Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026837 (muscle rigidity)
 1,077 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the study was to investigate the role of the ventromedial thalamic nucleus in the rigidity induced by morphine. Muscle rigidity was assessed using an electromyographic method (EMG) in non-anaesthesized rats with electrodes implanted unilaterally in the gastrocnemius soleus muscle. Subcutaneous (s.c.) injections of morphine in doses of 5, 10 or 20 mg/kg evoked tonic EMG activity in the gastrocnemius soleus muscle; this was estimated as muscle rigidity. Picrotoxin was injected bilaterally into the ventromedial nucleus in doses of 50-400 ng/0.5 microliter 30 min after morphine administration. Picrotoxin in doses of 200 and 400 ng attenuated the tonic EMG activity induced by morphine, 10 mg/kg s.c. Picrotoxin in a dose of 400 ng reduced the tonic activity induced by morphine, 20 mg/kg s.c. The results suggest that the thalamic ventromedial nucleus mediates the morphine-induced rigidity.
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PMID:GABA mechanisms of ventromedial thalamic nucleus in morphine-induced muscle rigidity. 302 5

Because evidence for the neurotransmitter role of dopamine in the gray matter of the spinal cord is accumulating, a question arises of whether or not spinal dopamine receptors are also involved in the effects of dopaminomimetics which are believed to induce beneficial effects in Parkinson's disease through an action thought to be mediated mainly by striatal dopamine receptors. To test this hypothesis muscimol and picrotoxin were injected unilaterally into the posterior part of the substantia nigra of rabbits permanently implanted with stainless-steel cannulae. Muscimol (a GABA-mimetic) enhanced locomotor activity, evoked a stereotyped behavior and contralateral rotations, and increased apomorphine-induced gnawing. Picrotoxin, a substance which inhibits GABA transmission, induced ipsilateral rotations, evoked catalepsy and muscle rigidity, and inhibited locomotor activity. Picrotoxin abolished apomorphine-induced gnawing, and increased haloperidol-mediated catalepsy. The catalepsy induced by an intranigral injection of picrotoxin, and the picrotoxin-evoked blockade of the apomorphine-induced gnawing disappeared within 16 h after the intranigral injection. Alterations in the apomorphine concentration in brain structures (n. caudatus and cerebral cortex) and in spinal cord after picrotoxin injection followed the same time course as the behavioral changes, and returned to the control values 16 h after injection of picrotoxin. Apomorphine was always injected 30 min before the rabbits were killed. Moreover, the substantial increase (to 300%) in apomorphine concentration in the spinal cord probably reflects the antagonism between behavioral changes induced by picrotoxin and the haloperidol catalepsy, rather than the decreased apomorphine concentrations observed in the brain structures. We suggest, therefore, that there exists a correlation between the behavioral effects, which are generally accepted as laboratory models of Parkinson's disease, and the enhanced apomorphine concentration in the spinal cord.
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PMID:Alterations in apomorphine concentration in spinal cord and brain follow the time course of catalepsies induced by different treatments. 686 47