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PubMed1986

Neophobia, conditioned taste aversion and EEG arousal after globus pallidus lesion.

Rats with unilateral or bilateral electrolytic lesions in the globus pallidus (GP) became aphagic and adipsic. Aphagia and adipsia lasted 2-3 days in rats with unilateral lesion, but were more persistent in animals with bilateral lesions. EEG arousal induced by nociceptive stimuli applied to the side of the body contralateral to the unilateral pallidal lesion was of shorter duration than that induced by ipsilateral stimulation; no difference was found between rats injured in left or right (GP). Total exploratory activity of rats with symmetrical or asymmetrical lesions, exposed to a novel environment for ten min, was not different from that of the control group, but the exploratory activity measured in a 60 sec block showed trends in the two injured groups being different than those in the controls. Rats with unilateral right or bilateral lesions showed a lower level of neophobia for saccharin than controls. Acquisition of conditioned taste aversion was similar in lesioned rats and controls, but extinction of the conditioned taste aversion was slower in the intact than in the injured animals.

Animals↗
PubMed2004

Globus pallidus internus stimulation in primary generalized dystonia: a H215O PET study.

Globus pallidus internus (GPi) deep brain stimulation (DBS) increasingly shows promising efficacy in the treatment of severe primary generalized dystonia. Functional imaging studies have shown previously that dystonia could be related to abnormal cortical activation during voluntary movement. In the present study, the effects of GPi DBS on regional cerebral blood flow (rCBF) during a motor task were studied in patients with primary generalized dystonia. rCBF was measured using H215O and PET in eight control subjects and six patients with dystonia treated with bilateral GPi DBS. Subjects were scanned at rest and while performing joystick movements. Dystonic patients were tested in two conditions: 'OFF' (stimulator bilaterally switched off) and 'ON' (unilateral stimulation). In the 'OFF' condition, compared with rest, motor activation of the most dystonic hand was associated with overactivity in the contralateral dorsolateral prefrontal cortex, gyrus frontalis medialis, superior frontal gyrus (area 10), frontoorbital cortex and thalamus. In the 'ON' condition, GPi DBS contralaterally to the most dystonic hand induced a decrease of the overactivation in the same areas, as well as the putamen. According to the present study, generalized dystonia is associated with prefrontal overactivation which can be reversed by effective GPi DBS.

Adolescent↗
PubMed1994

Electrophysiology of globus pallidus neurons in vitro.

1. We investigated the electrical properties of globus pallidus neurons intracellularly using brain slices from adult guinea pigs. Three types of neurons were identified according to their intrinsic electrophysiological properties. 2. Type I neurons (59%) were silent at the resting membrane level (-65 +/- 10 mV, mean +/- SD) and generated a burst of spikes, with strong accommodation, to depolarizing current injection. Calcium-dependent low-frequency (1-8 Hz) membrane oscillations were often elicited by membrane depolarization (-53 +/- 8 mV). A low-threshold calcium conductance and an A-current were also identified. The mean input resistance of this neuronal type was 70 +/- 22 M omega. 3. Type II neurons (37%) fired spontaneously at the resting membrane level (-59 +/- 9 mV). Their repetitive firing (< or = 200 Hz) was very sensitive to the amplitude of injected current and showed weak accommodation. Sodium-dependent high-frequency (20-100 Hz) subthreshold membrane oscillations were often elicited by membrane depolarization. This neuronal type demonstrated a low-threshold calcium spike and had the highest input resistance (134 +/- 62 M omega) of the three neuron types. 4. Type III neurons (4%) did not fire spontaneously at the resting membrane level (-73 +/- 5 mV). Their action potentials were characterized by a long duration (2.3 +/- 0.6 ms). Repetitive firing elicited by depolarizing current injection showed weak or no accommodation. This neuronal type had an A-current and showed the lowest input resistance (52 +/- 35 M omega) of the three neuron types. 5. Stimulation of the caudoputamen evoked inhibitory postsynaptic potentials (IPSPs) in Type I and II neurons. In Type II neurons the IPSPs were usually followed by rebound firing. Excitatory postsynaptic potentials and antidromic responses were also elicited in some Type I and II neurons. The estimated conduction velocity of the striopallidal projection was < 1 m/s (Type I neurons, 0.49 +/- 0.37 m/s; Type II neurons, 0.33 +/- 0.13 m/s).

Animals↗
PubMed1999

Stereotactic targeting of the globus pallidus internus in Parkinson's disease: imaging versus electrophysiological mapping.

OBJECTIVE: The reintroduction of pallidotomy for the treatment of Parkinson's disease (PD) has generated various opinions regarding the ideal anatomic or physiological location of the target within the globus pallidus. The role of microelectrode recording guidance in pallidotomy for the treatment of advanced PD is presently under debate. The purpose of this study was twofold. The first goal was to determine the degree of accuracy in the targeting of the globus pallidus internus (GPi) with magnetic resonance imaging (MRI), by comparing these results with the final placement of the thermolytic lesions (as defined by electrophysiological assessment). The second goal was to ascertain the somatotopic arrangement of the GPi in PD. METHODS: The analysis involved 50 patients with PD who underwent microrecording-guided pallidotomy. The theoretical coordinates for lesioning were calculated after definition of the intercommissural line by MRI. The actual placement of the lesions was determined after mapping of the GPi by microrecording, using stimulation to identify the sensorimotor region and its somatotopic organization. RESULTS: In most cases, the lesions were placed posterior and lateral to the targets chosen by MRI. Mapping by microrecording revealed differences of 2.3 +/- 1.55 mm and 3 +/- 1.9 mm in the mediolateral and anteroposterior coordinates, respectively. The actual lesion overlapped the theoretical target for only 45% of the patients. The somatotopic organization of the GPi was analyzed. Most of the units with sensorimotor activity or tremor-related activity were in the lateral portion of the nucleus. Upper limb and axial units were in the most lateral region and mainly in the ventral one-third of the nucleus. Lower limb responses were recorded mainly in the dorsal one-third of the nucleus. Tremor-related cells were found throughout the sensorimotor region of the nucleus. CONCLUSION: These results indicate that lesion targeting based on MRI alone is not sufficiently accurate to guarantee placement of the lesion in the sensorimotor region of the GPi.

Adult↗
PubMed1998

Differential effects of unilateral lidocaine infusion into the globus pallidus on consolidation and performance of inhibitory avoidance.

The striatum is involved in memory consolidation; also involved in this process is one of its two major efferent targets, namely, the substantia nigra. It is not clear, however, if the other target, the globus pallidus, participates in storage and/or performance of learned information. To examine this problem, male Wistar rats were trained in an inhibitory avoidance task and tested for retention 24 h afterward. Independent groups were infused, unilaterally, with 2% lidocaine in the pallidus either 2 min after training or 2 min before testing. No disturbances of memory were detected with posttraining infusion, but a significant deficit in retention was observed as a consequence of pretest infusion. Infusion of isotonic saline into the globus pallidus, or of lidocaine before testing into the parietal cortex, after training into the ventral thalamic nucleus, and both before training and testing into this thalamic nucleus were without effect. Taken together, the data indicate that unilateral inactivation of the GP interferes with retrieval of information derived from inhibitory avoidance training, but not with the early stages of memory consolidation of this task, and other work indicates that the pallidus may be involved in a late phase of this process.

Anesthetics, Local↗
PubMed1993

Adenosine A2a receptor modulation of electrically evoked endogenous GABA release from slices of rat globus pallidus.

Adenosine A2a receptors have been localized to GABAergic striatopallidal neurons, but their functional role is unknown. To address this question, the modulation of endogenous GABA release by adenosine A2a receptors was examined in slices of rat globus pallidus. The selective adenosine A2a receptor agonist CGS-21680 (3.0-10 nM) significantly increased electrically stimulated release (overflow) of GABA, with 10 nM CGS-21680 resulting in a 44% increase compared with the control. Both the nonselective adenosine receptor antagonist 8-phenyltheophylline (10 microM) and the selective A2a receptor antagonist KF-17837 (100 nM) abolished the CGS-21680-induced increase in GABA overflow. Higher concentrations of CGS-21680 (0.10-1.0 microM) decreased GABA overflow by approximately 25%. 8-Phenyltheophylline (10 microM) antagonized these effects, whereas KF-17837 (100 nM) did not, suggesting actions of CGS-21680 on other adenosine receptors at these concentrations. These results demonstrate that activation of adenosine A2a receptors augments electrically stimulated release of GABA from globus pallidus slices and suggest a mechanism by which adenosine may modulate GABAergic output from the striatopallidal efferent system.

Adenosine↗
PubMed1993

delta 9-Tetrahydrocannabinol and anandamide enhance the ability of muscimol to induce catalepsy in the globus pallidus of rats.

Doses of 3 or 30 micrograms of delta 9-tetrahydrocannabinol markedly increased the ability of 25 ng of muscimol to delay the descent of rats from a horizontal bar (descent latency) when these drugs were coadministered bilaterally into the globus pallidus. Intrapallidal injections of 30 micrograms of the putative endogenous cannabinoid, anandamide, also increased the effect of muscimol on descent latency. These data indicate that the production of catalepsy by cannabinoids may depend at least in part on an ability to enhance GABAergic transmission in the globus pallidus and support the hypothesis that anandamide is indeed an endogenous ligand for the cannabinoid receptor.

Amides↗
PubMed2005

Effect of intrastriatal 6-OHDA lesion on dopaminergic innervation of the rat cortex and globus pallidus.

The present study examined in the rat the effect of a partial lesion of the nigrostriatal dopaminergic pathway induced by intrastriatal injection of 6-hydroxydopamine (6-OHDA), on the dopaminergic innervation of the cortex and the globus pallidus as revealed using tyrosine hydroxylase (TH) immunoreactivity. Twenty-eight days after unilateral injection of 6-OHDA into the dorsal part of the striatum, TH-positive fiber density was reduced by 41% in the dorsal and central part of the structure, and was accompanied by a retrograde loss of 33% of TH-positive neurons in the substantia nigra (SN), while the ventral tegmental area was completely spared. In the SN, TH-positive cell loss was most severe in the ventral part of the structure (-55%). In the same animals, a substantial loss of TH-positive fibers was evident in the dorsal part of the globus pallidus, and involved both thick fibers of passage and thin varicose terminal axonal branches. In the cortex, a loss of TH-positive fibers was prominent in the cingulate area, moderate in the motor area and less affected in the insular area, while the noradrenergic innervation revealed using dopamine-beta-hydroxylase immunoreactivity was preserved in all of these cortical subregions. These results demonstrate that the intrastriatal 6-OHDA lesion model in rats produces a significant loss of dopaminergic axons in extrastriatal structures including the pallidum and cortex, which may contribute to functional sequelae in this animal model of Parkinson's disease.

Adrenergic Agents↗
PubMed1981

Neuronal responses of the globus pallidus to systemic administration of d-amphetamine: investigation of the involvement of dopamine, norepinephrine, and serotonin.

Systemic administration of d-amphetamine (d-AMP) caused significant increases in the unit activity of spontaneously firing neurons in the rat globus pallidus. Intravenous injection of 0.2 mg/kg of d-AMP produced an average increase of 32% while a cumulative dose of 6.4 mg/kg of d-AMP increased cell firing 81% above base line control. The excitatory effects of d-AMP on pallidal cells were effectively blocked and reversed by haloperidol. Increasing intravenous doses of l-amphetamine (l-AMP), totaling 12.8 mg/kg, caused a slight excitation of pallidal neurons. The average maximum increase was 18.3%. Minor rate-elevating effects were also observed after systemic administration of desmethylimipramine and clonidine. The serotonin uptake inhibitor, fluoxetine, produced varied changes in firing frequencies. Pretreatment with reserpine and alpha-methyl-p-tyrosine significantly attenuated the d-AMP-induced increase in pallidal activity. These results suggest that dopamine plays a prominent role in mediating the stimulatory effects of d-AMP on the firing rates of a population of globus pallidus cells in gallamine-paralyzed rats.

Animals↗
PubMed1979

Effects of interruption of the nigrostriatal pathway and of dopaminergic agents on the spontaneous activity of globus pallidus neurons in the awake monkey.

Interruption of the nigrostriatal pathway has been shown to change parameters of striatal activity. These changes are often difficult to explain because the functional structure of the striatum is not understood sufficiently. The function of the globus pallidus appears to be simpler. It transmits the output of the striatum to the thalamus and to the midbrain. Yet the effects of interruption of the nigrostriatal pathway on the activity of pallidal neurons are unknown. To study these effects the spontaneous activity of globus pallidus neurons was recorded in intact monkeys and in monkeys with lesions of the ventromedial midbrain tegmentum. The two groups of animals were studied with and without administration of dopaminergic agents. In intact monkeys medial pallidal neurons discharge uninterruptedly at high firing rates, while the discharge of most lateral pallidal neurons is interrupted by relatively long periods of silence. Lesions involving the nigrostriatal pathway change the firing patterns but not the mean firing rates of pallidal neurons. In lesioned monkeys pallidal neurons fire in bursts continuously: during movement, rest and sleepiness. Two lines of evidence strongly suggest that the bursting pallidal activities are a consequence of the interruption of the nigrostriatal dopaminergic pathway: (1) the percentage of bursting pallidal neurons is proportional to the amount of degeneration in the pars compacta of the ipsilateral substantia nigra; (2) chronic administration of dopamine antagonists, haloperidol and reserpine, reproduces in intact monkeys the bursting activities observed in lesioned animals. On the other hand, single injections of dopamine agonists, apomorphine and piribedil, silence the medial pallidum and concomittantly abolish the signs of parkinsonism displayed by lesioned monkeys.

Animals↗
PubMed2004

Modafinil prevents the MPTP-induced increase in GABAA receptor binding in the internal globus pallidus of MPTP-treated common marmosets.

The psychostimulant drug modafinil induces a reversal of motor deficits in MPTP treated primates and prevents MPTP toxicity to substantia nigra but its mechanism of action is not clear. In common marmosets acutely treated with MPTP in the presence or absence of modafinil, we have studied changes in GABA(A) receptor binding in the basal ganglia. MPTP treatment had no effect on [(3)H]-flunitrazepam (FNZ) binding density in the striatum or external globus pallidus (GPe) but increased [(3)H]-FNZ binding density in the internal globus pallidus (GPi). Administration of modafinil (10-100 mg/kg) with MPTP did not alter [(3)H]-FNZ binding density in the striatum or GPe. Low doses of modafinil (10 and 30 mg/kg) had no effect on the increased [(3)H]-FNZ binding density in the GPi but high dose modafinil (100 mg/kg) significantly decreased [(3)H]-FNZ binding density in GPi. These findings suggest that modafinil can selectively alter GABA binding density in the GPi either by preventing MPTP-induced toxicity or through an action on striatal output pathway related to its antiparkinsonian activity and its ability to inhibit MPTP toxicity.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1989

Neurons of the substantia nigra reticulata receive a dense GABA-containing input from the globus pallidus in the rat.

The lectin Phaseolus vulgaris leucoagglutinin (PHA-L) was used as an anterograde tracer to study the topographical distribution and synaptic organization of pallidonigral fibres in the rat. Injections of PHA-L in the lateral part of the globus pallidus led to anterograde labelling of a rich plexus of varicose fibres that arborized profusely in the central core of the rostral three quarters of the substantia nigra pars reticulata (SNr). However, few fibres were detected in SNr after PHA-L injection restricted to the most medial part of the globus pallidus. A small number of fibres was seen in the substantia nigra pars compacta after each injection. The most characteristic feature of the pallidonigral terminals was the formation of baskets around the perikarya and primary dendrites of SNr cells. Electron microscopic analysis revealed that the pallidonigral terminals contain pleomorphic vesicles and a large number of mitochondria and that they form symmetrical synaptic contacts. Furthermore, postembedding immunocytochemistry for gamma-aminobutyric acid (GABA) showed that they display GABA immunoreactivity. These findings demonstrate that, in the rat, the pallidonigral projection is a major source of GABA-containing terminals innervating pars reticulata cells and that the pattern of innervation is such that they may exert a powerful inhibitory control over these cells.

Animals↗
PubMed1997

High-frequency stimulation of the globus pallidus for the treatment of Parkinson's disease.

Long-term treatment of Parkinson's disease (PD) with levodopa is complicated by the development of motor fluctuations and dyskinesias. Posteroventral pallidotomy can improve tremor, bradykinesia, rigidity, and dyskinesias in PD. We performed chronic stimulation of the globus pallidus (CSGP) to duplicate the positive results of pallidotomy with reduced risk of permanent neurologic deficit in patients with advanced PD. The lead for CSGP was stereotactically implanted with the aid of microelectrode recordings in the globus pallidus pars interna. An electrical pulse generator was implanted in the subclavicular region. Stimulation settings were adjusted by computer. Five PD patients (four men, one woman) with disabling symptoms were enrolled. Three of the patients had bilateral implants. At 3 months following the last implant, four patients rated themselves as markedly improved, and one patient was moderately improved. The amount of time in the "on" state increased from 21% at baseline to 65% at 3-month follow-up (p < 0.05). There was a significant improvement in all subscales of the UPDRS (p < 0.05). One patient had an asymptomatic intracranial bleed, one patient had transient hemiparesis during surgery with stimulation, and one patient required surgical repositioning of the lead. Adverse effects caused by stimulation were minimal. CSGP is a safe and effective procedure in PD patients with motor fluctuations and dyskinesias.

Aged↗
PubMed2001

Intrapallidal D2 dopamine receptors control globus pallidus neuron activity in the rat.

Because activation of D2 dopamine receptors inhibits gamma-aminobutyric acid (GABA) release from intrapallidal nerve terminals, we measured the effects of modifiers of dopamine D2 receptors on the firing rate of single neurons in the globus pallidus (GP) of the anesthetized rat. The predominant effect of intrapallidal administration of the selective D2 agonist quinpirole was an increase in the rate of spontaneous firing while the D2 blocker sulpiride caused a decrease. The spontaneous firing of GP neurons is inhibited by stimulation of the GABAergic striatopallidal projection. We therefore measured the effects of modifiers of D2 receptors on striatal inhibition of GP neurons and found that intrapallidal quinpirole blocked the inhibitory effects of striatal stimulation while sulpiride enhanced them. These experiments show that both the spontaneous rate of firing of pallidal neurons and its modification by striatopallidal inputs is controlled by intrapallidal dopamine D2 receptors. In addition, taken together with other findings in the literature, our results suggest that activation of dopamine D2 receptors within the globus pallidus leads to inhibition of GABA release from presynaptic terminals.

Action Potentials↗
PubMed2003

Deficits induced by quinolinic acid lesion to the striatum in a position discrimination and reversal task are ameliorated by permanent and temporary lesion to the globus pallidus: a potential novel treatment in a rat model of Huntington's disease.

Symptoms in the early stages of Huntington's disease (HD) are assumed to reflect basal ganglia circuit dysfunction secondary to degeneration of striatal projections to the external segment of the globus pallidus (GPe). The hypothesis that GPe lesion would ameliorate HD symptoms by "normalizing" the circuit's functioning was tested in a rat model of this disease. The performance of rats sustaining quinolinic acid lesion to the striatum (a rat model of HD) in a position discrimination and reversal task was compared with the performance of rats sustaining in addition a bilateral excitotoxic lesion to the globus pallidus (GP) carried out simultaneously with the striatal lesion (Experiment 1) or 1 month after the striatal lesion (Experiment 2), as well as a unilateral temporary lesion of the GP (Experiment 3). The striatal lesion-induced deficit in the task was effectively reversed by a bilateral excitotoxic GP lesion carried out simultaneously or 1 month after the striatal lesion, as well as by a temporary unilateral GP inactivation. Given that a similar dysfunction of basal ganglia circuitry is thought to subserve the behavioral alterations seen in quinolinic acid lesioned rats and some of the symptoms in HD, these results raise the possibility that lesion or inactivation of the GPe may alleviate some of HD symptoms.

Animals↗
PubMed1991

The K(+)-evoked release of [3H]acetylcholine from slices of rat globus pallidus: modulation by delta-opioid receptors.

Previous investigations have shown that the activation of delta-opioid receptors depresses the release of acetylcholine (ACh) in the rat caudate putamen. This finding raised the possibility that the release of ACh is similarly modulated in the globus pallidus, a region containing a distinct population of cholinergic neurons and enriched in enkephalinergic nerve terminals. In the present study the pallidal release of ACh was characterized and the effects of delta-opioid receptor activation on this release were examined. The results show that this release is stimulated by high K+ in a concentration- and Ca(2+)-dependent manner. D-Pen2,L-Pen5-enkephalin (0.1-10 microM), a selective delta-opioid receptor agonist, produced a dose-related inhibition of the 25 mM K(+)-evoked tritium release. The maximal inhibitory effect, representing a 34% decrease in the K(+)-induced tritium release, was observed at a concentration of 1 microM. This opioid effect was attenuated by the selective delta-opioid receptor antagonist, ICI 174864 (1 microM). These findings support the role of a delta-opioid receptor in the modulation of ACh release in the rat globus pallidus.

Acetylcholine↗
PubMed1979

The spontaneous firing patterns of forebrain neurons. IV. Effects of bilateral and unilateral frontal cortical ablations on firing of caudate, globus pallidus and thalamic neurons.

To assess the effects of partial deafferentation of the neostriatum on spontaneous neuronal activity in the basal ganglia and related thalamic nuclei, ablations of frontal cortex were carried out in adult cats. Postoperative measures of interspike intervals of single neurons in the caudate nucleus, globus pallidus and ventral anterior-ventral lateral complex of the thalamus revealed a slowing of neuronal firing in these structures as compared with non-lesioned controls. The fact that deafferentation by cortical damage produces changes in neuronal firing in target neurons of the striatum (globus pallidus) and in thalamic neurons at least two synapses removed from the striatum is noteworthy. The possible extent to which these results might have been influenced by reduction of cortical inputs to or denervation of the thalamus is discussed.

Afferent Pathways↗
PubMed1995

Mineralization of the globus pallidus following excitotoxic lesions of the basal forebrain.

The excitotoxin N-methyl aspartic acid was injected into the rat nucleus basalis to destroy basal forebrain cholinergic (BFC) neurons. In long-term survival experiments (up to 11 months post-lesion), conspicuous mineralized deposits were found in the globus pallidus and to a lesser extent in the thalamus. Deposits stained in a manner consistent with a composition of calcium and iron. Typically, deposits were absent from the center of the injection site, where BFC cell loss was most severe, but were present within the ventral and lateral globus pallidus where there was substantial sparing of BFC neurons. The similarity of this pathology to basal ganglia calcification and its relationship to Alzheimer's Disease and Down's syndrome is discussed.

Alzheimer Disease↗