Differential antagonism of antiavoidance, cataleptic and ptotic effects of neuroleptics by biperiden

Oka, Makoto; Yamada, Kiyoko; Kamei, Chiaki; Yoshida, Kouichi; Shimizu, Masanao

doi:10.1254/jjp.29.435

Cited by 10 publications

(3 citation statements)

References 24 publications

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“…injection of quaternary atropine (atropine methylnitrate, Table I), that does not cross the blood-brain barrier. Biperiden, an antiparkinsonian drug which has antimuscarinic and NMDA receptor antagonist properties, also blocks the cataleptic effect of NOS inhibitors or haloperidol (Oka et al, 1979). It is interesting that one of the principal groups of cholinergic neurons is located in the nucleus tegmental pedunculopontinus (Hirsch et al, 1987).…”

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

confidence: 99%

Role of Nitric Oxide on Motor Behavior

et al. 2005

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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.

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

confidence: 99%

Role of Nitric Oxide on Motor Behavior

et al. 2005

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“…Haloperidol, biperiden, haloperidol þ biperiden, or saline were administered once daily for 14 consecutive days. The 2 mg/kg haloperidol dose was chosen since this dose of haloperidol induces catalepsy in almost all mice (Oka et al, 1979). Also, administration of 2 mg/kg haloperidol has been reported to yield plasma levels in rats that are relevant to that of humans who receive standard doses of haloperidol (Mahadik et al, 1988;Terry et al, 2003).…”

Section: Materials and Methods Animals And Drugsmentioning

confidence: 99%

Administration of haloperidol with biperiden reduces mRNAs related to the ubiquitin-proteasome system in mice

Iwata

Morioka

Iwabuchi

et al. 2005

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In order to find molecules affected by administration of an antipsychotic drug with an antimuscarinic drug, which is a common prescription used to prevent extrapyramidal adverse effects caused by the antipsychotic drugs, gene expression profiling in the frontal cortex was studied in mice. After 14 days of administration with 2 mg/kg haloperidol, a typical antipsychotic drug, and 2 mg/kg biperiden, a high-affinity antagonist for muscarinic receptors in the brain, approximately 500 mRNAs related to synaptic function were investigated. The levels of the mRNAs related to the ubiquitin-related systems were significantly reduced after the combined administration. However, the separate administration of either haloperidol or biperiden had little effect on the levels of the mRNAs. This result suggests that coadministration of haloperidol and biperiden specifically affects the ubiquitin-related system.

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“…Witkin et al (5) reported that certain neuroleptics such as chlorpromazine, triflupromazine and thiopropazate inhibited the pinna reflex in mice. It is well known that neuroleptics induce cataleptic behavior, and this behavior may be related to an imbalance between dopaminergic and cholinergic systems in the extrapyramidal tract connecting to the spinal cord (13). Considering the fact that Hi caused both cataleptic behavior and the inhibition of the pinna reflex, it is possible to assume that the mechanism of occurrence of the pinna reflex may be relevant to that of cataleptic behavior.…”

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confidence: 99%