Catalepsy and hypolocomotion induced by a nitric oxide donor: attenuation by theophylline

Dall'Igna, Oscar Phelippe Permigotti; Dietrich, Marcelo O.; Hoffmann, Ana; Neto, Waldemar Pires Ferreira; Vendite, Deusa; Souza, Diogo O.; Lara, Diogo R.

doi:10.1016/s0014-2999(01)01457-1

Cited by 13 publications

(6 citation statements)

References 26 publications

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“…In the present study, L-arg, although significantly decreasing the cataleptic effect of intrastriatal L-NAME, produced a small but significant cataleptic effect when administered alone. This result agrees with a reported cataleptic-inducing effect of a NO donor in mice (Dall'Igna et al 2001). Trabace and Kendrick (2000) suggested that NO can reduce DA concentrations in the striatum by increasing ONOO − (peroxynitrite) formation in a calcium-independent manner or increase them through a calcium-dependent mechanism involving sGC activation.…”

Section: Discussionsupporting

confidence: 93%

Intracerebroventricular administration of nitric oxide-sensitive guanylyl cyclase inhibitors induces catalepsy in mice

et al. 2007

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This study showed that pharmacological disruption of the endogenous NO-sGC signaling in the central nervous system induces long-lasting catalepsy in mice. Moreover, the cataleptic effect of NOS inhibition correlates with the decrease in NO( x ) products formation in the striatum. The results give further support to the hypothesis that NO plays a role in motor behavior control mediated, at least in part, by cyclic guanosine monophosphate production in the striatum.

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Section: Discussionsupporting

confidence: 93%

Intracerebroventricular administration of nitric oxide-sensitive guanylyl cyclase inhibitors induces catalepsy in mice

et al. 2007

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“…In the present study, the effectiveness of a slightly lower dose of sildenafil (1.5 mg/kg) suggests a slight shift to the left in the curve for the attenuation of learning impairment induced by L-NAME. These findings are consistent with other inverted U-shaped curves commonly reported for the central effects of NO-related compounds, including effects on motor behavior (Dall'Igna et al 2001), which can be independent of effects on cognition (see above). Similarly, evidence suggests that NO effects on blood pressure are dissociable from effects on cognition Prickaerts et al 1997).…”

Section: Discussionsupporting

confidence: 93%

Phosphodiesterase inhibition by sildenafil citrate attenuates a maze learning impairment in rats induced by nitric oxide synthase inhibition

et al. 2005

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“…Mice mutant for the neuronal NOS isoform have altered locomotor abilities (Kriegsfeld et al, 1999) and rats and mice treated with various NOS inhibitors show problems with fine motor control (Starr and Starr, 1995;Dzoljic et al, 1997;Araki et al, 2001;Dall'Igna et al, 2001;Uzbay, 2001;Del Bel et al, 2002). NO antagonizes the increase in locomotor activity found after dopamine agonists administration (Starr and Starr, 1995).…”

Section: Nitric Oxide and Motor Behavior: The Catalepsy Testmentioning

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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Catalepsy and hypolocomotion induced by a nitric oxide donor: attenuation by theophylline

Cited by 13 publications

References 26 publications

Intracerebroventricular administration of nitric oxide-sensitive guanylyl cyclase inhibitors induces catalepsy in mice

Intracerebroventricular administration of nitric oxide-sensitive guanylyl cyclase inhibitors induces catalepsy in mice

Phosphodiesterase inhibition by sildenafil citrate attenuates a maze learning impairment in rats induced by nitric oxide synthase inhibition

Role of Nitric Oxide on Motor Behavior

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