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At least 613 records · Page 34Linked to original sources
PubMed1978

Computer analysis of interacting dopaminergic and cholinergic control mechanisms in the extrapyramidal system.

The experimental results of many authors suggest that the output activity of the extrapyramidal motor control system depends on a balance between the levels present of the chemical transmitters dopamine and acetylcholine. In this paper it is proposed that these results are best explained by two feedback regulatory systems interconnected with positive interaction--in the sense of the relative gain array (Bristol, 1966). Using the computer-aided design procedure CAIAD, a simple two-input two-output model is simulated so as to give responses similar to those observed when dopaminergic or cholinergic drugs are applied. The effect of reducing the gain in one control loop corresponds to the effect of lesioning part of the extrapyramidal system in the brain. In addition, the effect of an anti-schizophrenic drug such as haloperidol is interpreted as a disturbance input on one of the interacting paths.

Acetylcholine↗
PubMedDate not supplied

Adult onset of stuttering as a presenting sign in a parkinsonian-like syndrome: a case report.

Stuttering onset in adulthood is rare. With no prior history of stuttering or demonstrable neurological insult, diagnosis is often that of a conversion reaction. Stuttering as the first sign of a parkinsonian-like syndrome in extrapyramidal disease has only been reported once in the previous 30 years (Koller, 1983). The present case study differs from and builds upon the case reports in the literature, and describes a 29-year-old white male who began stuttering purportedly secondary to psychological stress. The fluency evaluation revealed severe stuttering characterized by multiple repetitions and/or blocks, with 20 or more repetitions per word routinely noted during both conversational speech and oral reading. No starters or secondary stuttering characteristics, no specific word fears or avoidances, and no situational fears were exhibited. The subsequent neurological examination found resting tremor in hands and legs, lingual fasciculations, gait imbalance, and numbness and tingling of the hands and feet, all of which were progressive in nature. Rehabilitation initially focused on fluency therapy, but then included psychiatric therapy, and finally medical intervention. Fluency and psychiatric therapies were unsuccessful in eliminating stuttering. Following a diagnosis of parkinsonian-like syndrome, medical intervention with carbidopa-levodopa resulted in dramatic improvement of motor, sensory, and fluency symptoms. It is important to consider extrapyramidal disease as an etiological factor in patients with adult onset of stuttering.

Adult↗
PubMed1985

Primate model of parkinsonism: selective lesion of nigrostriatal neurons by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine produces an extrapyramidal syndrome in rhesus monkeys.

Systemic administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to rhesus monkeys (1.0-2.5 mg/kg i.v.) produces irreversible damage to nigrostriatal neurons. Dopaminergic neurons in the dorsolateral part of striatum were the most vulnerable. The major clinical signs of an extrapyramidal syndrome, but not resting tremor, appeared only in MPTP-treated monkeys suffering from more than 80% reduction in striatal dopamine. No chronic changes in the mesolimbic dopaminergic system were observed. Immunocytochemical staining of the mid-brain with a tyrosine hydroxylase antiserum indicated that MPTP produced a significant decrease of dopaminergic cell bodies in the A9, but not in the A10 ventrotegmental area. Despite greater than 80% decrease in A9 nigral cell bodies, the dopamine content decreased only by 50%. Sprouting of the surviving nigral A9 neurons was observed histologically and neurochemically in the area above substantia nigra. The present behavioral, neurochemical and histological results indicate that MPTP produces an ideal primate model for studying parkinsonism. Selective lesion of more than 80% of the nigrostrial neurons by MPTP is sufficient to produce the major clinical signs of the extrapyramidal syndrome in idiopathic parkinsonism.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1985

Role of female gonadal hormones in the CNS: clinical and experimental aspects.

The large body of evidence presented indicates that in the brain the action of sex hormones cannot be thought as restricted to the regulation of endocrine functions and mating behavior. Estrogens and progesterone seem to act in numerous regions of the CNS to regulate motor as well as limbic functions. Furthermore, the data reviewed indicate that these hormones may modulate neuronal activity through a wide variety of mechanisms. More studies should focus on such mechanisms in order to better understand the role of sex hormones in the CNS and to devise ways of limiting their effects on depression, epilepsy etc. It is known that in peripheral target organs these hormones modulate cell activities by binding to specific receptors which can recognize the DNA sequence and activate the transcription of selected genes (135, 136). There is evidence supporting the hypothesis that this mechanism of action has been conserved also in the brain. First, the brain receptors for progesterone and estrogens are functionally and biochemically indistinguishable from those in the periphery (4, 5): they may be concentrated in neuronal nuclei and bind chromatin "in vitro" (7). Second, a temporal relationship has been observed between administration of steroids and the increase of polymerase II activity (137) and protein synthesis (4, 5). Third, various hormone-induced behaviors may be blocked by inhibitors of the protein synthesis (138, 139, 140, 141). However, sex hormones must be capable to regulate neuronal functions by mechanisms other then genomic. In fact, the topical application of estrogen or progesterone on nervous tissue results in a rapid change of membrane potential (60, 71). Such a rapid effect is not likely to be the consequence of nuclear action, but rather must be related to events occurring on the cell surface. It has been hypothesized that sex steroids affect the fluidity of the cell membrane, therefore modifying the ion transport or neurotransmitter receptor activity (142). If this were the case we would expect to observe a similar effect after application of any steroid. Experimental evidence demonstrates that not all the steroids affect the nervous membrane potential. Moreover, two steroids, estradiol and progesterone, have been described to modulate membrane potential in an opposite way (66, 67, 69, 75). At the moment, there is no evidence for the presence of steroid receptors on neuronal membranes which could mediate the described phenomena.(ABSTRACT TRUNCATED AT 400 WORDS)

Amygdala↗
PubMed1996

Extrapyramidal effects of methanandamide, an analog of anandamide, the endogenous CB1 receptor ligand.

Recent evidence has demonstrated that arachidonylethanolamide ("anandamide", AEA), the major endogenous ligand of CB1 receptors, inhibits motor behavior in rats, as does (-)delta 9-tetrahydrocannabinol (THC), the prototypical tricyclic cannabinoid derived from Cannabis sativa preparations. However, its effects were of shorter duration, as compared to THC, likely due to its rapid breakdown by an amidase activity. The present work has been designed to examine the motor effects of AM356(R-methanandamide), an analog of AEA that possesses higher metabolic stability to amidase hydrolysis. We have studied the dose-response and time-course effects of R-methanandamide, i.p. administered, on ambulatory activity, frequency of stereotypy and time spent in inactivity measured in an open-field test. Results were as follows. R-Methanandamide, as THC and AEA, inhibited motor behavior. Thus, it decreased ambulation and stereotypy and increased the time spent in inactivity, usually in a dose-related manner, 10 min after administration. However, the motor deficit caused by the highest dose of R-methanandamide was usually more pronounced than that caused by a similar dose of AEA. These inhibitory effects persisted 30 min after the administration of R-methanandamide, as occurred with AEA and THC. Interestingly, at 60 min after administration, the effects of AEA disappeared, likely because of its breakdown to arachidonic acid and ethanolamine, but this did not occur with R-methanandamide whose effects persisted even until 180 min after treatment as occurred with THC. In summary, R-methanandamide inhibits motor behavior in a manner (its effects were persistent) that resembles the effects of THC rather than the effects of AEA (its effects were of rapid onset but shorter duration). This fact supports the use of R-methanandamide as a valuable tool for studying the physiological roles of the anandamidergic system.

Animals↗