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Results for “Catalepsy”

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At least 37 records · Page 2Linked to original sources
PubMed1978

A study of the sites of interaction between dopamine and 5-hydroxytryptamine for the production of fluphenazine-induced catalepsy.

The effect of reducing 5-hydroxytryptamine (5-HT) concentration within various areas of the central dopamine (DA) system on catalepsy has been investigated. The neurotoxin 5,7-dihydroxytryptamine was used to selectively deplete 5-HT in the striatum, nucleus accumbens septi, tuberculum olfactorium or substantia nigra. Localised depletion of 5-HT within the nucleus accumbens septi and substantia nigra reduced the cataleptic effects of the neuroleptic agent fluphenazine, while lesions of the striatum or tuberculum olfactorium were without effect. Each injection of neurotoxin resulted in a 38--47% depletion of 5-HT in the target site: DA levels were not significantly altered. The results suggest that varied dopamine/5-hydroxytryptamine interactions within the nucleus accumbens may contribute to the action of the neuroleptic. The reduction of fluphenazine-induced catalepsy produced by 5-HT depletion within the substantia nigra supports the concept of a controlling influence of 5-HT on nigro-striatal DA function.

Animals↗
PubMed1979

Dopaminergic antagonism and catalepsy in the developing rat.

The cataleptic effect of the dopaminergic blockers spiroperidol and haloperidol was investigated in developing rats. Both neuroleptics were found to produce less catalepsy in 15 day old rats than in either 10 or 20 day old animals. It is proposed that the decrement in catalepsy occurring between 10 and 15 days of age is related to increased dopaminergic activity in the neostriatum. The reversal of this phenomenon by 20 days may be a consequence of maturation of cholinergic local circuit neurons.

Aging↗
PubMed2026

The influence of neuroprotector isatin on haloperidolinduced catalepsy and proteomic profile of mice brain.

Isatin (indol-2,3-dione) is an endogenous regulator found in humans and animals. It interacts with numerous target proteins and exhibits a wide range of biological activities, including neuroprotective action in animal models of Parkinson's disease (PD) induced by administration of neurotoxins MPTP (1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine) or rotenone. An antipsychotic drug haloperidol, which impairs neurotransmitter balance in the nigrostriatal pathway, models dopamine deficiency and promotes the development of motor disorders characteristic of PD. In this work, the effect of two doses of isatin (10 mg/kg and 80 mg/kg) on the haloperidol catalepsy and on the proteomic profile of mice brain was investigated. The pretreatment of animals with isatin (1 h before haloperidol administration) reduced the occurrence of haloperidol catalepsy. The administration of haloperidol and also isatin with haloperidol influenced the relative content of a number of proteins associated with PD and other neurodegenerative diseases.

Animals↗
PubMed1979

Production of catalepsy and depletion of brain monoamines by a butyrophenone derivative.

1 The cataleptic and monoamine-depleting effects of a butyrophenone derivative (4'-fluoro-4-[[4-(p-fluorophenyl)-3-cyclohexen-1-yl]-amino]-butyrophenone hydrochloride, U-32, 802A) were studied in rats and mice and compared with those of tetrabenazine. 2 Catalepsy was evaluated by means of a modified grid test which allowed the repetition of the test in the same animal several times without affecting the results. Both drugs produced a dose-related cataleptic state of similar time course. 3 Like tetrabenazine, U-32, 802A induced a large reduction in the content of 5-hydroxytryptamine, dopamine and noradrenaline in different parts of the brain, with a concomitant elevation in the metabolites 5-hydroxyindol-3-yl acetic acid and homovanillic acid. The time courses of the catalepsy and the reduction in brain monoamines were very similar. 4 The activity of U-32, 802A suggested that the drug, although chemically a butyrophenone, might act primarily at the presynaptic organelle for storage of monoamines in a way similar to tetrabenazine.

Animals↗
PubMedDate not supplied

[Comparative neurochemical and physiological characteristics of catalepsy-like rest and sleep].

In vertebrates (excluding mammals), the rest is presented also by a special functional condition of the catalepsy type. In hens, its total duration is higher in the day-time, than in the twilight; it is completely absent at night. This natural condition in hens may be imitated by photogenic catalepsy which is developed in response to rhythmic illumination of animals. Cytospectrophotometric investigation of single cells of the supraoptic nucleus indicates that with respect to absence of changes in absolute content (per 1 cell) of protein in the neurons cataleptiform rest in hens does not differ from the sleep in rats. However, in contrast to sleep this immobilization is associated with the decrease of RNA content of the neurons, as well as with the absence of accumulation of proteins and RNA in gliocytes. During cataleptiform rest, insiginficant changes were found in the content of proteins and RNA in cells of ectomammilar nucleus of the additional optic system and thalamic round nucleus. Cataleptiform (photogenic) immobilization in hens is presumably a metabolically passive form of rest as compared to the sleep in rats, which is characterized by anabolic processes in the brain.

Animals↗
PubMed1979

Effect of haloperidol on reflex activation of rat alpha-motoneurones. A possible explanation for akinesia and catalepsy?

Effects of haloperidol on rat flexor and extensor alpha-motoneurones were studied in ventral roots of laminectomized rats under halothane anesthesia. The alpha-motoneurones were activated by tetanic stimulation of low-threshold afferents (group I and II), either of the ipsilateral peroneal nerve ("flexor alpha-motoneurones") or gastrocnemius-soleus nerve ("extensor alpha-motoneurones"). Haloperidol, given in the doses of 0.075, 0.15 and 0.30 mg/kg i.p. inhibited the reflex activation of flexor alpha-motoneurones; higher doses seemed to be more effective than lower ones. Apomorphine (2 mg/kg s.c.) partially antagonized the inhibitory action of haloperidol with some latency. Higher doses of haloperidol (0.15-0.60 mg/kg i.p.) also inhibited the reflex activation of extensor alpha-motoneurones; this inhibitory effect was, at least for a short time, antagonized by apomorphine (2 mg/kg s.c.). The threshold for reflex activation both of flexor and extensor alpha-motoneurones was raised by haloperidol and lowered by a subsequent administration of apomorphine. Our results suggest that akinesia and catalepsy, induced in rats by haloperidol might be, at least in part, due to a decrease in sensitivity of alpha-motoneurones to proprioceptive stimuli.

Animals↗
PubMed1979

Potentiation of haloperidol-induced catalepsy by dopamine agonists: possible involvement of central 5-hydroxytryptamine.

Apomorphine (0.12--2 mg/kg, SC) and d-amphetamine (1--8 mg/kg, IP) were each able, at certain doses, to potentiate the cataleptic state produced by the neuroleptic agent, haloperidol (1 mg/kg, IP). In subsequent biochemical experiments, in which the effects of combinations of apomorphine or d-amphetamine and haloperidol on brain monoamine levels were studied, this behavioural observation was seen to be related to an enhanced utilisation of 5-hydroxytryptamine (5-HT) in certain brain regions. The results suggest not only the possible involvement of 5-HT in the production of catalepsy, but also that the effects of these 'classical' dopamine agonists on other central transmitter systems should be considered when interpreting their various behavioural responses.

Animals↗
PubMedDate not supplied

The effect of baclofen and aminoxyacetic acid on catalepsy in the rat.

Gabaergic compounds, baclofen and aminoxyacetic acid (AOAA) potentiate the catalepsy induced by neuroleptics. This effect indicates their functional antagonism towards the central dopaminergic system. Both compounds exert a central antiserotonin effect. Baclofen, but not AOAA, also shows weak cholinolytic properties. However, the potentiation of cataleptogenic action of neuroleptics by baclofen and AOAA is not related to their effect on the central serotonergic or cholinergic systems.

5-Hydroxytryptophan↗
PubMed1979

Effect of drugs influencing central serotonergic mechanisms on haloperidol-induced catalepsy.

Pretreatment with quipazine, a serotonin agonist, and clomipramine, a selective serotonin neuronal uptake blocker, was found to potentiate the cataleptic effect of haloperidol in a dose-dependent manner in rats. Pretreatment with methysergide, a serotonin antagonist, reduced the cataleptic effect of haloperidol. The results indicate that the cataleptic effect of neuroleptics depends on the balance between the dopaminergic and serotonergic systems, and that the serotonergic system exerts an inhibitory influence on the dopaminergic system.

Animals↗
PubMed1978

6-OHDA lesion to the dorsal noradrenergic bundle alters morphine-induced locomotor activity and catalepsy.

Rats show an initial depression in locomotor activity in response to doses of morphine greater than 5 mg/kg during the first hour after injection which is followed by a prolonged hyperactive phase. The effect of bilateral 6-hydroxydopamine (6-OHDA) lesions to the dorsal noradrenergic bundle on this biphasic action of morphine was studied. These lesions were found to significantly potentiate the locomotor depressant effects of morphine at 10.0 and 20.0 mg/kg while leaving the subsequent stimulant action of morphine unchanged. The cataleptic action of morphine at 20.0 mg/kg as measured in a separate test was also potentiated. These lesions were found to deplete hippocampal and cortical noradrenaline (NA) to 3% and hypothalamic NA to 32% of control values and also to cause significant increases in cerebellar and spinal NA. These data suggest a role for NA in the depressant effects of morphine but not in its subsequent stimulant actions which appear to be mediated by other neurochemical systems.

Animals↗