Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “BASAL GANGLIA”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 127 records · Page 7Linked to original sources
PubMed1998

Dopamine-glutamate interactions in the basal ganglia.

In an attempt to formulate a working hypothesis of basal-ganglia functions, arguments are considered suggesting that the basal ganglia are involved in a process of response selection i.e. in the facilitation of "wanted" and in the suppression of "unwanted" behaviour. The meso-accumbal dopamine-system is considered to mediate natural and drug-induced reward and sensitization. The meso-striatal dopamine-system seems to fulfill similar functions: It may mediate reinforcement which strengthens a given behaviour when elicited subsequently, but which is not experienced as reward or hedonia. Glutamate as the transmitter of the corticofugal projections to the basal ganglia nuclei and of the subthalamic neurons is critically involved in basal ganglia functions and dysfunctions; for example Parkinson's disease can be considered to be a secondary hyperglutamatergic disease. Additionally, glutamate is an essential factor in the plasticity response of the basal-ganglia. However, opposite to previous suggestions, the NMDA-receptor blocker MK-801 does not prevent psychostimulant- nor morphine-induced day to day increase (sensitization) of locomotion. Also the day to day increase of haloperidol-induced catalepsy was not prevented by MK-801.

Basal Ganglia↗
PubMed1975

Basal ganglia calcification as a late radiation effect.

Basal ganglia calcification following radiation therapy has rarely been documented in the literature. A case of diffuse bilateral basal ganglia calcification developing 6 years after irridiation of a hypothalamic glioma is presented. Review of previous reports and other causes of basal ganglia calcification are discussed.

Astrocytoma↗
PubMed2002

Interictal and ictal EEG activity in the basal ganglia: an SEEG study in patients with temporal lobe epilepsy.

PURPOSE: The interictal and ictal EEG activity in the basal ganglia in patients with temporal lobe epilepsy were studied during invasive EEG monitoring. METHODS: Eight epilepsy surgery candidates, each with a proven mesiotemporal seizure-onset zone, participated in the study. We used two invasive EEG methods to determine the seizure-onset zone. In both methods, diagonal electrodes were targeted into the amygdalohippocampal complex via a frontal approach and were passed through the basal ganglia with several leads. We analyzed 16 partial epileptic seizures, four of which became secondarily generalized. RESULTS: No epileptic interictal or ictal discharges were noticed in the basal ganglia. The interictal activity in the basal ganglia was a mixture of low-voltage beta activity and medium-voltage alpha-theta activity. When the ictal paroxysmal activity remained localized to the seizure-onset zone, the activity of the basal ganglia did not change. The spread of epileptic activity to other cortical structures was associated with the basal ganglia EEG slowing to a theta-delta range of 3-7 Hz. This slowing was dependent on the spread of ictal discharge within the ipsilateral temporal lobe (related to the investigated basal ganglia structures); alternatively, the slowing occurred in association with the regional spread of ictal activity from the mesiotemporal region to the temporal neocortex contralaterally to the investigated basal ganglia. Secondary generalization was associated with a further slowing of basal ganglia activity. CONCLUSIONS: The basal ganglia do not generate specific epileptic EEG activity. Despite the absence of spikes, the basal ganglia participate in changing or reflect changes in the distribution of the ictal epileptic activity.

Adult↗
PubMedDate not supplied

[Functional anatomy of the basal ganglia].

INTRODUCTION: The cerebral cortex of mammals is massively interconnected with the basal ganglia. The manner in which the basal ganglia process information has been accepted since it was described in the 1980s. It is not a definitive model and many aspects of it still need clarification. DEVELOPMENT: The corpus striatum (ST) forms the entrance to the basal ganglia circuit (BG) and receives numerous afferent fibres from the cerebral cortex. Similarly, the internal segment of the globus pallidus (GPi) and the substantia nigra pars reticulata (SNpr) form the main nuclei for exit from the circuit and have an inhibitory effect on the pre-motor neurones of the ventral lamina of the thalamus. Between the entrance nucleus and the exit structures are two parallel systems of projection known as the direct and indirect pathways. The direct pathway projects monosynaptically only on the Gpi/SNpr complex. The indirect pathway projects polysynaptically on to the GR/SNpr complex after passing through the external segment of the globus pallidus (Gpe) and subthalamic nucleus. Imbalance in the activity of these two circuits will lead to alterations in discharge from the Gpi/SNpr complex which will cause bradykinesia or hyperkinesia. The bradykinesia or akinesia would be caused by increased gabaergic inhibition of the thalamic premotor neurones as a result of excessive discharge of the Gpi/SNpr complex. CONCLUSION: Current exploration of the electrophysiology of the basal ganglia and careful analysis of the clinical findings in lesions circumscribed to certain parts of the thalamus, subthalamus and internal globus pallidus in patients with Parkinson's disease, have led to the appearance of paradoxical effects, according to the current basal ganglia model.

Basal Ganglia↗
PubMed2004

Pedunculopontine nucleus and basal ganglia: distant relatives or part of the same family?

The basal ganglia are more highly interconnected with the pedunculopontine tegmental nucleus (PPN) than with any other brain region. Regulation and relay of basal ganglia activity are two key functions of the PPN. The PPN provides an interface for the basal ganglia to influence sleep and waking, and the two structures are similarly implicated in learning, reward and other cognitive functions. Perturbations of basal ganglia activity have consequences for the PPN and vice versa, exemplified by their interdependencies in motor function and Parkinson's disease. Thus, close anatomical and physiological links between the PPN and basal ganglia make it increasingly difficult to consider the two as separate functional entities.

Animals↗
PubMed2002

Neuropsychiatry of the basal ganglia.

This review aims to relate recent findings describing the role and neural connectivity of the basal ganglia to the clinical neuropsychiatry of basal ganglia movement disorders and to the role of basal ganglia disturbances in "psychiatric"' states. Articles relating to the relevant topics were initially collected through MEDLINE and papers relating to the clinical conditions discussed were also reviewed. The anatomy and connections of the basal ganglia indicate that these structures are important links between parts of the brain that have classically been considered to be related to emotional functioning and brain regions previously considered to have largely motor functions. The basal ganglia have a role in the development and integration of psychomotor behaviours, involving motor functions, memory and attentional mechanisms, and reward processes.

Basal Ganglia↗
PubMed2003

The basal ganglia and motor control.

This paper briefly reviews the functional anatomy of the basal ganglia and their relationships with the thalamocortical system. The basal ganglia, including the striatum, pallidum, subthalamic nucleus, and substantia nigra, are involved in a number of parallel, functionally segregated cortical-subcortical circuits. These circuits support a wide range of sensorimotor, cognitive and emotional-motivational brain functions. A main role of the basal ganglia is the learning and selection of the most appropriate motor or behavioral programs. The internal functional organization of the basal ganglia is very well suited for such selection mechanisms, both in development and in adulthood. The question of whether clumsiness may be, at least in part, attributed to dysfunction of the basal ganglia is discussed in the context of the differential, complementary, or interactive roles of the basal ganglia and the cerebellum in the development of motor control.

Animals↗
PubMed2006

Preservation of the direct and indirect pathways in an in vitro preparation of the mouse basal ganglia.

We have developed a slice preparation of the mouse basal ganglia which contains portions of the striatum, external pallidum, subthalamic nucleus and substantia nigra and the neocortex. This basal ganglia slice is unique in preserving functional direct and indirect connections between the striatum and the substantia nigra as well as interconnectivity between the globus pallidus and the subthalamic nucleus. We used fiber tract tracing studies and electrophysiological recordings to demonstrate the full functionality of these pathways. Deposits of 1,1'-dioctadecyl-3,3,3',3'-tetra-methylindocarbocyamine perchlorate in the different basal ganglia resulted in labeled fibers in each of their target nuclei. Confirming these results, electrical stimulation of the different nuclei elicited whole-cell recorded postsynaptic potentials in their target neurons with an appropriate pharmacological profile. Electrical and glutamate activation of the striatum evoked bursts of glutamatergic and GABAergic activities in whole-cell recorded nigral neurons indicating that the direct and indirect pathways are operative in this slice. It also showed that the responses evoked are not due to fibers en passant but to the activation of striatal cell bodies. These findings provide the first direct evidence for a preserved basal ganglia circuitry in vitro and make the basal ganglia slice a suitable preparation for analyzing the activity of the direct and indirect pathways in physiological and pathological conditions.

Animals↗
PubMed1988

Psychiatric complications of some basal-ganglia disorders.

Many basal-ganglia disorders are complicated by psychological disturbances and most are aggravated by emotional tension. These relationships are considered in the context of parkinsonism, Sydenham's chorea, Huntington's disease, Wilson's disease and a number of generalized and localized varieties of dystonia.

Basal Ganglia Diseases↗
PubMedDate not supplied

The basal ganglia and chunking of action repertoires.

The basal ganglia have been shown to contribute to habit and stimulus-response (S-R) learning. These forms of learning have the property of slow acquisition and, in humans, can occur without conscious awareness. This paper proposes that one aspect of basal ganglia-based learning is the recoding of cortically derived information within the striatum. Modular corticostriatal projection patterns, demonstrated experimentally, are viewed as producing recoded templates suitable for the gradual selection of new input-output relations in cortico-basal ganglia loops. Recordings from striatal projection neurons and interneurons show that activity patterns in the striatum are modified gradually during the course of S-R learning. It is proposed that this recoding within the striatum can chunk the representations of motor and cognitive action sequences so that they can be implemented as performance units. This scheme generalizes Miller's notion of information chunking to action control. The formation and the efficient implementation of action chunks are viewed as being based on predictive signals. It is suggested that information chunking provides a mechanism for the acquisition and the expression of action repertoires that, without such information compression would be biologically unwieldy or difficult to implement. The learning and memory functions of the basal ganglia are thus seen as core features of the basal ganglia's influence on motor and cognitive pattern generators.

Animals↗
PubMed2005

Role of the basal ganglia in balance control.

In this review paper, we summarize the important contributions of the basal ganglia to the regulation of postural control. After a brief overview of basal ganglia circuitries, the emphasis is on clinical observations in patients with focal lesions in parts of the basal ganglia, as the impairments seen here can serve to highlight the normal functions of the basal ganglia nuclei in postural control. Two particularly relevant functions are discussed in detail: first, the contribution of the basal ganglia to flexibility and to gaining control of balance-correcting responses, including the ability to lend priority to the elements of a postural task; and second, processing afferent information by the basal ganglia, which is increasingly recognized as being highly relevant for postural control.

Adaptation, Physiological↗
PubMed1986

A computer model of neuronal pathways in the basal ganglia.

Disorders of the basal ganglia and the extrapyramidal motor system exhibit an imbalance of neurotransmitter concentrations in affected neurons. For three synapses with dopamine, acetylcholine, and gamma-amino butyric acid (GABA), mathematical models of synaptic transmission are developed. To describe the kinetics of transmitter substances, compartment analysis is used. Membrane potential behaviour is described by the Hodgkin-Huxley equations with an additional equation accounting for a presynaptic calcium current mediating transmitter release. At the postsynaptic site, activated receptor molecules control the activity of ion channels, eliciting either inhibitory or excitatory postsynaptic potentials. A simple model of the feedback loop connecting the caudate nucleus and the substantia nigra is simulated on a digital computer using the simulation language ACSL. A comparison of the control case with a model of Parkinson's disease shows a shift of eigenvalues towards zero in the diseased state.

Acetylcholine↗
PubMed2004

[Association of basal ganglia damage with Chinese agraphia].

OBJECTIVE: To study the clinical features of Chinese agraphia caused by basal ganglia damage. METHODS: The Chinese speaking and writing abilities of 38 patients with basal ganglia damage were evaluated with aphasia battery and agraphia battery of Chinese, respectively, and the agraphia quotient (AgQ) and the scores for writing abilities calculated. RESULTS: Of the 38 patients, 21 had left basal ganglia injury, which was responsible for aphasia in 18 and agraphia also in 18 patients. Another 14 patients had right basal ganglia injury and caused aphasia in 1 case and agraphia in 4. The rest 3 patients had injuries of the basal ganglia on both sides that resulted in aphasia in all and agraphia in 2 of them. Significant difference was noted in the incidence of agraphia between patients with left and those with right basal ganglia injuries, characterized by difficulty in building the Chinese characters, mistakes in writing the characters and disability of writing at the level of sentences and paragraphs of Chinese. CONCLUSION: Basal ganglia damage may result in Chinese agraphia, due to, hypothetically, hypoperfusion, dysfunction of integration center, circuit damage and impaired function in extracting the graphical features of the Chinese characters from memory.

Adolescent↗
PubMed1999

The functional anatomy of the basal ganglia of birds.

To study how the basal ganglia can control movement in birds, we have reinvestigated the connections of the pigeon dorsal pallidum. Our results indicate that avian basal ganglia appear to control movement through major projections to several premotor pretectal and tegmental centres which innervate the tectum, and through a minor projection to a possible motor thalamic centre which innervates the Wulst. For such control, separate striatopallidal output circuits appear to exist in birds that are remarkably similar to those described in mammals, suggesting that avian and mammalian basal ganglia may control movement through similar mechanisms, and that the morphological substrate for such control evolved earlier than previously thought.

Animals↗
PubMed1989

Psychopathological alterations in cases of symmetrical basal ganglia sclerosis.

Psychopathological alterations caused by symmetrical basal ganglia sclerosis of different etiologies are described, involving cases with parathyroid gland/hormone dysfunction (some of them familial), patients after thyroidectomy, and patients with basal ganglia calcification of uncertain etiology. Initial symptomatology in a group of 62 patients is reported; chronic symptoms in another group of 35 patients were evaluated. Estimates of volume of the basal ganglia calcifications were made, in addition to precise topographical localizations by CT. In 40% the initial symptoms noted were psychiatric, compared with 50% who first presented neurological symptoms. In the group of chronic cases practically all showed intellectual impairment. There was a marked preponderance of organic affective syndromes (initially 21%, chronic 65%): the affective chronic patients can be subdivided into 37% depressive, 20% bipolar, 11% manic cases. We could find no direct relationships with regard to etiology, localization, volume or symptoms, except that extensive calcifications occur after parathyroid hormone deficiencies due to thyroidectomy and lead to more severe mental deterioration.

Basal Ganglia Diseases↗
PubMedDate not supplied

Basal ganglia: anatomy, pathology, and imaging characteristics.

Several cases of bilateral basal ganglia lesions seen in magnetic resonance imaging initiated a review of the anatomy, pathology, and differential diagnoses of this region. There are a variety of disease entities that present as symmetrical basal ganglia abnormalities. Although these findings may not indicate a specific diagnosis, knowledge of the characteristics of diseases that affect this area can limit the differential considerations. Clinical information is often essential for narrowing the possible pathology that can be found here. The purpose of this article is to review the anatomy of the basal ganglia, the pathologies, clinical histories, and imaging characteristics that can cause bilateral basal ganglia lesions.

Basal Ganglia↗
PubMed1998

A review of differences between basal ganglia and cerebellar control of movements as revealed by functional imaging studies.

The role of the basal ganglia and cerebellum in the control of movements is unclear. We summarize results from three groups of PET studies of regional CBF. The results show a double dissociation between (i) selection of movements, which induces differential effects in the basal ganglia but not the cerebellum, and (ii) sensory information processing, which involves the cerebellum but not the basal ganglia. The first set of studies concerned motor learning of a sequence of finger movements; there was a shift of activation in the anterior-posterior direction of the basal ganglia which paralleled changes in the motor areas of the frontal cortex. During new learning, the dorsolateral prefrontal cortex and striatum (caudate nucleus and anterior putamen) were activated. When subjects had to select movements, the premotor cortex and mid-putamen were activated. With automatic (overlearned) movements, the sensorimotor cortex and posterior putamen were activated. When subjects paid attention to overlearned actions, activation shifted back to the dorsolateral prefrontal cortex and striatum. The cerebellum was not activated when subjects made new decisions, attended to their actions or selected movements. These results demonstrate components of basal ganglia-(thalamo)-cortical loops in humans. According to earlier studies in animals we propose that the basal ganglia may be concerned with selecting movements or the selection of appropriate muscles to perform a movement selected by cortical areas (e.g. premotor cortex). Secondly, a visuomotor co-ordination task was examined. In the absence of visual control over arm movements, subjects were required to use a computer mouse to either generate new lines or to re-trace lines on a computer screen. The neocerebellum (hemispheres of the posterior lobe, cerebellar nuclei and cerebellar vermis), not the basal ganglia, was more engaged when lines were re-traced (compared with new line generation). Animal experiments have shown that error detection (deviation from given lines) and correction occurs during line re-tracing but not line generation. Our data suggest that the neocerebellum (not the basal ganglia) is involved in monitoring and optimizing movements using sensory (proprioceptive) feedback. Thirdly, the relative contribution of sensory information processing to the signal during active/passive execution of a motor task (flexion and extension of the elbow) was examined; it was found that 80-90% of the neocerebellar signal could be attributed to sensory information processing. The basal ganglia were not involved in sensory information processing. They may be concerned with movement/ muscle selection (efferent motor component); the neocerebellum may be concerned with monitoring the outcome (afferent sensory component) and optimizing movements using sensory (feedback) information.

Basal Ganglia↗
PubMed2000

Expression and distribution of CYP2C enzymes in rat basal ganglia.

The function and integrity of the basal ganglia is modulated by sex steroids whose activity may be controlled by P450 enzymes, such as members of the CYP2C subfamily. The expression of CYP2C enzymes in rat basal ganglia was examined by immunohistochemistry along with some of the factors that might control their expression. Whereas no CYP2C11 or CYP2C12 immunoreactivity was detected in the basal ganglia of either male or female rats, marked CYP2C13 immunoreactivity was evident in neurones of the subthalamic nucleus, substantia nigra, and interpeduncular nucleus. Strong CYP2C13 immunoreactivity was also expressed in the cortex, olfactory tubercle, hippocampus, dentate gyrus, hypothalamic nuclei, medial habenular nucleus, red nucleus, and medial forebrain bundle. Similar results were found in male and female rats. Following 6-hydroxydopamine lesioning of the nigro-striatal tract, tyrosine hydroxylase immunoreactivity was absent and CYP2C13 immunoreactivity was decreased markedly in the substantia nigra pars compacta, implying its presence in dopaminergic neurones. Modulation of sex steroids, using castrated rats, had no effect on the number of CYP2C13 positive neurones in the substantia nigra pars compacta. These results indicate that CYP2C13 protein is constitutively and widely expressed in rat brain. However, its expression is not sex-specific and is unaffected by castration. The role of CYP2C13 in brain is unknown but it may be involved in the generation of neurosteroids and catecholoestrogens.

Animals↗