Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In view of the recently demonstrated extra-endocrine central actions of hypothalamic releasing hormones, we have investigated the effects of prolyl-leucyl-glycinamide (PLG) and thyrotropin releasing hormone (TRH) on morphine-induced catalepsy. Although acute administration of PLG (10 mg kg-1 s.c.) slightly attenuated the cataleptic response, chronic PLG treatment (10 mg kg-1 s.c. for 10 days) virtually abolished morphine-induced catalepsy. TRH, administered subcutaneously, exhibited little or no anti-cataleptic activity. These results are discussed in relation to the possible central site of narcotic-induced catalepsy and the therapeutic potential of PLG in Parkinson's disease.
 ...
PMID:Antagonism of morphine-induced catalepsy by L-prolyl-L-leucyl-glycinamide. 3 58

The effects of the morphinan drugs dextrorphan, dextromethorphan and levorphanol were tested towards the cataleptic activity induced by 1 mg/kg of haloperidol i.p. in rats. The influence of the morphinans was compared to that of the N-methyl-D-aspartate competitive antagonist, 2-amino-5-phosphonovaleric acid. 2-Amino-5-phosphonovaleric acid (0.5 mumoles, i.c.v.), dextrorphan (7.5-15 mg/kg, i.p.) and dextromethorphan (15-30 mg/kg, i.p.) significantly reduced the degree of catalepsy in the haloperidol-treated rats within 15 min. Conversely, levorphanol (15-30 mg/kg, i.p.) significantly increased the degree of catalepsy in the haloperidol-treated rats within 15 min. Naloxone (2 mg/kg, i.p.) counteracted the potentiating effects of levorphanol. These findings demonstrate a differential influence of the morphinan stereoisomers dextrorphan and levorphanol on experimental catalepsy, and suggest a potential use of dextromethorphan in the treatment of Parkinson's disease.
 ...
PMID:Differential effects of morphinan drugs on haloperidol-induced catalepsy in rats: a comparative study with an N-methyl-D-aspartate antagonist. 168 12

Current long-term treatment of Parkinson's disease is inadequate, and improved symptomatic and neuroprotective therapies are needed. Recent interest has focused on the use of antagonists of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor in Parkinson's disease. Abnormally increased activity of the subthalamic nucleus is postulated to play a central pathophysiological role in the signs of Parkinson's disease, and NMDA antagonists may provide a means of decreasing this activity selectively. Like dopaminergic agonists, NMDA antagonists can reverse the akinesia and rigidity associated with monoamine depletion or neuroleptic-induced catalepsy. Very low doses of NMDA antagonists markedly potentiate the therapeutic effects of dopaminergic agonists. There is evidence that the beneficial effects of anticholinergic drugs and amantadine may be mediated, in part, by NMDA receptor blockade. Moreover, NMDA antagonists provide profound protection of dopaminergic neurons of the substantia nigra in the MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) and methamphetamine models of Parkinson's disease. The clinical use of NMDA antagonists may prove useful in Parkinson's disease to treat symptoms and retard disease progression.
 ...
PMID:N-methyl-D-aspartate antagonists in the treatment of Parkinson's disease. 147 53

Behavioural and some neurochemical effects of Ro 40-7592 (3,4-dihydroxy-4'-methyl-5-nitrobenzophenone), a new COMT inhibitor, were studied in rats and mice. Ro 40-7592 increased the effect of L-DOPA (plus benserazide) on locomotor activity, reserpine-induced hypothermia, and catalepsy induced by pimozide, haloperidol and fluphenazine. Locomotor hyperactivity induced by amphetamine or nomifensine, as well as stereotypy induced by amphetamine (but not apomorphine), were also increased by Ro 40-7592. The drug stimulated exploratory activity in the open field test. It decreased the levels of HVA and 3-MT, increased the level of DOPAC but did not change the levels of dopamine in the striatum, nucleus accumbens and frontal cortex. These results indicate that Ro 40-7592 may improve the therapy with L-DOPA (plus decarboxylase inhibitor) of Parkinson's disease.
 ...
PMID:Behavioural and neurochemical effects of Ro 40-7592, a new COMT inhibitor with a potential therapeutic activity in Parkinson's disease. 197 8

Subcutaneous administration of fluphenazine elicits catelepsy that can be attenuated by the glutamate antagonists MK801 and phencyclidine (PCP). 3-[-(+)-2-carboxy piperazine-4-yl]-propyl-1-phosphanate (CPP) was found to be ineffective in this model. Intrastriatal injections of sulpiride or fluphenazine were also found to induce catalepsy which could be attenuated by MK801 and PCP. These results illustrate that nondopaminergic compounds might possibly be of value in the treatment of Parkinson's disease. Furthermore it was demonstrated that this paradigm can be utilized to investigate neurotransmitter interactions within the striatum. This was clearly emphasized by the observation that bilateral administration of MK801 into the striatum increased basal locomotor activity.
 ...
PMID:Neuroleptic-induced catalepsy as a model of Parkinson's disease. II. Effect of glutamate antagonists. 197 10

N-methyl-D-aspartic acid (NMDA; 40 mg/kg, i.p.) did not elicit catalepsy, but it potentiated the cataleptic effect of haloperidol and GABAB receptor agonist, baclofen. MK-801 (0.2 mg/kg, i.p.), NMDA-receptor antagonist, reversed haloperidol- but not baclofen-induced catalepsy. MK-801 also potentiated the anticataleptic effect of scopolamine and bromocriptine against haloperidol-induced catalepsy. Dihydropyridine (DHP) calcium-channel antagonists such as nimodipine and nitrendipine (10 mg/kg, i.p.), reversed the anticataleptic effect of MK-801, and potentiated the cataleptic effect of haloperidol, as well as baclofen. These observations indicate the involvement of NMDA receptors in catalepsy, and suggest a potential clinical implication of NMDA-receptor antagonists in Parkinson's disease.
 ...
PMID:Role of N-methyl-D-aspartate (NMDA) receptors in experimental catalepsy in rats. 215 85

The N-methyl-D-aspartate (NMDA) antagonist MK-801 was administered to rats in three doses (0.08, 0.16, 0.33 mg/kg) in order to examine its effects on catalepsy that was induced by haloperidol (0.5 mg/kg). The degree of catalepsy was assessed 30 and 60 min after application of drugs by placing the rat on a horizontal bar, on a podium and on a vertical grid. Animals having received saline and haloperidol showed a higher degree of catalepsy than animals having received MK-801 and haloperidol (except for the lowest dose of MK-801). These findings may suggest a therapeutic potential of MK-801 and possibly of other NMDA antagonists in the treatment of Parkinson's disease.
 ...
PMID:Anticataleptic effects of the N-methyl-D-aspartate antagonist MK-801 in rats. 254

Several reports have indicated that melatonin influences motor activity in animals and humans. Melatonin has been reported to attenuate the rigidity and tremor of Parkinson's disease. Some of the behavioral effects (e.g., analgesic and anticonvulsant properties) of melatonin have been reported to be mediated through interactions with the endogenous opioid peptides. We investigated the effect of melatonin on reserpine-induced catalepsy in the rat and, additionally, examined whether this effect is modified by opioid peptides. Melatonin was found to attenuate markedly the duration of reserpine-induced catalepsy. These effects were potentiated by administration of the opiate agonist nalbuphine hydrochloride, while naloxone partially reversed the catalepsy reducing effect of melatonin. These findings suggest that the motor effects of melatonin may involve critical interactions with opioid peptides, and support the postulated reciprocal interactions between melatonin and opioid peptides that previously have been demonstrated for the analgesic and anticonvulsant properties of melatonin.
 ...
PMID:Attenuation of reserpine-induced catalepsy by melatonin and the role of the opioid system. 258 45

The present study evaluates the effects of MPTP-induced striatal DA depletions on sensorimotor behavior in mice. While MPTP produces no obvious behavioral deficits under normal conditions, acute stress (cold swim) or injection of low doses of haloperidol results in marked akinesia, catalepsy, and sensory neglect. Thus, significant behavioral impairments do accompany the neurotoxicity observed after MPTP administration in mice and render this a valuable animal model for studying mechanisms underlying Parkinson's disease.
 ...
PMID:Acute stress or neuroleptics elicit sensorimotor deficits in MPTP-treated mice. 325 74

Haloperidol-induced (0.25-1.0 mg/kg) catalepsy in rats is characterized by rhythmic time fluctuations. Marked catalepsy was accompanied by slow regular waves at 2-4 and 5-7 min period. Natural or L-dopa-induced inhibition of the process involves the phase of irregular and frequent fluctuations. The study of time fluctuations of the muscular tone are believed important for predicting the development of drug-induced Parkinson's disease.
 ...
PMID:[Minute rhythms of haloperidol catalepsy in rats]. 394 22


1 2 3 4 5 6 7 8 9 10 Next >>