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PubMed2005

Blood manganese concentration is elevated in iron deficiency anemia patients, whereas globus pallidus signal intensity is minimally affected.

OBJECTIVES: To determine whether blood manganese (Mn) concentration is elevated in patients with iron deficiency anemia (IDA), and whether this affects signal intensities in the globus pallidus. METHODS: Twenty-seven patients with IDA and 10 control subjects were tested for blood Mn, and brain magnetic resonance images (MRI) were also examined. Seventeen of the 27 patients were followed-up after iron therapy. RESULTS: IDA patients had a mean blood Mn concentration of 2.05 +/- 0.44 microg/dl, which was higher than controls. The mean pallidal index (PI) of anemic patients was not different from that of controls. There was a correlation between log blood Mn and PI (rho = 0.384, P = 0.048; n = 27) in IDA patients. None of the patients showed increased signals in the globus pallidus in T1-weighted MRI. Blood Mn levels decreased and hemoglobin levels increased after iron therapy (P < 0.05). CONCLUSION: Although blood Mn is elevated in IDA patients, there is no increase in globus pallidus MRI signal intensity. These findings stand in contrast to those of our other studies showing patients with chronic liver disease or occupational Mn exposure have elevated signal intensities remarkably.

Adult↗

PubMed2003

Pre-synaptic kainate receptors in GABAergic and glutamatergic axon terminals in the monkey globus pallidus.

Although the localization and role of kainate receptors in the CNS remain poorly known, complex, and rather unusual, pre-synaptic auto- and heteroreceptor functions have been disclosed in various brain regions. Basal ganglia nuclei, including the globus pallidus, are enriched in GluR6/7 immunoreactivity. Using electron microscopic immunocytochemistry for GluR6/7 combined with post-embedding immunogold labeling for GABA, we demonstrate that GluR6/7 immunoreactivity is enriched in a large subpopulation of small unmyelinated, presumably pre-terminal, axons as well as GABAergic and putative glutamatergic axon terminals in the internal and external segments of the globus pallidus in monkey. Our findings suggest that kainate receptors are located to subserve pre-synaptic modulation of inhibitory and excitatory transmission in the primate globus pallidus.

Animals↗

PubMed1992

Cholinergic innervation of the human striatum, globus pallidus, subthalamic nucleus, substantia nigra, and red nucleus.

The anatomical organization of cholinergic markers such as acetylcholinesterase, choline acetyltransferase, and nerve growth factor receptors was investigated in the basal ganglia of the human brain. The distribution of choline acetyltransferase-immunoreactive axons and varicosities and their relationship to regional perikarya showed that the caudate, putamen, nucleus accumbens, olfactory tubercle, globus pallidus, substantia nigra, red nucleus, and subthalamic nucleus of the human brain receive widespread cholinergic innervation. Components of the striatum (i.e., the putamen, caudate, olfactory tubercle, and nucleus accumbens) displayed the highest density of cholinergic varicosities. The next highest density of cholinergic innervation was detected in the red nucleus and subthalamic nucleus. The level of cholinergic innervation was of intermediate density in the globus pallidus and the ventral tegmental area and low in the pars compacta of the substantia nigra. Immunoreactivity for nerve growth factor receptors (NGFr) was confined to the cholinergic neurons of the basal forebrain and their processes. Axonal immunoreactivity for NGFr was therefore used as a marker for cholinergic projections originating from the basal forebrain (Woolf et al., '89: Neuroscience 30:143-152). Although the vast majority of striatal cholinergic innervation was NGFr-negative and, therefore, intrinsic, the striatum also contained NGFr-positive axons, indicating the existence of an additional cholinergic input from the basal forebrain. This basal forebrain cholinergic innervation was more pronounced in the putamen than in the caudate. The distribution of NGFr-positive axons suggested that the basal forebrain may also project to the globus pallidus but probably not to the subthalamic nucleus, substantia nigra, or red nucleus. The great majority of cholinergic innervation to these latter three structures and to parts of the globus pallidus appeared to come from cholinergic neurons outside the basal forebrain, most of which are probably located in the upper brainstem. These observations indicate that cholinergic neurotransmission originating from multiple sources is likely to play an important role in the diverse motor and behavioral affiliations that have been attributed to the human basal ganglia.

Acetylcholinesterase↗

PubMed1992

Persistent effects of manganese on effortful responding and their relationship to manganese accumulation in the primate globus pallidus.

Manganese produces signs and symptoms that suggest involvement of the basal ganglia, especially the globus pallidus and substantia nigra. Overt neurological signs have been reported in primates exposed to high levels of manganese (over 100 mg/kg) but little is known about the effects of lower doses. To examine these issues, three cebus monkeys were trained to operate a response device with their arms and legs by executing a rowing-like movement against a 3.9- to 4.1-kg spring through an arc length of 10 cm under a multiple fixed-ratio fixed-interval schedule of reinforcement. Over the course of 450 days, these monkeys were administered acute doses of 5 or 10 mg/kg iv of manganese chloride using a multiple baseline experimental design. Doses as low as 5 mg/kg provoked a large increase in the number of incomplete responses. The onset of manganese's effect appeared within days of exposure and developed over the course of several weeks. Its magnitude declined over the course of months, but after a cumulative dose of 10 to 40 mg/kg it did not return to baseline. Action tremor appeared at cumulative doses greater than 40 mg/kg and dystonia was never observed at the cumulative doses examined. Behavioral microanalysis revealed that manganese's effects initially appeared as increased variability of interresponse times and response duration. Later, the response pattern during the fixed ratio component shifted to one of progressively increasing durations through the course of the ratio. Magnetic resonance imaging revealed that the behavioral effects of manganese corresponded to an apparent increase in the manganese content of the globus pallidus and substantia nigra.

Animals↗

PubMed2000

[Chronic electric stimulation of the internal globus pallidus and subthalamic nucleus in Parkinson disease].

PATHOPHYSIOLOGY: In Parkinson's disease, the neurodegenerative process of the nigrostriatal dopaminergic pathways induces an increase in activity of the subthalamic nucleus and the medial globus pallidus, which cause inhibition of thalamo-cortical outputs explaining parkinsonism. HIGH-FREQUENCY DEEP BRAIN STIMULATION: The adverse effects induced by lesions of subcortical structures (thalamotomy, pallidotomy) have increased interest in chronic electrical stimulation proposed as a new therapy in Parkinson's disease. This technique is reversible and can be modulated with less adverse effects. TWO TARGETS: Two targets may be proposed in case of severe motor fluctuations: the medial globus pallidus and the subthalamic nucleus. Pallidial stimulation improves dramatically levodopa-induced dyskinesia and, with a variable degree, the parkinsonian triad. Subthalamic stimulation rapidly reverses akinesia, rigidity and tremor and also dyskinesias which progressively tend to diminish after decreasing L-dopa dosage. LONG-TERM EFFICACY: A follow-up period of a few years has confirmed that the beneficial effect is maintained. However, stimulation dose not prevent the development of certain symptoms (postural impairment, cognitive decline). LIMITED INDICATIONS: Chronic electrical stimulation of medial globus pallidus and subthalamic nucleus may be proposed for parkinsonian patients with severe motor fluctuations associated with abnormal involuntary movements which are not controlled by different medical therapies. Parkinsonian symptoms must still be levodopa responsive and cause severe clinical disability severely limiting daily living activities. Cognitive impairment and other severe pathologies are contraindications.

Electric Stimulation Therapy↗

PubMed2006

Magnetic resonance images of the globus pallidus in patients with idiopathic portal hypertension: a quantitative analysis of the relationship between signal intensity and the grade of portosystemic shunt.

BACKGROUND AND AIM: To elucidate a quantitative relationship between hyperintensity of the globus pallidus on T1-weighted magnetic resonance images (MRI) and portosystemic shunt (PSS) in portal hypertension. METHODS: Fifteen patients with idiopathic portal hypertension (IPH) and 44 patients with liver cirrhosis (LC) underwent brain MRI to asses signal intensity at the globus pallidus and Doppler sonography to examine the blood flow volume of PSS. Blood manganese (Mn) levels were examined in 36 patients and neuropsychological tests were performed in 15 patients without overt hepatic encephalopathy. RESULTS: Pallidal hyperintensity on MRI was more prominent in patients with IPH than in patients with LC. There was no correlation between MRI pallidal hyperintensity and the severity of liver dysfunction or hepatic encephalopathy. The grade of hyperintensity correlated well with the grade of PSS. The correlation was stronger in patients with IPH than in patients with LC. The plasma ammonia level and whole blood Mn level significantly correlated with MRI pallidal hyperintensity, but blood Mn level showed a stronger correlation than plasma ammonia. CONCLUSION: Hyperintensity of the globus pallidus on T1-weighted MRI correlated with the development of PSS independent of liver cell function. This brain image should be an index of the grade of PSS rather than a landmark of chronic liver failure.

Globus Pallidus↗

PubMed1993

Metabolism in the globus pallidus after fetal implants in rats with nigral lesions.

The effect of fetal mesencephalic implants on glucose utilization in selected brain structures and on apomorphine-induced rotational behavior was measured in rats with a unilateral lesion of the substantia nigra. Ipsilateral, but not contralateral, implants decreased the rotational behavior induced by apomorphine. In addition, the nigral lesion decreased glucose utilization in the dorso- and ventrolateral quadrants of the striatum and in the entopeduncular nucleus but increased glucose utilization in the ipsilateral globus pallidus and lateral habenula. The increased metabolism in the globus pallidus was attenuated by ipsilateral, but not contralateral, mesencephalic implants which also decreased glucose utilization in the dorsomedial caudate nucleus. These results indicate that the ability of an ipsilateral mesencephalic graft to ameliorate the motor behavior in rats with nigral lesions is associated with changes in the functional activity of the ipsilateral globus pallidus.

Analysis of Variance↗

PubMed1996

Neurospectroscopic alterations and globus pallidus hyperintensity as related magnetic resonance markers of reversible hepatic encephalopathy.

In patients with chronic hepatic encephalopathy, proton magnetic resonance spectroscopy can be used to detect specific metabolic abnormalities in the brain; MRI shows a hyperintense globus pallidus on T1-weighted sequences. We investigated the relationship between these two MR findings in a series of 25 patients with the use of quantitative data and a multiple regression analysis model. The cerebral increase in glutamine compounds and the decrease in myoinositol and choline correlated separately with globus pallidus hyperintensity, and each was complementary in accounting for this imaging finding. Such as association suggests that spectroscopic and imaging alterations are two different expressions of the reversible events that occur in the brain of patients with hepatic encephalopathy in that both disappear after liver transplantation. Globus pallidus hyperintensity seems to be a global indicator of the cerebral metabolic disorder, and the spectroscopic pattern denotes the specific metabolic alterations.

Aged↗

PubMed2001

Neostriatal and globus pallidus stimulation induced inhibitory postsynaptic potentials in entopeduncular neurons in rat brain slice preparations.

Recent anatomical studies revealed that the entopeduncular nucleus of the rat receives GABAergic inputs from both the neostriatum and the globus pallidus. The present study was undertaken to reveal the physiological features of these inputs using the intracellular recording method in rat brain slice preparations. Most of the entopeduncular nucleus neurons generated repetitive firing without spike accommodation with intracellular current stimulation and thus were classified as Type-I. A small number of neurons were classified as Type-II since they generated spikes with pronounced accommodation. Most of the Type-I, but none of Type-II, entopeduncular nucleus neurons exhibited monosynaptic GABAergic inhibitory postsynaptic potentials (IPSPs) after stimulation of the neostriatum and the globus pallidus. Neostriatal stimulation induced long latency IPSPs while pallidal stimulation induced long latency IPSPs compounded with short latency IPSPs. The IPSPs were mediated by GABA(A) receptors. The unitary IPSPs to striatal stimulation were small while those to pallidal stimulation were large in amplitude and able to reset ongoing rhythmic firing. The short latency IPSPs induced by pallidal stimulation reversed at a somatic membrane potential that was a few millivolts more depolarized than the long latency IPSPs, suggesting that the striatal inputs were evoked in more distal portions of the neurons than the pallidal inputs. Repetitive activation of these inputs resulted in a poor amplitude summation but a prolongation of the duration of the IPSPs. The results of the present study indicate that the pallidal projection to the entopeduncular nucleus is physiologically significant and that the neostriatum and the globus pallidus play important roles in controlling the activity of the entopeduncular nucleus, although in different ways.

Animals↗

PubMed1997

Morphology of globus pallidus neurons: its correlation with electrophysiology in guinea pig brain slices.

Intracellular recordings obtained from globus pallidus neurons in guinea pig revealed, on the basis of their membrane properties, the existence of at least two major (types I and II) and one minor (type III) groups of neurons. Type I neurons were silent at the resting membrane level and generated a burst of spikes with strong accommodation to depolarizing current injection. Type II neurons fired at the resting membrane level or with small membrane depolarization, and their repetitive firing (< or = 200 Hz) was very sensitive to the amplitude of injected current and showed weak accommodation. Type III neurons did not fire spontaneously at the resting membrane level. The neurons were morphologically characterized by intracellular injection of biocytin following the electrophysiological recordings. Among the major groups, the soma size of type I neurons (40 x 23 microns) was larger than that of type II neurons (29 x 17 microns). Both types of neurons had three to six primary dendrites. Dendritic spines were very sparse. Occasionally, dendrites exhibited varicosities, especially in their terminal branches. Dendritic fields were disc-like in shape and were perpendicular to striopallidal fibers. Most of the axons had intranuclear collaterals. Main axonal branches projected rostrally or caudally, and in some neurons one axonal branch could be followed caudally, and another rostrally, into the striatum. These two types were major neurons in the globus pallidus and were considered to be projection neurons. Type III neurons were small (18 x 12 microns), and their dendrites were covered with numerous spines. They were considered to be interneurons.

Animals↗

PubMed1991

Met-enkephalin release from slices of the rat striatum and globus pallidus: stimulation by excitatory amino acids.

The present study evaluated the effects of high K+ and four excitatory amino acids (EAAs) on the release of met-enkephalin-like immunoreactivity (ME-i.r.) from slices of the rat striatum and globus pallidus. High K+ (15-50 mM) increased the release of ME-i.r. in a concentration-dependent manner in both regions, the release response in the globus pallidus being consistently greater than in the striatum. This release was highly Ca(++)-dependent and was significantly enhanced in the absence of external Mg++. D-2-Amino-7-phosphonoheptanoic acid (0.5 mM), a competitive N-methyl-D-aspartate (NMDA) receptor antagonist, did not alter this enhanced action of K+, suggesting that the activation of NMDA receptors by an endogenous agonist did not contribute to the enhancement. Exposure of pallidal or striatal slices to four EAA receptor agonists, NMDA, L-glutamate, kainate (KA) and quisqualate, increased the release of ME-i.r. above the base line, an effect that was Ca(++)-dependent. Both L-glutamate and NMDA, at concentrations of 1 and 5 mM, produced a graded increase in the ME-i.r. release, but a higher concentration (10 mM) produced a lower release. In both regions the NMDA (5 mM)-evoked release was effectively inhibited by Mg++ (1.2 mM), 3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP) (5 microM), a competitive NMDA receptor antagonist and thienylcyclohexylpiperidine (10 microM), a noncompetitive NMDA receptor antagonist. Tetrodotoxin (0.3 microM), a Na+ channel blocker, did not affect the NMDA-evoked release of ME-i.r. in the striatum, but decreased it by 52% in the globus pallidus.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acids↗

PubMed1989

Dyskinesia in the primate following injection of an excitatory amino acid antagonist into the medial segment of the globus pallidus.

Injection of an excitatory amino acid antagonist, kynurenic acid, into the medial segment of the globus pallidus of the conscious monkey elicited dyskinesia of the contralateral limbs. In most respects the dyskinesia was indistinguishable from the disorder that is produced by ablation of the subthalamic nucleus, or injection of a GABA antagonist into the subthalamic nucleus. Injections of kynurenic acid into the lateral segment of the globus pallidus, by contrast, did not provoke dyskinesia. The effect of kynurenic acid is attributed to the blockade of neurotransmission from the subthalamic nucleus to the medial pallidal segment, and the results suggest that the neurotransmitter utilised by this pathway is an excitatory amino acid.

Animals↗

PubMed1990

Blockade of excitatory neurotransmission in the globus pallidus induces rigidity and akinesia in the rat: implications for excitatory neurotransmission in pathogenesis of Parkinson's diseases.

Bilateral microinjections of the selective N-methyl-D-aspartate (NMDA) antagonist, (-)-2-amino-7-phosphonoheptanoate (AP7), 0.02-0.5 nmol, into the globus pallidus and ventral-posterior portions of the caudate-putamen result in an increase in the muscle tone (rigidity) and catalepsy (akinesia) in rats. NMDA blocked the actions of AP7 on motility in sensitive regions of the globus pallidus and caudate-putamen. Topographical differences in the action of AP7 in the striatum were detected in the dorsal-ventral and rostral-caudal direction. Microinjections of AP7 into the nucleus accumbens induced neither an increase in the muscle tone nor catalepsy in rats, while ventral regions of the caudate-putamen were sensitive to both actions of AP7. Microinjections of AP7 into the dorsal caudate-putamen resulted in a moderate or no increase in the muscle tone. AP7 failed to induce catalepsy from dorsal regions of the caudate-putamen. These data identify the globus pallidus and a defined subregion of the caudate-putamen as crucial sites where excitatory neurotransmission acts to regulate the final set-point of the respective output neurons providing modulation of the passage of motor information through the basal ganglia.

2-Amino-5-phosphonovalerate↗

PubMed2006

Lesions in monkey globus pallidus externus exacerbate parkinsonian symptoms.

To further define the role of the external segment of the globus pallidus (GPe) in the development of parkinsonian motor signs, two rhesus monkeys were made parkinsonian with the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Behavioral assessments of bradykinesia and akinesia as well as single neuron recordings in the internal segment of the globus pallidus (GPi) were performed in both monkeys before and after ablating the sensorimotor portion of GPe. The effects of apomorphine on behavior and neuronal activity were also assessed in the parkinsonian monkeys before and after GPe ablation. We found that lesions in GPe exacerbated parkinsonian symptoms, altered neuronal activity in GPi, and reduced the therapeutic effects of apomorphine. These results support the hypothesis that GPe can influence GPi neuronal activity and is directly involved in parkinsonism. In addition, these data suggest that the inclusion of GPe in pallidotomy lesions for the treatment of Parkinson's disease can block the beneficial effects of antiparkinsonian medications and should be avoided.

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

PubMed1984

Behaviorally specific limb use deficits following globus pallidus lesions in rats.

The effects of bilateral globus pallidus lesions were observed in rats trained to perform a somatosensory/proprioceptive guided forelimb reaching task. Postlesion reaching became very inaccurate, characterized by gross abnormalities in limb and body posture. Postural abnormalities and paw use deficits were not observed in other situations. These results suggest that pallidal damage does not result in a simple motor deficit but interferes with motor performance when movements depend upon somesthetic and proprioceptive feedback.

Animals↗

PubMed1981

A microiontophoretic study of morphine on single neurons in the rat globus pallidus.

The microiontophoretic application of morphine to single globus pallidus neurons in morphine naive rats resulted in a depression of both spontaneous and glutamate-evoked firing of these neurons. Seventy percent of all pallidal neurons on which morphine was tested exhibited some degree of depression of neuronal discharge; no excitatory effect ws observed to morphine on any pallidal neurons. The depressant effects of morphine, but not those of dopamine, could be antagonized by the microiontophoretic application of the morphine antagonist naloxone, indicating that the morphine-induced depression of pallidal neuronal activity was a specific morphine action. This effect of morphine is most likely mediated by the opiate receptors on pallidal neurons that have been proposed to function in enkephalinergic-mediated synaptic transmission.

Animals↗

PubMed1998

Tolerance to catalepsy following chronic haloperidol is not associated with changes in GABA release in the globus pallidus.

In vivo microdialysis was used to investigate the relationship between extracellular GABA levels in rat globus pallidus following acute (1st injection) and chronic (29th injection) haloperidol (Hal) (0.25 mg kg-1 day-1, s.c.) with the presence and absence of catalepsy, respectively. There was no difference in basal pallidal GABA levels in the drug naive and chronically treated rats. Furthermore, pallidal GABA release was not affected following injection with Hal in either group although there was a prolonged catalepsy in the drug naive group and a tolerance to catalepsy in the chronically treated group. A previous microdialysis study employing similar experiment protocol showed that Hal increases striatal GABA release in drug naive rats and increases basal striatal GABA levels following chronic treatment. The results of the current study demonstrate that these effects are not reflected in the globus pallidus and suggest that striatal GABA interneurons and/or GABA projection neurons to extrapallidal nuclei such as the substantia nigra pars reticulata may be involved in initiating catalepsy following acute Hal and mediating the tolerance to catalepsy observed following chronic Hal.

Animals↗

PubMed1995

Thalamic distribution of projection neurons to the primary motor cortex relative to afferent terminal fields from the globus pallidus in the macaque monkey.

To examine quantitatively the pathway from the internal segment of the globus pallidus to the primary motor cortex through the thalamus, we compared the distribution of thalamocortical neurons projecting to the motor cortex with the distribution of afferent terminal fields from the pallidum in the ventrolateral nuclear group of the thalamus in four Japanese monkeys by using the anterograde and retrograde double-labeling method. In each monkey, different fluorescent retrograde tracers (Fast Blue and Diamidino Yellow) were injected separately into the distal and proximal forelimb areas of the primary motor cortex after physiological mapping with intracortical microstimulation. In the same individual monkeys, an anterograde tracer, wheatgerm agglutinin conjugated to horseradish peroxidase, was injected into the internal segment of the globus pallidus after the forelimb part was identified physiologically. A small group of projection neurons to the distal and proximal representations of the motor cortex were found in the terminal fields from the pallidum, but a majority of the projection neurons were distributed outside the terminal area in the thalamus. These results confirm the existence of the pathway from the pallidum through the thalamus to the primary motor cortex, but also indicate that the primary motor cortex receives its major thalamic inputs from outside of the pallidal projection area, and that the pallidum sends its major outputs to nonprimary motor areas through the thalamus.

Afferent Pathways↗