaemontana divaricata leaves extracts viz. aqueous and ethanolic at different doses (50, 100 and 150 mg/kg i.p.) were studied using haloperidol (1 mg/kg, i.p.) induced catalepsy in rats which is a useful animal model for screening drugs for Parkinsons disease. Both the extracts were found to reduce catalepsy significantly (P<0.001) as compared to the haloperidol treated rats showing greater effect at 150 mg/kg i.p. dose. Thus the present study reveals the anti-cataleptic activity of Tabernaemontana divaricata evaluating the traditional folklore medicinal use of the plant.DOI: http://dx.doi.org/10.3329/icpj.v3i3.17891 International Current Pharmaceutical Journal, February 2014, 3(3): 240-242

show abstract

Section: Discussionmentioning

confidence: 99%

Effect of various extracts of Tabernaemontana divaricata on haloperidol induced catalepsy in rats

Raj

Balasubramaniam²,

Nadeem³

2014

Int Curr Pharm J

View full text Add to dashboard Cite

show abstract

“…Whereas L-NOARG had an additive effect with haloperidol (Marras et al, 1995), apomorphine, a DA agonist, inhibits L-NOARG catalepsy (Table I). Although there are contradictory results (Silva et al, 1995) most Bel et al, 1998;Klemm, 1983;Klemm, 1985;Ushijima et al, 1997 Silva et al, 1999;Prinssen et al, 2002 Amantadine (NMDA antagonist) ± − Danysz et al 1994;Moore et al, 1993;Papa et al, 1993;Yoshida et al, 1994;Del Bel, unpublished results Note. −: inhibition; +: activation; 0: no effect.…”

Section: Motor Effects Of Nos Inhbitors: Possible Mechanisms Of Actionmentioning

confidence: 91%

Role of Nitric Oxide on Motor Behavior

et al. 2005

View full text Add to dashboard Cite

The present review paper describes results indicating the influence of nitric oxide (NO) on motor control. Our last studies showed that systemic injections of low doses of inhibitors of NO synthase (NOS), the enzyme responsible for NO formation, induce anxiolytic effects in the elevated plus maze whereas higher doses decrease maze exploration. Also, NOS inhibitors decrease locomotion and rearing in an open field arena. These results may involve motor effects of this compounds, since inhibitors of NOS, NG-nitro-L-arginine (L-NOARG), N(G)-nitro-L-arginine methylester (L-NAME), N(G)-monomethyl-L-arginine (L-NMMA), and 7-Nitroindazole (7-NIO), induced catalepsy in mice. This effect was also found in rats after systemic, intracebroventricular or intrastriatal administration. Acute administration of L-NOARG has an additive cataleptic effect with haloperidol, a dopamine D2 antagonist. The catalepsy is also potentiated by WAY 100135 (5-HT1a receptor antagonist), ketanserin (5HT2a and alfal adrenergic receptor antagonist), and ritanserin (5-HT2a and 5HT2c receptor antagonist). Atropine sulfate and biperiden, antimuscarinic drugs, block L-NOARG-induced catalepsy in mice. L-NOARG subchronic administration in mice induces rapid tolerance (3 days) to its cataleptic effects. It also produces cross-tolerance to haloperidol-induced catalepsy. After subchronic L-NOARG treatment there is an increase in the density NADPH-d positive neurons in the dorsal part of nucleus caudate-putamen, nucleus accumbens, and tegmental pedunculupontinus nucleus. In contrast, this treatment decreases NADPH-d neuronal number in the substantia nigra compacta. Considering these results we suggest that (i) NO may modulate motor behavior, probably by interfering with dopaminergic, serotonergic, and cholinergic neurotransmission in the striatum; (ii) Subchronic NO synthesis inhibition induces plastic changes in NO-producing neurons in brain areas related to motor control and causes cross-tolerance to the cataleptic effect of haloperidol, raising the possibility that such treatments could decrease motor side effects associated with antipsychotic medications. Finally, recent studies using experimental Parkinson's disease models suggest an interaction between NO system and neurodegenerative processes in the nigrostriatal pathway. It provides evidence of a protective role of NO. Together, our results indicate that NO may be a key participant on physiological and pathophysiological processes in the nigrostriatal system.

show abstract

“…We postulated Þve possibilities to explain why carteolol improves neuroleptic-induced catalepsy in rats: the Þrst attributes the phenomenon to an anticholinergic e¤ect (Klemm 1985), the second to a stimulative e¤ect on postsynaptic dopamine receptors, the third to 5-HT 1A receptor agonistic activity (Kulikov et al 1994), the fourth to 5-HT 2 receptor blocking activity (Balsara et al 1979) and the Þfth to b-adrenoceptor blocking activity (Ono et al 1986;Tikal 1989). However, the Þrst, second, third and fourth possibilities are unlikely for carteolol.…”

Section: Discussionmentioning

confidence: 98%

“…In addition, anticholinergic drugs and propranolol, which improve neuroleptic-induced catalepsy in laboratory animals (Klemm 1985;Ono et al 1986;Tikal 1989), are e¤ective in neuroleptic-induced akathisia in humans, which suggests that part of the mechanism of neurolepticinduced catalepsy is identical with that of neurolepticinduced akathisia, although the symptoms of neuroleptic-induced catalepsy are di¤erent from those of neuroleptic-induced akathisia. Thus, it has been suggested that drugs which improve neurolepticinduced catalepsy in laboratory animals may be e¤ective in neuroleptic-induced akathisia in humans.…”

Section: Introductionmentioning

confidence: 94%

The attenuating effect of carteolol hydrochloride, a β-adrenoceptor antagonist, on neuroleptic-induced catalepsy in rats

et al. 1997

View full text Add to dashboard Cite

It is known that beta-adrenoceptor antagonists are effective in the treatment of akathisia, one of the extrapyramidal side effects that occur during neuroleptic treatment. Neuroleptic-induced catalepsy, a model of neuroleptic-induced extrapyramidal side effects, was considered suitable as a model for predicting neuroleptic-induced akathisia in humans, although neuroleptic-induced catalepsy was not considered a specific test for neuroleptic-induced akathisia. Therefore, the effects of carteolol, a beta-adrenoceptor antagonist, on haloperidol-induced catalepsy in rats were behaviorally studied and compared with those of propranolol and biperiden, a muscarinic receptor antagonist. Carteolol, as well as propranolol and biperiden, inhibited the haloperidol-induced catalepsy. The inhibitory effect of carteolol was almost comparable to that of propranolol, but was weaker than that of biperiden. Carteolol did not evoke postsynaptic dopamine receptor-stimulating behavioral signs such as stereotypy and hyperlocomotion in rats. Carteolol did not antagonize the inhibitory effects of haloperidol on apomorphine-induced stereotypy and locomotor activity in rats. In addition, carteolol did not evoke 5-HT1A receptor-stimulating behavioral signs such as flat body posture and forepaw treading and did not inhibit 5-hydroxytryptophan-induced head twitch in rats. Finally, carteolol did not inhibit physostigmine-induced lethality in rats. These results strongly suggest that carteolol improves haloperidol-induced catalepsy via its beta-adrenoceptor antagonistic activity and is expected to be effective in the treatment of akathisia without attenuating neuroleptic-induced antipsychotic effects due to its postsynaptic dopamine receptor antagonistic activity.

show abstract

Evidence for a cholinergic role in haloperidol-induced catalepsy

Cited by 59 publications

References 14 publications

Effect of various extracts of Tabernaemontana divaricata on haloperidol induced catalepsy in rats

Effect of various extracts of Tabernaemontana divaricata on haloperidol induced catalepsy in rats

Role of Nitric Oxide on Motor Behavior

The attenuating effect of carteolol hydrochloride, a β-adrenoceptor antagonist, on neuroleptic-induced catalepsy in rats

Contact Info

Product

Resources

About