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PubMed1991

Further investigations into the pathophysiology of MPTP-induced parkinsonism in the primate: an intracerebral microdialysis study of gamma-aminobutyric acid in the lateral segment of the globus pallidus.

The technique of intracerebral microdialysis has been employed to examine the extracellular level of gamma-aminobutyric acid (GABA) within the lateral segment of the globus pallidus of two cynomolgus monkeys, before and after the induction of parkinsonism with N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Microdialysis probes were acutely implanted through indwelling cannulae positioned at several sites above the lentiform nuclei in the conscious primates, and the basal and potassium (100 mM) evoked amino acid levels were monitored for 3 h. These procedures were repeated at fresh sites within the lateral globus pallidus following the induction of parkinsonism with MPTP. The levels of a number of amino acids, including Asn, Ala, Gln, Ser, and Tau were unchanged following MPTP treatment, whereas both the basal and K(+)-evoked release of GABA was consistently increased. This observation represents further corroboration of the evidence for increased GABAergic input to the lateral globus pallidus in MPTP-induced parkinsonism.

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

PubMed1984

Identification of different subpopulations of neostriatal neurones projecting to globus pallidus or substantia nigra in the monkey: a retrograde fluorescence double-labelling study.

Fluorescent tracers (Nuclear Yellow, True Blue, Fast Blue) were injected, in various combinations, into the globus pallidus and substantia nigra in three marmosets. Examination of perikarya in the ipsilateral neostriatum, well removed from pallidal injection sites, revealed that the predominant pattern was of single-labelled cells, retrogradely labelled from either the globus pallidus or substantia nigra. It is suggested, on the basis of this evidence and data previously available, that the striatum contains at least three types of efferent neurones, one projecting exclusively to the globus pallidus, one projecting exclusively to the substantia nigra, and another projecting to both structures.

Animals↗

PubMed2004

Globus pallidus: a target brain region for divalent metal accumulation associated with dietary iron deficiency.

Recently, iron deficiency has been connected with a heterogeneous accumulation of manganese in the rat brain. The striatum is particularly vulnerable, for there is a significant negative correlation between accumulated manganese and gamma-aminobutyric acid levels. The effect of dietary iron deficiency on the distribution of zinc and copper, two other divalent metals with essential neurobiological roles, is relatively unexplored. Thus, the primary goal of this study was to examine the effect of manipulating dietary iron and manganese levels on the concentrations of copper, iron, manganese and zinc in five rat brain regions as determined with inductively coupled plasma mass spectrometry analysis. Because divalent metal transporter has been implicated as a transporter of brain iron, manganese, and to a lesser extent zinc and copper, another goal of the study was to measure brain regional changes in transporter levels using Western blot analysis. As expected, there was a significant effect of iron deficiency (P < 0.05) on decreasing iron concentrations in the cerebellum and caudate putamen; and increasing manganese concentrations in caudate putamen, globus pallidus and substantia nigra. Furthermore, there was a significant effect of iron deficiency (P < 0.05) on increasing zinc concentration and a statistical trend (P = 0.08) toward iron deficiency-induced copper accumulation in the globus pallidus. Transporter protein in all five regions increased due to iron deficiency compared to control levels (P < 0.05); however, the globus pallidus and substantia nigra revealed the greatest increase. Therefore, the globus pallidus appears to be a target for divalent metal accumulation that is associated with dietary iron deficiency, potentially caused by increased transporter protein levels.

Animals↗

PubMed1997

Dopamine-adenosine interactions in the striatum and the globus pallidus: inhibition of striatopallidal neurons through either D2 or A2A receptors enhances D1 receptor-mediated effects on c-fos expression.

D1 receptors located on striatonigral neurons and D2 receptors located, together with A2A receptors, on striatopallidal neurons are known to interact functionally. Using in situ hybridization, we examined the effects of D1 and D2 agonists and of an A2A antagonist on c-fos mRNA in identified striatal neurons and in globus pallidus. The full D1 agonist, SKF 82958 (1 mg/kg), induced a homogenous increase of c-fos mRNA in the striatum. This increase occurred to a similar extent in D1 and D2 receptor-containing striatal neurons. Conversely, the D2 agonist, quinelorane (2 mg/kg), decreased c-fos mRNA in these populations but increased it in globus pallidus. The adenosine A2A receptor antagonist, SCH 58261 (5 mg/kg), also decreased c-fos mRNA in D2 receptor-containing neurons in striatum but did not affect pallidal c-fos mRNA. Concomitant administration of either D1 plus D2 agonists or D1 agonist plus A2A antagonist caused a potentiation of c-fos mRNA in striatal neurons expressing the D1 receptor and in globus pallidus. However, only the combination of D1 and D2 agonists modified the c-fos mRNA expression to a "patchy" distribution. Our data show that (1) c-fos expression can be activated through D1 and inhibited through A2A or D2 receptors in both striatal output pathways in normal rats, and (2) D2 receptor stimulation as well as A2A receptor blockade can interact with D1 receptor activation to potentiate c-fos expression in the striatum and the globus pallidus. The data also suggest that the topological alteration of c-fos expression after coadministration of D1 and D2 agonists involves D2 receptors located on interneurons or presynaptically on dopaminergic nerve terminals.

Adenosine↗

PubMed1984

Lesions of the globus pallidus and striatum attenuate ketocyclazocine-induced feeding.

A large body of evidence suggests that endogenous opioids are involved in the regulation of feeding. As the striatum and globus pallidus have relatively high concentrations of opioid receptors, these areas are possible sites of action for the stimulatory effects of opiates on feeding. To test these possibilities, male rats were lesioned bilaterally in the globus pallidus or striatum. Nocturnal food intake was then measured after the subcutaneous administration of the opiate antagonist, naloxone (0-10 mg/kg). Spontaneous daytime intake was measured after the subcutaneous administration of the kappa opiate agonist ketocyclazocine (0-10 mg/kg). Neither pallidal nor striatal lesions affected the sensitivity of naloxone in reducing food intake. On the other hand, both lesioned groups were 10-100 times less sensitive to the stimulatory effects of ketocyclazocine. These results suggest that the globus pallidus and striatum may be target areas for the stimulatory effects of exogenous opiates on food intake. Additionally, the relationship of these areas to the dopaminergic nigrostriatal tract suggests that feeding regulation may involve an interaction between dopaminergic and opioid systems.

Animals↗

PubMed2001

Abnormal activity in the globus pallidus in off-period dystonia.

Pallidotomy was performed in a parkinsonian patient with off-period foot dystonia. Dystonia appeared at the beginning of surgery and disappeared after the first microelectrode penetration of the globus pallidus, perhaps a micropallidotomy effect. Neuronal recording during dystonia revealed that the mean firing rates were low in both the internal and external segments of the globus pallidus, and that firing was irregular in the internal segment of the globus pallidus, compared with firing patterns in offstate parkinsonian patients without dystonia. These firing patterns immediately changed into those of nondystonic, off-state parkinsonism after relief of dystonia These results suggest that off-period dystonia results from the same physiological change in the basal ganglia as that in primary dystonia.

Dystonia↗

PubMed1991

Dopamine D1 receptors in the sub-commissural part of the globus pallidus and their role in oro-facial dyskinesia in cats.

The possible role of dopamine D1 receptors in the sub-commissural part of the globus pallidus in the induction of oro-facial dyskinesia was studied in cats. The present study reveals two findings. Firstly, bilateral injections of the D1 agonist (+/-)-SK& F38393 into the ventral pallidal area elicited oro-facial dyskinesia, which was quantified in terms of numbers of tongue protrusions. The results show that the dose-effect curve was bell-shaped (1.0, 1.75, 2.5, 5.0 micrograms/0.5 microliters (+/-)-SK&F38393). The oro-facial dyskinesia elicited by (+/-)-SK&F38393 was highly comparable to the oro-facial dyskinesia elicited by injections of the GABA antagonist picrotoxin or the acetylcholine agonist carbachol into the sub-commissural part of the globus pallidus. Secondly, the inactive enantiomer of SK&F38393, i.e. S(-)-SK&F38393, was found to be ineffective in eliciting oro-facial dyskinesia when injected in a dose equivalent to 50% of the most effective dose of the racemic mixture of (+/-)-SK&F38393. Furthermore, the effect elicited by 2.5 micrograms/0.5 microliters (+/-)-SK&F38393 was significantly attenuated by local injection of the D1 antagonist R(+)-SCH23390 in a dose which had no effect itself (1.0 micrograms/0.5 microliters). These findings indicate that the effects elicited by (+/-)-SK&F38393 are D1-specific. The present results thus clearly indicate that dopamine D1 receptors within the sub-commissural part of the globus pallidus are involved in mediating oro-facial dyskinesia in cats.

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

PubMed2003

Dual effects of intermittent or continuous L-DOPA administration on gene expression in the globus pallidus and subthalamic nucleus of adult rats with a unilateral 6-OHDA lesion.

Intermittent oral doses of levodopa (L-DOPA) are routinely used to treat Parkinson's disease, but with prolonged use can result in adverse motor complications, such as dyskinesia. Continuous administration of L-DOPA achieves therapeutic efficacy without producing this effect, yet the molecular mechanisms are unclear. This study examined, by in situ hybridization histochemistry, the effects of continuous or intermittent L-DOPA administration on gene expression in the globus pallidus and subthalamic nucleus of adult rats with a unilateral 6-hydroxydopamine (6-OHDA) lesion of the nigrostriatal pathway. Results were compared to 6-OHDA-treated rats receiving vehicle. Our results provide original evidence that continuous L-DOPA normalizes the 6-OHDA-lesion-induced increase in mRNA levels encoding for the 67 kDa isoform of glutamate decarboxylase in neurons of the globus pallidus and cytochrome oxidase subunit I mRNA levels in the subthalamic nucleus. The extent of normalization did not differ between the continuous and intermittent groups. In addition, intermittent L-DOPA induced an increase in the mRNA levels encoding for the 65 kDa isoform of glutamate decarboxylase in globus pallidus neurons ipsilateral to the lesion and a bilateral increase in c-fos mRNA expression in the subthalamic nucleus. These results suggest that continuous L-DOPA tends to normalize the 6-OHDA-lesion-induced alterations in cell signaling in the pallido-subthalamic loop. On the other hand, we propose that chronic intermittent L-DOPA exerts a dual effect by normalizing cell signaling in a subpopulation of neurons in the globus pallidus and subthalamic nucleus while inducing abnormal signaling in another subpopulation.

Animals↗

PubMedDate not supplied

[Participation of the globus pallidus in the organization of stereotyped behavior in the cat].

Electrical stimulation of the globus pallidus of cats produces a stereotype behaviour like that following the injection of high doses of d,1-amphetamine. This drug enhances pallidal response. On the other hand, pallidal stimulation facilitates formation of amphetamine-induced stereotypy which weakens after bilateral destruction of the globus pallidus. Neuroleptic haloperidol in very low doses abolishes pallidal as well as amphetamine-induced stereotypy. As supposed pallidal stereotypy may be connected with the disturbance of nigro-strio-pallidal relations.

Amphetamine↗

PubMed1994

Mapping of globus pallidus and ventral pallidum lesions that produce hyperkinetic treading.

The purpose of this study was to identify sites where striatopallidal lesions produce two distinct sensory-triggered hyperkinetic syndromes: (1) exaggerated forelimb treading alone to oral taste infusions and (2) sensorimotor exaggerated treading plus enhanced aversive reactions to taste infusions. The behavioral characteristics of these syndromes have been described previously (Berridge, K.C. and Cromwell, H.C., Behav. Neurosci., 104 (1990) 778-795). Bilateral excitotoxin lesions were made using quinolinic acid (10 micrograms in 1 microliter) in the caudate/putamen, nucleus accumbens, globus pallidus or ventral pallidum/substantia innominata. In order to identify the precise center, borders, severity and size of lesion sites that caused these hyperkinetic treading syndromes, neuron counts (modified fractionator technique) and glial fibrillary acidic protein immunoreactivity (GFAP-IR) densitometry were used in a stereological mapping analysis. The site of lesions that produced the hyperkinetic treading syndrome without enhanced aversion was found to be restricted to the globus pallidus (GP). Damage exceeding 60% neuron loss bilaterally within a 0.8 x 1.0 x 1.0 mm subregion of the ventromedial GP produced this syndrome. The site of lesions that produced the combined syndrome of hyperkinetic treading and aversive enhancement was ventral to the globus pallidus, within the ventral pallidum/substantia innominata (VP/SI). Damage exceeding 70% neuron loss bilaterally within a 1.0 x 0.5 x 1.0 mm diameter subregion of the ventromedial ventral pallidum/substantia innominata produced this syndrome. This subterritory was located immediately lateral to the border of the lateral hypothalamus. Bilateral lesions to the caudate/putamen or nucleus accumbens did not produce either hyperkinetic treading syndrome. These results are discussed in terms of the connectivity of the ventral pallidal/substantia innominata and globus pallidus regions and in terms of neuropathological models of hyperkinetic disorders.

Animals↗

PubMed1981

[Different effects of conditioning stimulation of the caudate nucleus and globus pallidus on the paroxysmal activity of the cat amygdala].

The conditioning stimulation of the globus pallidus both in chronic and acute cats determined a more effective inhibition than caudate nucleus activation on the evoked paroxysmal activity in the amygdala. Lesions by means of kainic acid of the entopeduncular nucleus, has resulted in a significant decrease of the caudate inhibitory effect. The hypothesis we assumed is about a role of the globus pallidus in the control of the evoked amygdaloid after-discharge.

Amygdala↗

PubMed2000

Enhanced levels of endogenous cannabinoids in the globus pallidus are associated with a reduction in movement in an animal model of Parkinson's disease.

In recent years, cannabinoid receptors and their endogenous ligands (endocannabinoids) have been identified within the brain. The high density of CB1 cannabinoid receptors within the basal ganglia suggests a potential role for endocannabinoids in the control of voluntary movement and in basal ganglia-related movement disorders such as Parkinson's disease. However, whether endocannabinoids play a role in regulating motor behavior in health and disease is unknown. Here we report the presence in two regions of the basal ganglia, the globus pallidus and substantia nigra, of the endocannabinoids 2-arachidonoylglycerol (2AG) and anandamide. The levels of the latter compound are approximately threefold higher than those previously reported in any other brain region. In the reserpine-treated rat, an animal model of Parkinson's disease, suppression of locomotion is accompanied by a sevenfold increase in the levels of the 2AG in the globus pallidus, but not in the other five brain regions analyzed. Stimulation of locomotion in the reserpine-treated rat by either of the two selective agonists of D2 and D1 dopamine receptors, quinpirole and R-(+/-)-3-allyl-6-chloro-7, 8-dihydroxy-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine hydrobromide (Cl-APB), respectively, results in the reduction of both anandamide and 2AG levels in the globus pallidus. Finally, full restoration of locomotion in the reserpine-treated rat is obtained by coadministration of quinpirole and the selective antagonist of the cannabinoid CB1 receptor subtype, SR141716A. These findings indicate a link between endocannabinoid signaling in the globus pallidus and symptoms of Parkinson's disease in the reserpine-treated rat, and suggest that modulation of the endocannabinoid signaling system might prove useful in treating this or other basal ganglia-related movement disorders.

Animals↗

PubMed1990

A postmortem quantitative study of iron in the globus pallidus of schizophrenic patients.

Several postmortem studies have reported the presence and probable overabundance of basal ganglia mineralization in schizophrenic patients. In order to study this problem in a quantitative fashion we analyzed the mineral content of the globus pallidus in 9 schizophrenic patients and 10 age-matched controls with a Loats computer image analysis system. No significant differences were noted between schizophrenic patients and controls in regard to gender, age, or mineral content of the globus pallidus. The mean content of iron per internal segment of globus pallidus was greater in schizophrenic patients, but the large variation and small number of patients in our sample may have accounted for the negative findings.

Adult↗

PubMed1997

D2 receptor-mediated inhibition of GABA release by endogenous dopamine in the rat globus pallidus.

Attempting to better understand the role of the dopaminergic innervation in the rat globus pallidus, we examined here whether or not endogenous dopamine modulates the release of [3H]GABA in superfused pallidal slices. The superfusion medium contained elevated (15 mM) potassium. The release of endogenous dopamine was induced by the dopamine releaser drug, methamphetamine. Methamphetamine (100 microM) inhibited by 46% the release of [3H]GABA. Methamphetamine inhibition was completely blocked by reserpinization of the rats. It was also completely blocked by the D2 dopamine receptor antagonist sulpiride (10 microM). Sulpiride alone caused a 105% increase in GABA release. The increase was not observed in slices from reserpinized rats. Quinpirole (10 microM), a D2 dopamine receptor agonist, inhibited (43%) [3H]GABA release. The results suggest that endogenous dopamine exerts an inhibitory effect on GABA release in the rat globus pallidus. The effect is mediated by D2 receptors presumably located on striatopallidal axon terminals.

Animals↗

PubMed1990

Effects of dopamine D1 and D2 agonists and antagonists injected into the nucleus accumbens and globus pallidus on jaw movements of rats.

The effects of bilateral injections of selective D1 and D2 agonists and antagonists into the anteromedial part of the nucleus accumbens and the globus pallidus on apomorphine-induced jaw movements were studied in ketamine-anaesthetized rats after C1 spinal transection. Both SCH 23390 (0.1 and 1 micrograms) and 1-sulpiride (5 and 25 ng) injected into the nucleus accumbens suppressed the display of jaw movements after apomorphine (0.5 mg/kg i.v.). Injection of 1-sulpiride (5 and 25 ng) into the globus pallidus also blocked the effect of apomorphine, whereas SCH 23390 (1 microgram) injected into the same site was ineffective in this respect. Simultaneous application of the selective D1 and D2 agonists, SKF (1 or 5 micrograms) + quinpirole (10 micrograms), into the nucleus accumbens strongly potentiated the effect induced by local administration of each drug alone; a comparable, but smaller, effect was seen after simultaneous injections of these agents into the globus pallidus. These results show that dopaminergic mechanisms within the nucleus accumbens are involved in apomorphine-induced jaw movements, and that the expression of these movements requires concurrent activation of D1 and D2 receptors.

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

PubMed1990

Nigrostriatal lesion alters neurophysiological responses to selective and nonselective D-1 and D-2 dopamine agonists in rat globus pallidus.

The effects of the selective D-1 dopamine agonist SKF 38393, the selective D-2 agonist quinpirole, and the nonselective D-1/D-2 agonist apomorphine on spontaneous activity of globus pallidus neurons were compared in normal control rats and rats with unilateral 6-hydroxydopamine induced lesions of the nigrostriatal pathway. In control, unlesioned rats, SKF 38393 (0.4 and 10 mg/kg, i.v.) caused no significant net change in the activity of globus pallidus neurons, although some individual cells showed significant increases or decreases in discharge rates following 10 mg/kg SKF 38393 administration. In animals with unilateral 6-hydroxydopamine induced lesions, SKF 38393 caused greater increases and decreases in the discharge rates of a larger percentage of pallidal cells recorded on the ipsilateral side than in control, unlesioned animals. These rate changes were effectively reversed by the D-1 antagonist SCH 23390, but not by the D-2 antagonist YM-09151-2. Quinpirole (0.3 mg/kg, i.v.) produced modest rate increases in control, unlesioned animals and significantly larger rate increases in nigrostriatal lesioned animals. YM-09151-2, but not SCH 23390, effectively reversed quinpirole's effects in the lesioned animals. As previously reported, the nonselective D-1/D-2 agonist apomorphine (0.3 mg/kg, i.v.) produced large increases in discharge rates of pallidal cells in control, unlesioned rats. In contrast, in nigrostriatal lesioned rats, the discharge rates of some ipsilateral pallidal neurons were markedly increased, others were decreased, and some were unaffected following apomorphine administration. The dopamine antagonist spiroperidol partially to fully reversed these rate changes. In summary, apomorphine's neurophysiological profile appears to be an exaggeration of the D-1 agonist profile in the globus pallidus of these lesioned animals. The degree of change observed after apomorphine administration is consistent with results from other studies that have indicated that a synergistic interaction between effects triggered by stimulation of the two receptor subtypes can occur in these animals, as in control, unlesioned animals. However, these results further show that in rats with unilateral nigrostriatal lesions, the denervated dopamine receptors or the processes they mediate are altered so that they no longer have the requirement seen in controls for concurrent stimulation of the complementary dopamine receptor subtype for expression of the selective agonist effects.

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

PubMed2006

Involvement of globus pallidus in the antiparkinsonian effects of adenosine A(2A) receptor antagonists.

An involvement of globus pallidus (GP) in the antiparkinsonian effects of A(2A) receptor antagonists has been proposed on the basis of the selective localization of A(2A) receptors on the striatopallidal pathway. In order to investigate this possibility, the present study evaluated rotational behavior in unilaterally 6-hydroxydopamine-lesioned rats following infusion of the water-soluble A(2A) receptor antagonist SCH BT2 into GP. SCH BT2 (5 microg/1 microl) altered neither motor behavior nor produced postural asymmetry by itself. However, when infused concomitantly with a parenteral subthreshold dose of l-DOPA (3 mg/kg i.p.) capable of inducing modest contralateral rotational behavior (34.7 +/- 20.7/1 h), SCH BT2 significantly potentiated the number of contraversive rotations (167.4 +/- 16.3/1 h). These results suggest that A(2A) receptors located in the globus pallidus may be involved in the antiparkinsonian effects of A(2A) antagonists.

Adenosine A2 Receptor Antagonists↗

PubMed1985

Behavioural effects in rats of unilateral and bilateral injections of opiate receptor agonists into the globus pallidus.

Unilateral injections of a putative kappa-opiate receptor agonist, ethylketocyclazocine, into the globus pallidus of rats caused dose-dependent ipsiversive circling which was inhibited by prior systemic administration of the opiate receptor antagonist naloxone. Neither a putative delta-opiate receptor agonist ( [D-Ala2, D-Leu5]enkephalin) nor a putative mu-opiate receptor agonist (Tyr-D-Ala-Gly-MePhe-Met(0)-ol) induced circling behaviour after unilateral intrapallidal injection. Bilateral intrapallidal injection of the delta-opiate receptor agonist or the mu-opiate receptor agonist caused an increase in locomotor activity which in both cases was reduced by systemic administration of naloxone. A specific delta-receptor antagonist, (N,N-bisalyl-Tyr-Gly-Gly-psi-(CH2S)-Phe-Leu-OH) had no effect on the increase in locomotor activity caused by the delta-opiate receptor agonist. Bilateral intrapallidal injection of the kappa-opiate receptor agonist had no effect on locomotor activity. It is suggested that different opiate receptor subtypes within the globus pallidus differentially mediate circling and locomotor behaviour.

Animals↗