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PubMed2003

Correlated multisecond oscillations in firing rate in the basal ganglia: modulation by dopamine and the subthalamic nucleus.

Previous studies from this laboratory have shown that many neurons in the basal ganglia have multisecond (<0.5 Hz) periodicities in firing rate in awake rats. The frequency and regularity of these oscillations are significantly increased by systemically injected dopamine (DA) agonists. Because oscillatory activity should have greater functional impact if shared by many neurons, the level of correlation of multisecond oscillations was assessed by recording pairs of neurons in the globus pallidus and substantia nigra pars reticulata in the same hemisphere, or pairs of globus pallidus neurons in opposite hemispheres in awake, immobilized rats. Cross-correlation (90-180 s lags) and spectral analysis were used to characterize correlated oscillations. Thirty-eight percent of pairs recorded in baseline (n=50) demonstrated correlated multisecond oscillations. Phase relationships were near 0 or 180 degrees. DA agonist injection significantly increased the incidence of correlation (intra- and interhemispheric) to 94% (n=17). After DA agonist injection, phase relationships of globus pallidus/substantia nigra neuron pairs were exclusively concentrated near 180 degrees, and phases of interhemispheric pairs of globus pallidus neurons were concentrated near 0 degrees. After subthalamic nucleus lesion (n=8), the incidence of correlated multisecond oscillations (or of multisecond oscillations per se) was not changed, although the consistent phase relationship between the globus pallidus and substantia nigra pars reticulata was disrupted. Subthalamic lesion also blocked apomorphine-induced decreases in oscillatory period and increases in oscillation amplitude, and significantly attenuated apomorphine-induced changes in mean firing rate. The data demonstrate that multisecond oscillations in the basal ganglia can be correlated between nuclei, and that DA receptor activation increases the level of correlation and organizes internuclear phase relationships at these multisecond time scales. While the subthalamic nucleus is not necessary for generating or transmitting these slow oscillations, it is involved in DA agonist-induced modulation of mean firing rate, oscillatory period, and internuclear phase relationship. These data further support a role for DA in modulating coherent oscillatory activity in the basal ganglia, and for the subthalamic nucleus in shaping the effects of DA receptor stimulation on basal ganglia output.

Animals↗

PubMed2004

An electron microscope immunocytochemical study of GABA(B) R2 receptors in the monkey basal ganglia: a comparative analysis with GABA(B) R1 receptor distribution.

Functional gamma-aminobutyric acid (GABA)(B) receptors are heterodimers made up of GABA(B) R1 and GABA(B) R2 subunits. The subcellular localization of GABA(B) R2 receptors remains poorly known in the central nervous system. Therefore, we performed an ultrastructural analysis of the localization of GABA(B) R2 receptor immunoreactivity in the monkey basal ganglia. Furthermore, to characterize better the neuronal sites at which GABA(B) R1 and GABA(B) R2 may interact to form functional receptors, we compared the relative distribution of immunoreactivity of the two GABA(B) receptors in various basal ganglia nuclei. Light to moderate GABA(B) R2 immunoreactivity was found in cell bodies and neuropil elements in all basal ganglia nuclei. At the electron microscope level, GABA(B) R2 immunoreactivity was commonly expressed postsynaptically, although immunoreactive preterminal axonal segments were also frequently encountered, particularly in the globus pallidus and substantia nigra, where they accounted for the third of the total number of GABA(B) R2-containing elements. A few labeled terminals that displayed the ultrastructural features of glutamatergic boutons were occasionally found in most basal ganglia nuclei, except for the subthalamic nucleus, which was devoid of GABA(B) R2-immunoreactive boutons. The relative distribution of GABA(B) R2 immunoreactivity in the monkey basal ganglia was largely consistent with that of GABA(B) R1, but some exceptions were found, most noticeably in the globus pallidus and substantia nigra, which contained a significantly larger proportion of presynaptic elements labeled for GABA(B) R1 than GABA(B) R2. These findings suggest the possible coexistence and heterodimerization of GABA(B) R1 and GABA(B) R2 at various pre- and postsynaptic sites, but also raise the possibility that the formation of functional GABA(B) receptors in specific compartments of basal ganglia neurons relies on mechanisms other than GABA(B) R1/R2 heterodimerization.

Animals↗

PubMed2005

Cellular localization of AMPA type glutamate receptor subunits in the basal ganglia of pigeons (Columba livia).

Corticostriatal and thalamostriatal projections utilize glutamate as a neurotransmitter in mammals and birds. The influence on striatum is mediated, in part, by ionotropic AMPA-type glutamate receptors, which are heteromers composed of GluR1-4 subunits. Although the cellular localization of AMPA-type subunits has been well characterized in mammalian basal ganglia, their localization in avian basal ganglia has not. We thus carried out light microscopic single- and double-label and electron microscopic single-label immunohistochemical studies of GluR1-4 distribution and cellular localization in pigeon basal ganglia. Single-label studies showed that the striatal neuropil is rich in GluR1, GluR2, and GluR2/3 immunolabeling, suggesting the localization of GluR1, GluR2 and/or GluR3 to the dendrites and spines of striatal projection neurons. Double-label studies and perikaryal size distribution determined from single-label material indicated that about 25% of enkephalinergic and 25% of substance P-containing striatal projection neuron perikarya contained GluR1, whereas GluR2 was present in about 75% of enkephalinergic neurons and all substance-P -containing neurons. The perikaryal size distribution for GluR2 compared to GluR2/3 suggested that enkephalinergic neurons might more commonly contain GluR3 than do substance P neurons. Parvalbuminergic and calretininergic striatal interneurons were rich in GluR1 and GluR4, a few cholinergic striatal interneurons possessed GluR2, but somatostatinergic striatal interneurons were devoid of all subunits. The projection neurons of globus pallidus all possessed GluR1, GluR2, GluR2/3 and GluR4 immunolabeling. Ultrastructural analysis of striatum revealed that GluR1 was preferentially localized to dendritic spines, whereas GluR2/3 was found in spines, dendrites, and perikarya. GluR2/3-rich spines were generally larger than GluR1 spines and more frequently possessed perforated post-synaptic densities. These results show that the diverse basal ganglia neuron types each display different combinations of AMPA subunit localization that shape their responses to excitatory input. For striatal projection neurons and parvalbuminergic interneurons, the combinations resemble those for the corresponding cell types in mammals, and thus their AMPA responses to glutamate are likely to be similar.

ATP-Binding Cassette Transporters↗

PubMed2001

Basal ganglia as a sensory gating devise for motor control.

Basal ganglia lie between the cerebral cortex and the thalamus, and have dense fiber connections between them. These connections form 4-5 distinct loops or circuits to allow parallel processing of information. Among them, the most intensively studied is the motor loop, which comprises 2 distinct direct and indirect pathways. The direct pathway disinhibits the powerful inhibition of the internal segment of the globus pallidus/substantia nigra pars reticulata upon thalamic ventrolateral nuclei with a net result of facilitatory influence upon the motor cortex. By contrast, the indirect pathway exerts an inhibitory effect. Overall this dual system provides a center (excitatory)-surround (inhibitory) mechanism to focus its effect on selected cortical neurons. Although putative transmitters, inhibitory or excitatory nature of these projections and their receptors are mostly known, the functional role of the loop in motor control is not precisely understood. Several lines of evidence have recently been presented to support the view that this center-surround mechanism is used to focus the output to a specific group of muscles required for performing a specific task. This operation is made possible through opening the sensory channel for the expected sensory feed-back afferents during movement. Thus one of the important functions of basal ganglia seems to be the gating of sensory input for motor control.

Animals↗

PubMed1995

Postvaricella basal ganglia infarction in children.

Two patients presented with acute neurologic deficits attributable to contralateral basal ganglia infarction 1 to 3 months after episodes of chickenpox. Both presented with hemiparesis with one patient also demonstrating ipsilateral choreoathetosis. In both patients MR revealed unilateral basal ganglia infarction. Cerebral angiography findings in one patient were normal; in the second, there was unilateral narrowing of the common carotid artery and of proximal branches of the anterior and middle cerebral artery.

Adrenal Cortex Hormones↗

PubMed2001

Function of the 'direct' and 'indirect' pathways of the basal ganglia motor loop: evidence from reciprocal aiming movements in Parkinson's disease.

The purpose of this study was to test the validity of a neural-network model of the basal ganglia developed by Bischoff and colleagues (A. Bischoff, Modeling the basal ganglia in the control of arm movements (Doctoral dissertation, University of Southern California, 1998). Dissertation Abstr. Int. 59-08B (1998) 3924, 0208; A. Bischoff, M.A. Arbib, Modeling the role of basal ganglia and supplementary motor areas in sequential arm movements, Abstr. Soc. Neurosci. 23 (1997) 466; A. Bischoff, M.A. Arbib, C.J. Winstein, Modeling the role of the basal ganglia in reciprocal aiming task, Proceedings of the Fourth Annual Joint Symposium on Neural Computation, University of Southern California, Los Angeles, 7, 1997, pp. 20-27), and to examine the effects of levodopa on aiming movement performance. Findings confirm the model predictions for repetitive aiming movements. Individuals with late stage Parkinson's disease demonstrated longer movement times and longer pauses between aiming sequences compared to controls. Levodopa only slightly improved bradykinesia but not akinesia in these patients.

Adult↗

PubMed2006

Basal ganglia activation in Parkinson's disease.

The objective of this study was to compare basal ganglia activation in patients with Parkinson's disease to that of healthy controls, using functional MRI (fMRI). Six mildly-affected patients, off antiparkinsonian medications for at least 12h, and seven age-matched controls performed a unilateral motor switching task during fMRI data acquisition. Clear differences in basal ganglia activation were seen, with control subjects showing greater activation during both the left and right movement sessions. We observed activation of right sided basal ganglia structures in both groups, particularly with right sided movements, with caudate activation noted most frequently. This observation is consistent with right caudate involvement in the learning of new tasks and in association with externally paced movements.

Adult↗

PubMed1980

Basal ganglia calcification in postoperative hypoparathyroidism.

The presence of bilateral basal ganglia calcification was sought in nine patients with post-operative and two patients with primary hypoparathyroidism, using computerized axial tomography (CAT) and plain skull radiographs. Calcification was detected with CAT in seven patients; five with post-operative and both with primary hypoparathyroidism, but in only one was it demonstrable on plain X-ray films. The presence of calcification appeared to be related to the duration of the disease and possibly the degree of control of serum calcium. Six of the seven patients with cerebral calcification also had cataracts. The incidence of basal ganglia calcification in hypoparathyroidism is probably much greater than previously recognized, especially in post-operative hypoparathyroidism.

Adult↗

PubMed1988

Receptor autoradiography as a tool for the study of the phylogeny of the basal ganglia.

Recent studies on the neurotransmitter organization of the basal ganglia and forebrain in lower vertebrates suggest that, in contrast to the old concepts of the phylogeny of the brain, there are many similarities between the chemical organization of the brain throughout evolution. By examining neurotransmitter receptors using in vitro autoradiography we have attempted to further our understanding of the evolution of the brain. Receptors enriched in different parts of the basal ganglia in mammals appear to be also enriched in the homologous areas in lower vertebrates. Thus, for example, dopamine and muscarinic receptors, but not serotonin-1A, are enriched in the paleostriatum augmentatum while GABA/benzodiazepine receptors are enriched in the paleostriatum primitivum corresponding with their localization to the caudate-putamen and globus pallidus respectively. Our results support the concept of a more conservative evolution of the vertebrate brain and demonstrate the usefulness of receptor autoradiography in the understanding of brain evolution.

Animals↗

PubMed1979

Clinical correlations of CT scan-detected calcifications of the basal ganglia.

A review of CT scans of 7,081 patients demonstrated calcifications of the basal ganglia in 53. The calcifications were evident in the skull roentgenograms of only 4 patients out of 40 in whom both CT scans and plain roentgenograms were available, demonstrating the superior resolution of this new method. Seventy-five percent of the patients were older than 50 years of age. Of the younger patients, 5 had had prior cranial irradiation; 1 had received cranial irradiation and intrathecal methotrexate therapy for meningeal leukemia; and 2 others had deep-seated arteriovenous malformations. Serum concentrations of calcium and phosphorus were normal in all 46 patients in whom they were measured. We conclude that the detection of small calcifications of the basal ganglia in persons above 50 years of age is infrequently associated with either clinical signs of basal ganglia dysfunction or calcium and phosphorus abnormalities. Calcium deposition in these patients may be related to vascular changes associated with aging. In younger patients a specific pathogenetic factor or underlying process is infrequently found.

Adolescent↗

PubMed2006

Receptor-receptor interactions as studied with microdialysis. Focus on NTR/D2 interactions in the basal ganglia.

Using mono and dualprobe(s) microdialysis in the basal ganglia of the freely moving rat evidence has been obtained that neurotensin (NT) in threshold concentrations can counteract the D(2) agonist (intrastriatally perfused) induced inhibition of striatal dopamine (DA) release and of pallidal GABA release from the striato-pallidal GABA pathway, effects that are blocked by a NTR(1) antagonist SR48692. These results indicate the existence of antagonistic intramembrane NTR/D(2) receptor interactions in the striatal DA terminals and in the somato-dendritic regions of the striato-pallidal GABA neurons. By the NT-induced reduction of the D(2) mediated signals at the striatal pre- and postjunctional level DA transmission is switched towards a D(1) mediated transmission leading to increased activity in the striatopallidal and striatonigral GABA pathways. The former action will contribute to the motor inhibition and catalepsy found with NT treatment and underlies the use of NT receptor antagonists as a treatment strategy for Parkinson's disease. Nigral NT by an antagonistic NTR/D(2) receptor interaction in the DA cell body and dendrites may also increase nigral DA release leading to a D(2) mediated inhibition of the nigrothalamic GABA pathway. Such an effect, will instead result in antiparkinsonian actions. Thus, increases in NT transmission will have different consequences for the motor system depending upon where in the basal ganglia the increase takes place.

Animals↗

PubMed2004

Cognitive and motor functioning in a patient with selective infarction of the left basal ganglia: evidence for decreased non-routine response selection and performance.

Focal damage to the basal ganglia is relatively rare, and little is known about the cognitive effects of damage to specific basal ganglia structures. A 28-year-old, highly educated male (patient RI) sustained a unilateral left ischemic infarction involving primarily the putamen and secondarily the head of the caudate and the anterior internal capsule. Two detailed neuropsychological assessments, at 3 and 16 months post-infarction, revealed that a majority of cognitive abilities were spared. RI's general intelligence, simple attention, concept formation, cognitive flexibility, and explicit memory were unaffected. Select cognitive abilities were affected, and these appeared to be related to direct involvement of the putamen and/or to indirect disruption of circuits between the basal ganglia and frontal lobes. Consistent with involvement of the left putamen, RI showed micrographia with his right hand. Interestingly, his micrographia was context-dependent, appearing only when verbal expression was involved (e.g., present when writing spontaneously, but not when copying sentences or when drawing). Evidence of disruption to frontal systems included variably decreased sustained attention, mildly decreased ability to generate words and to generate ideas, and significantly impaired abstraction ability in both verbal and visual modalities. Although there are several possible interpretations for these findings, this pattern of cognitive and motor functioning is consistent with neuroimaging research suggesting that the frontal/subcortical circuit between the putamen and frontal motor areas plays a role in non-routine response selection and performance.

Adult↗

PubMed1993

Bilateral basal ganglia lesions: pediatric differential considerations.

Computed tomography (CT) and magnetic resonance (MR) imaging have dramatically improved the ability to visualize the deep gray structures of the basal ganglia (primarily, the caudate nucleus, putamen, and globus pallidus). Any process that alters cerebral metabolism can lead to basal ganglia damage. This article presents the spectrum of disease that may be seen with bilateral basal ganglia abnormalities in the pediatric population. A simplified approach to the differential diagnosis of these entities is based on acute versus chronic conditions and radiologic manifestations. Acute processes include hypoxia, hypoglycemia, carbon monoxide poisoning, hemolytic-uremic syndrome, osmotic myelinolysis, and encephalitis. Chronic conditions include inherited ("inborn errors of metabolism," Huntington disease, and dysmyelinating diseases) or acquired (sequelae of acute disorders) conditions that represent abnormal biochemical or structural processes within the basal ganglia. Elimination of acute causes gives little hope for improvement. Recognition of chronic disorders is important for counseling purposes, since most of these conditions have specific patterns of inheritance.

Acute Disease↗

PubMed2003

Metabotropic glutamate 5 receptor blockade alleviates akinesia by normalizing activity of selective basal-ganglia structures in parkinsonian rats.

Glutamate overactivity within the basal ganglia has been shown to be central to the expression of motor symptoms in advanced stages of Parkinson's disease, and metabotropic glutamate receptors (mGluRs) represent promising targets for new therapeutic strategies in this pathology. Little is known, however, about the cellular and behavioral changes occurring in the early stages of the disease when dopamine depletion is moderate. Here, we report that rats with partial bilateral dopamine lesions exhibit akinetic deficits associated with dramatically increased neuronal metabolic activity in selective structures of the basal ganglia such as the subthalamic nucleus and the substantia nigra pars reticulata, but not in the entopeduncular nucleus. Furthermore, chronic treatment with the mGluR5 antagonist 2-methyl-6-(phenylethylnyl)-pyridine alleviated the akinesia and was associated with a normalization of the activity of these two overactive structures. These data stress the therapeutic potential of mGluR5 antagonists in the treatment of parkinsonian patients in the early stages of the disease.

Animals↗

PubMed1995

Behavioral laterality in individuals with Gilles de la Tourette's syndrome and basal ganglia alterations: a preliminary report.

This study aims to investigate whether abnormalities in structural basal ganglia asymmetries in Tourette's syndrome (GTS) have functional significance. Eleven adult GTS patients and 11 normal controls who had participated in the previous MRI study where GTS patients lacked the normal left-greater-than-right (L > R) lenticular asymmetry were re-recruited. They were administered a battery of lateralizing neuropsychological tasks believed to require intact basal ganglia function. GTS subjects lacked normal functional asymmetries on these measures, as predicted. The neuropsychological measures also accounted for a significant portion of the variance in the severity of tic symptoms. These findings suggest that GTS subjects who lack normal basal ganglia structural asymmetries also lack normal functional asymmetries on related neuropsychological measures.

Adult↗

PubMed2000

Effect of basal ganglia injury on central dopamine activity in Gulf War syndrome: correlation of proton magnetic resonance spectroscopy and plasma homovanillic acid levels.

BACKGROUND: Many complaints of Gulf War veterans are compatible with a neurologic illness involving the basal ganglia. METHODS: In 12 veterans with Haley Gulf War syndrome 2 and in 15 healthy control veterans of similar age, sex, and educational level, we assessed functioning neuronal mass in both basal ganglia by measuring the ratio of N-acetyl-aspartate to creatine with proton magnetic resonance spectroscopy. Central dopamine activity was assessed by measuring the ratio of plasma homovanillic acid (HVA) and 3-methoxy-4-hydroxyphenlyglycol (MHPG). RESULTS: The logarithm of the age-standardized HVA/MHPG ratio was inversely associated with functioning neuronal mass in the left basal ganglia (R(2) = 0.56; F(1,27) = 33.82; P<.001) but not with that in the right (R(2) = 0. 04; F(1,26) = 1.09; P =.30). Controlling for age, renal clearances of creatinine and weak organic anions, handedness, and smoking did not substantially alter the associations. CONCLUSIONS: The reduction in functioning neuronal mass in the left basal ganglia of these veterans with Gulf War syndrome seems to have altered central dopamine production in a lateralized pattern. This finding supports the theory that Gulf War syndrome is a neurologic illness, in part related to injury to dopaminergic neurons in the basal ganglia.

Basal Ganglia Diseases↗

PubMed2000

Projections from basal ganglia to tegmentum: a subcortical route for explaining the pathophysiology of Parkinson's disease signs?

Functional changes in the organisation of neuronal circuitries are generally used to explain parkinsonian motor symptoms and levodopa-induced dyskinesias. Based on information from histology and neurophysiological microrecordings of specific basal ganglia nuclei, the most widely accepted scheme is based on a central loop which starts in the cerebral cortex, makes multiple relays in the basal ganglia, and returns to the cerebral cortex. Transcranial magnetic stimulation studies, however, reveal no significant differences in the excitability of the motor cortex between normal subjects and patients with Parkinson's disease. Furthermore, electrophysiological and audiospinal facilitation studies indicate that the activity of reticular nuclei is altered in Parkinson's disease. It therefore appears that a circuit with the cortex as the only recipient of basal ganglia output is an oversimplification. This paper explores the relationships between various basal ganglia nuclei and proposes a subcortical pathway via which modifications in the basal ganglia may influence motor function.

Animals↗

PubMed2004

Brainstem and basal ganglia lesions in xeroderma pigmentosum group A.

Xeroderma pigmentosum group A (XPA) is a hereditary disorder characterized by cutaneous symptoms and progressive neurodegeneration. Since XPA patients exhibit peripheral neuropathy, neuronal deafness, rigidity, dysphagia, and laryngeal dystonia, it is indispensable for investigation of the neurodegeneration to analyze brainstem and basal ganglia lesions clinically and pathologically; we have previously shown the role of oxidative stress in the development of basal ganglia lesions. Here we immunohistochemically examined the expression of neurotransmitters, calcium-binding proteins, and neuropeptides in the brainstem, basal ganglia, and thalamus in 5 XPA autopsy cases. In the brainstem, immunoreactivity for tyrosine hydroxylase, tryptophan hydroxylase, and calbindin-D28K was severely reduced throughout the brainstem in all the XPA cases. Nevertheless, the expressions of parvalbumin, substance P, and methionine-enkephalin in the brainstem were comparatively preserved; the exception being reduced immunoreactivity for them in the cochlear and dorsal column nuclei in 3 cases. The large cell neurons in the putamen were preferentially reduced, the immunoreactivity for tyrosine hydroxylase reflecting the dopaminergic afferent and efferent pathways was severely affected, and the expression of 3 calcium binding proteins (i.e. parvalbumin, calbindin-D28K, and calretinin) was disturbed in various ways. The expression of substance P and methionine-enkephalin, which are involved in the efferent pathways in the basal ganglia, in the globus pallidus and substantia nigra was spared. It is speculated that the selective damage to the dopamine system in the basal ganglia and the disturbed monoaminergic expression in the brainstem could be related to clinical abnormalities such as the rigidity, laryngeal dystonia, and several neurophysiological changes. Functional analysis of autopsy brains will facilitate clarification of the pathogenesis of the neurodegeneration in XPA.

Adolescent↗