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[Possible mechanisms of firing patterns reorganization of the neurons of the output nuclei basal ganglia].

Previously proposed unitary modification rules and known experimental data were used for understanding possible mechanisms of reorganization of firing patterns of neurons in the output basal ganglia nuclei. According to the suggested mechanism, a switch from regular-spiking to bursting activity evoked by systemic inactivation of N-methyl-d-aspartate (NMDA) receptors or dopaminic receptors mainly depends on modifications of cortico-striatal synapses whereas the opposite effect of inactivation of the same receptors directly on the output basal ganglia cells is less effective. We hypothesized that some of the output basal ganglia nuclei neurons which can generate bursting discharges due to inactivation of NMDA and dopaminic receptors are glutamatergic or cholinergic cells.

Animals↗

Computer tomography in basal ganglia calcification.

The computer tomographic findings in basal ganglia calcification are presented. The incidence is much higher than previously recognised in all forms of hypoparathyroidism, on accout of the sensitivity of CT as compared to conventional radiography.

Basal Ganglia Diseases↗

Intracellular pH measurements of the whole head and the basal ganglia in chronic liver disease: a phosphorus-31 MR spectroscopy study.

The purpose of this study was to determine the intracellular pH of the whole head and in voxels localized to the basal ganglia in patients with chronic liver disease using phosphorus-31 magnetic resonance spectroscopy (31P MRS). The study group compromised 82 patients with biopsy-proven cirrhosis (43 Child's grade A, 25 Child's grade B and 14 Child's grade C). Eleven subjects showed no evidence of neuropsychiatric impairment on clinical, psychometric and electrophysiological testing, 37 showed evidence of minimal hepatic encephalopathy and 34 had overt hepatic encephalopathy. Unlocalized 31P MRS of the whole head was performed in 48 patients and 10 healthy volunteers. Localized 31P MRS of the basal ganglia was performed in the 34 patients and in 20 healthy volunteers. The intracellular pH values were calculated from the chemical shift difference between the inorganic phosphate (P) and phosphocreatine (PCr) resonances. The percentage inorganic phosphate (%Pi), phosphocreatine (%PCr) and betaNTP signals, relative to the total 31P signal, and peak area ratios of inorganic phosphate and phosphocreatine, relative to betaNTP were also measured. There were no differences between patients and volunteers in intracellular pH in 31P MR spectra measured from the whole head or the basal ganglia. There was no correlation between the severity of encephalopathy (West Haven criteria) or liver dysfunction (Child score) and intracellular pH values. There was also no significant change in the inorganic phosphate, phosphocreatine or betaNTP resonances in spectra acquired from the whole head. However, in spectra localized to the basal ganglia, there was a significant increase in mean P/NTP (p=0.02) and PCr/NTP (p=0.009). The mean %Pi and mean %PCr were also increased (p=0.06; p=0.05, respectively), but there was no significant change in mean %betaNTP. When the patient population was classified according to the severity of encephalopathy, those with overt disease had a higher mean P/NTP and %Pi (p=0.03; p=0.01), compared to the reference population. Our results suggest that there are detectable bioenergetic abnormalities in patients with minimal hepatic encephalopathy or stable, overt chronic hepatic encephalopathy, but any associated intracellular pH change is probably a secondary, rather than a primary phenomenon.

Adult↗

Electrophysiological effects of SKF 38393 in rats with reserpine treatment and 6-hydroxydopamine-induced nigrostriatal lesions reveal two types of plasticity in D1 dopamine receptor modulation of basal ganglia output.

To examine the role of D1 dopamine receptors in modulating basal ganglia output and how this role may be altered by changes in dopaminergic transmission, the effects of a D1 dopamine agonist on firing rates of substantia nigra pars reticulata (SNpr) neurons were determined in reserpine-treated rats and compared with effects observed in nigrostriatal-lesioned and normal rats. It was confirmed that systemic administration of the D1 dopamine agonist SKF 38393 (10 mg/kg i.v.) induces a small (averaging 20% above base line) increase in firing rates of SNpr neurons in normal rats and significantly inhibits SNpr single unit activity in rats studied 6 to 26 weeks after 6-hydroxydopamine (6-OHDA)-induced substantia nigra dopamine cell lesion. In contrast to results obtained after 6-OHDA lesions, SKF 38393 administration consistently and significantly increased the firing rates of SNpr neurons in rats treated for 6 days with reserpine (1 mg/kg/day s.c.); increases averaged 88% above base line. Five days after the 6-day reserpine treatment was discontinued, administration of SKF 38393 still induced a pronounced increase in SNpr activity. These increases were reversed by the administration of the D1 dopamine antagonist SCH 23390. SKF 38393 also significantly increased the firing rates of a subpopulation of SNpr neurons in rats treated with only a single dose of reserpine (10 mg/kg s.c. 4-7 hr). The difference between responses in reserpine and 6-OHDA-treated rats was not due to the shorter time course of the reserpine treatments, as SKF 38393 did not consistently affect the activity of SNpr neurons 7 days after 6-OHDA nigral dopamine cell lesion. When the subchronic reserpine treatment was administered to rats lesioned previously with 6-OHDA, D1 dopamine agonist-mediated inhibition of SNpr neuronal activity was obtained. The results show that SNpr responses to D1 dopamine agonist administration after reserpine treatment are enhanced ("supersensitive") relative to normal, whereas SNpr responses to D1 dopamine agonists in animals with 6-OHDA-induced dopamine cell degeneration are opposite to those observed in normal and in reserpinized animals. Current models of basal ganglia function predict that D1 dopamine agonists should reduce activity in the SNpr, because D1 dopamine receptors on striatonigral neurons are thought to stimulate striatonigral firing rates and to enhance the release of tau-aminobutyric acid in the SNpr. The present results call for modification of these concepts.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

The basal ganglia and the locomotor regions.

This review cites evidence suggesting that the pedunculopontine nucleus (PPN), long known as a site of termination for basal ganglia outputs, is equivalent to the mesencephalic locomotor region (MLR), an area known to modulate spinal locomotion oscillators. The presence of cholinergic cells in this area also identifies it with the CH-5 cell group. In keeping with its cellular make-up, evidence is reviewed suggesting that the descending output of the PPN/MLR is cholinergic. This output may be under nigral GABAergic control which, in turn, may be under subthalamic influence. From various lines of evidence, it appears that the PPN/MLR receives elements of information from the motor cortex and basal ganglia centers involved in postural control. This area may be involved in the relay of information useful in the control of the center of gravity and other postural functions during locomotion. Pathological evidence is reviewed implicating basal ganglia afferents to the PPN/MLR (Parkinson's disease) and PPN/MLR efferents (Alzheimer's disease) in the deficits in locomotion observed in certain disorders.

Alzheimer Disease↗

Cognitive- and movement-related potentials recorded in the human basal ganglia.

Sources of potentials evoked by cognitive processing of sensory and motor activities were studied in 9 epilepsy surgery candidates with electrodes implanted in the basal ganglia (BG), mostly in the putamen. Several contacts were also located in the pallidum and the caudate. The recorded potentials were related to a variety of cognitive and motor activities (attentional, decisional, time estimation, sensory processing, motor preparation, and so on). In five different tests, we recorded P3-like potentials evoked by auditory and visual stimuli and sustained potential shifts in the Bereitschaftspotential and Contingent Negative Variation protocols. All of the studied potentials were generated in the BG. They were recorded from all over the putamen. Various potentials on the same lead or nearby contacts were recorded. A functional topography in the BG was not displayed. We presume that the cognitive processes we studied were produced in clusters of neurons that are organized in the basal ganglia differently than the known functional organization, e.g., of motor functions. The basal ganglia, specifically the striatum, may play an integrative role in cognitive information processing, in motor as well as in nonmotor tasks. This role seems to be nonspecific in terms of stimulus modality and in terms of the cognitive context of the task.

Adult↗

The biochemistry of the basal ganglia and Parkinson's disease.

The metabolic pathways for five transmitters in the basal ganglia are briefly described; the results of determinations of their concentrations, of their rate-limiting enzymes and of their degradation products are summarized. The changes found in Parkinson's disease are described. While dopamine synthesis in the basal ganglia is defective in this condition, abnormalities of other transmitters occur, and their possible significance is discussed.

Acetylcholine↗

Prognosis in traumatic basal ganglia haematoma.

Twenty two patients with traumatic basal ganglia haematoma were studied. The mean Glasgow Coma Score on admission was 7. 17 patients had sustained high acceleration/deceleration injuries. The location and size of haematoma did not correlate with prognosis. Outcome was poor in 7 patients, while 8 patients died.

Adolescent↗

[Electron microscopic and histochemical study of the localization of adenylate cylase and acetylcholinesterase in the synapses of the rat cerebral cortex and basal ganglia].

Synapses of the brain cortex and basal ganglia of the rat were studied by means of electron histochemical reactions to adenylate cyclase and acetylcholinesterase. Three types of synapses, viz. cholinergic, adrenergic and mixed, were identified. Typification was carried out on the basis of presynaptic terminal vesicle characteristics and localization of the mentioned enzymes of the synapse receptor area.

Acetylcholinesterase↗

Macro-architecture of basal ganglia loops with the cerebral cortex: use of rabies virus to reveal multisynaptic circuits.

We have used retrograde transneuronal transport of rabies virus to examine basal ganglia connections with the cerebral cortex. We injected rabies into the primary motor cortex (M1) or into Area 46 of cebus monkeys. A 4-day survival time was long enough to allow transport of rabies from the injection site to 'third-order' neurons in the basal ganglia. After either M1 or Area 46 injections, third-order neurons were found in the external segment of the globus pallidus (GPe), striatum and subthalamic nucleus (STN). In each of these nuclei, the third-order neurons that innervate M1 were spatially separated from those that innervate Area 46. Thus, distinct basal ganglia-thalamocortical circuits innervate M1 and Area 46. Next, we injected a conventional tracer into M1 to define its terminations in the putamen and STN. We found that the regions of the putamen and STN that receive input from M1 are the same as those that contain third-order neurons after M1 injections of virus. On the other hand, virus injections into M1 also labeled a relatively dense group of third-order neurons in a region of the ventral putamen that is not innervated by M1. This region of the putamen is the target of efferents from the amygdala. Thus, the ventral putamen may provide a route for the limbic system to influence motor output. Overall, our results indicate that basal ganglia circuits with the cerebral cortex can be characterized by both open- and closed-loop macro-architectures.

Animals↗

Reduced basal ganglia volume in HIV-1-associated dementia: results from quantitative neuroimaging.

Although brain atrophy is a common neuroradiologic and pathologic finding in patients with HIV-1 infection, especially those with HIV-1-associated dementia complex, it is not clear whether specific regions of the brain are differentially responsible for tissue loss. In this study, we measured volumes of basal ganglia structures on MRIs for three groups: HIV-1-infected homosexual men with HIV-1-associated dementia complex (HIV+ demented), HIV-1-infected homosexual men without HIV dementia (HIV+ nondemented), and noninfected homosexual men. All groups were comparable on age and years of education, and the HIV+ groups were comparable on level of immunosuppression. Total brain volume was smaller in the HIV+ nondemented patients in comparison with HIV- control subjects; the HIV+ demented patients demonstrated even smaller brain volumes than the HIV+ nondemented patients. Smaller basal ganglia volumes, after corrections for intracranial volume, distinguished HIV+ demented patients from the other two groups; there were no differences between the HIV+ nondemented and HIV- groups on basal ganglia volumes. This study suggests that HIV infection causes generalized brain atrophy, but that the clinical features of HIV dementia develop with selective basal ganglia atrophy, consistent with the characterization of HIV dementia as subcortical.

AIDS Dementia Complex↗

[The role of the basal ganglia in control of motor activity].

Morphological, histochemical and functional analysis of the role of basal ganglia in the motor control is presented. The inhibiting effect of basal ganglia on the motor activity, their role in programming the slow and stereotyped movements, and the presentation of emotional and memory centres to the motor mechanisms of behaviour is emphasised.

Animals↗

Neurochemically specified subsystems in the basal ganglia.

The fibre pathways associated with the basal ganglia include through-conduction lines and side-loops associated with the striatum, pallidum and substantia nigra. Each of these regions is now known to contain subdivisions differing from one another in the neurotransmitter-related compounds they contain. This paper includes an outline of these new findings and a commentary on some of their functional implications.

Acetylcholine↗