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GABAA receptor-mediated K(+)-evoked GABA release from globus pallidus--analysis using microdialysis.

Presynaptic modulation of gamma-aminobutyric acid (GABA) release in the globus pallidus of rat was examined using in vivo microdialysis procedures. The addition of nipecotic acid (0.5 mM), a neuronal GABA uptake inhibitor, into perfusate, resulted in an increase in the basal GABA released from the globus pallidus. GABA release from the globus pallidus was also augmented dose-dependently by the addition of KCI. Muscimol, a GABAA receptor agonist, caused a significant suppression of the high potassium (100 mM)-evoked release of GABA, and this suppressive effect of muscimol was antagonized invariably by bicuculline, a GABAA receptor antagonist. On the other hand, baclofen, a GABAB receptor agonist, did not induce any significant changes in the 100 mM KCl-evoked GABA release. Similarly, 3-aminopropylphosphonous acid, a GABAB receptor agonist, failed to suppress the GABA release induced by high (100 mM) and low (50 mM) concentrations of KCl from the globus pallidus. Furthermore, CGP 54626A,-a GABAB receptor antagonist, had no significant effect on these KCl-evoked GABA releases. These results suggest that presynaptic modulation of GABA release in the globus pallidus may be mediated by the GABAA autoreceptor.

Animals↗

[Morphometrical-statistical structure analysis of human striatum, pallidus and subthalamic nucleus. II. Globus pallidus].

1. The pallidum of 13 hemispheres of 11 human brains of normal adults was studied by morphometric-statistical methods. 2. The values obtained on paraffin-embedded frontal serial sections were corrected individually for shrinkage in order to get comparable fresh values. 3. The mean fresh volume of the pallidum laterale of males (1220 mm3) was 13% higher than that of females (1065 mm3). The corresponding mean values of the pallidum mediale were 520 mm3 (male) and 430 mm3 (female), the difference being 17%. The difference between sexes failed to be significant. The lateral segment accounted for about 70% of the total volume of the pallidum. 4. The pallidum occupied 0,32% or ca. 1 over 300 of the volume of the hemisphere. 5. The numeric cell densities showed no significant age or sex differences. The mean value of the lateral pallidum was 437 nerve cells/mm3 and of the medial part 327 nerve cells/mm3, the difference being highly significant (p less than 0,001). 6. The pallidum laterale showed a numerical density of 66000 glial cells/mm3, the medial segment had 62000 glial cells/mm3, the difference just reaching the 5% -- level of significance. 7. On the average the ratio of glial cells to nerve cells was 158:1 in the lateral pallidum, and 159:1 in the medial part. The difference was statistically significant (p less than 0,01). 8. The mean of the total number of nerve cells in the pallidum laterale amounted to 540000 for males and 465000 for females. The corresponding values of the medial part were 171000 (male) and 143000 (female). The total number of pallidal nerve cells is just about as high as the number of large striatal nerve cells (670000 (male) and 570000 (female). 9. In the pallidum laterale we calculated the total number of glial cells to be 82 million for males and 63 million for females. In the medial pallidum we found 32 million (male) and 26 million (female). 10. The total numbers of nerve and glial cells were well correlated in the lateral as well as in the medial segment (r = 0,636 and r = 0,734, respectively). 11. The volumetric nerve cell densities showed no significant differences between sexes. The values were 0,36 Vol.-% lateral and 0,31 Vol.-% medial. This difference failed to be significant. 12. The volumetric densities of the glial cell nuclei were equal in both segments, the value being 0,43 Vol.-%. They were strictly correlated (r = 0,830). 13. The mean volume of a nerve cell in the medial segment (9600 mum3) was 19% higher (p less than 0,05) than in the lateral segment (8100 mum). 14. The mean volume of a nucleus of a glial cell showed only insignificant differences, being lateral 65 mum3 and medial 70 mum3. 15. The various morphometric data indicated a closer correlation between striatum and pallidum laterale than between striatum and pallidum mediale. Within the striatum, the putamen showed a better correlation with the pallidum than the nucleus caudatus.

Cell Count↗

The effects of globus pallidus lesions on dopamine-dependent motor behaviour in rats.

Motor effects of bilateral lesions of the globus pallidus induced by quinolinic acid (30 and 60 nmol in 0.5 microl) were investigated in rats. Globus pallidus lesions with 60 nmol quinolinic acid produced a significant reduction of spontaneous motor activity measured by a reduced locomotor activity in an open field and by a reduced sniffing activity in an experimental chamber. In addition, D-amphetamine (1 mg/kg, i.p.)-induced hyperlocomotion and D-amphetamine (3 mg/kg, i.p.)-induced stereotyped sniffing were significantly reduced in animals with quinolinic acid lesions (60 nmol). Globus pallidus lesions with 60 nmol quinolinic acid potently reversed catalepsy induced by systemic administration of the dopamine D1 receptor antagonist SCH23390 (0.75 and 1 mg/kg, i.p.) or the dopamine D2 receptor antagonist raclopride (1.25 and 5 mg/kg, i.p.), while lesions with 30 nmol quinolinic acid exerted anti-cataleptic effects which were only partly significant. In line with current models of basal ganglia functions, these findings indicate that inactivation of the globus pallidus reduced spontaneous motor activity and motor hyperactivity after dopamine receptor stimulation. However, the present data also demonstrate that inactivation of the globus pallidus reversed motor hypoactivity induced by a blockade of dopamine D1 and D2 receptors. Therefore, a more complex functional model of the globus pallidus is required to account for the opposite effects on motor behaviour observed after lesions of this basal ganglia nucleus.

Animals↗

Neuronal globus pallidus activity in patients with generalised dystonia.

We studied 516 globus pallidus neurons in dystonic patients. The firing rate was analysed. We classified the burst activity into tonic, burst, and pause patterns. Mean +/- SD firing rates and tonicity score for internal globus pallidus (GPi) and external globus pallidus (GPe) were 54.6 +/- 28.6; 58.01 +/- 39.1 and 1.18 +/- 0.55; 0.95 +/- 0.43, respectively. Differences in percentage appearance of tonic, burst, or paused neurons were not statistically significant for GPi versus GPe. GPi firing features in dystonic patients were closely similar to those of GPe. This could suggest that the abnormally patterned output from GPi would not result from increased differential inhibitory/excitatory input arising from the direct/indirect pathway but rather be transmitted from GPe, striatum, or either centromedian nucleus.

Adolescent↗

Changes in globus pallidus with (pre)term kernicterus.

OBJECTIVE: We report serial magnetic resonance (MR) and sonographic behavior of globus pallidus in 5 preterm and 3 term infants with kernicterus and describe the clinical context in very low birth weight preterm infants. On the basis of this information, we suggest means of diagnosis and prevention. METHODS: Charts and MR and ultrasound images of 5 preterm infants and 3 term infants with suspected bilirubin-associated brain damage were reviewed. Included were preterm infants with severe hearing loss, quadriplegic hypertonia, and abnormal hypersignal of globus pallidus on T2-weighted MR imaging (MRI). In 1 infant who died on day 150, the diagnosis was confirmed during the neonatal period. The others were picked up as outpatients and scanned at 12 or 22 months' corrected age. Three instances of term kernicterus were included for comparison of serial MRI in the neonatal period and early infancy: they were caused by glucose-6-phosphate dehydrogenase deficiency, urosepsis, and dehydration plus fructose 1-6 biphosphatase deficiency. RESULTS: Five preterm infants of 25 to 29 weeks' gestational age presented with total serum bilirubin (TSB) levels below exchange transfusion thresholds commonly advised. Mixed acidosis was present in 3 infants around the TSB peak. The bilirubin/albumin molar ratio was >0.5 in all, in the absence of displacing drugs. All failed to pass bedside hearing screen tests and had severe hearing loss on auditory brain response testing. Symmetrical homogeneous hyperechogenicity of globus pallidus was the alerting feature in 1 infant. Globus pallidus was hyperintense on T1-weighted MR images in this child. The other infants presented with severe developmental delay as a result of dyskinetic quadriplegia and hearing loss. Globus pallidus was normal on T1- but hyperintense on T2-weighted MR images at 12 or 22 months' corrected age. Subthalamic involvement was documented in coronal fluid attenuated inversion recovery MRI in 2 infants. The term infants with classical clinical presentation in the neonatal period had MR behavior similar to the preterms, but pallidal injury was not recognized with targeted sonographic examination. Their neonatal MR images demonstrated pallidal T1 hyperintensity and mild T2 hyperintensity. CONCLUSION: Acidotic very low birth weight preterm infants with low serum albumin levels develop MR-confirmed pallidal injury and hearing loss facing "accepted" TSB levels. Serial MRI documents a shift from acute mainly T1 hypersignal to permanent T2 hypersignal in globus pallidus within the late neonatal period. Subthalamic and not thalamic involvement helps to differentiate from ischemic or metabolic disorder. As newborns, these infants are rigid and have severe apnea, before developing hypertonic quadriplegia in infancy.

Echoencephalography↗

Alteration of neuronal responses in the subthalamic nucleus following globus pallidus and neostriatal lesions in rats.

Kainic acid (2-4 days) or ibotenic acid (7-9 days) lesions of the globus pallidus or neostriatum altered the responsiveness of subthalamic nucleus neurons to electrical stimulation of the agranular frontal cortex. Three changes in responsiveness were seen following pallidal lesion: a) An increase in the proportion of responding cells as compared to controls (approximately 90% vs. 60%); b) an increase in the total duration of the evoked response (62.5 ms vs. 28.6 ms); 3) an increase in magnitude of response (9.76 spikes per stimulus vs. 3.24). Both an increase in firing rate (17.94 spikes/s vs. 8.23) and a change to a bursty spontaneous firing pattern were seen. Lesion of the neostriatum had fewer but opposite effects including decreased firing rate (7.21 spikes/s) and decreased total response duration (18.9 ms). These results suggest that the normal tonic inhibition of the subthalamic nucleus by the globus pallidus may play an important role in controlling subthalamic neuronal spontaneous activity and responsiveness. The neostriatum may influence the subthalamic nucleus via the globus pallidus. Globus pallidus lesions may have important consequences on the specificity of cortical control of the subthalamic nucleus and may alter subthalamic influence on basal ganglia output.

Animals↗

Lesions of the globus pallidus, entopeduncular nucleus and substantia nigra alter dopamine mediated circling behaviour.

Unilateral kainic acid lesions of the globus pallidus in the rat caused weak spontaneous circling at 3 and 10 days after surgery. Unilateral kainic acid lesions of the entopeduncular nucleus caused no spontaneous circling at any time after surgery. Systemic administration of apomorphine to such lesioned animals caused ipsiversive circling in both groups. Pallidal lesions in animals with a prior ipsilateral 6-OHDA lesion of the medial forebrain bundle attenuated apomorphine-induced, but not amphetamine-induced, circling. Entopeduncular nucleus lesions in the 6-OHDA lesioned animal attenuated both apomorphine- and (+)-amphetamine-induced circling. Kainic acid lesions of the globus pallidus or entopeduncular nucleus did not alter nigral glutamic acid decarboxylase (GAD) activity. Unilateral electrolytic lesions of the globus pallidus or entopeduncular nucleus caused ipsiversive circling in response to apomorphine. An electrolytic lesion of the globus pallidus in animals with a prior 6-OHDA lesion did not alter (+)-amphetamine-induced circling but reversed the direction of apomorphine-induced circling. Electrolytic lesions of the entopeduncular nucleus enhanced (+)-amphetamine-induced circling and attenuated apomorphine-induced circling. Nigral GAD activity was reduced by electrolytic lesions of the globus pallidus but not by those of the entopeduncular nucleus. Large kainic acid lesions in the area of the substantia nigra caused weak spontaneous contraversive circling 3 days after surgery, and ipsiversive circling in response to the systemic administration of apomorphine. Similar lesions in animals with a prior ipsilateral 6-OHDA lesion of the medial forebrain bundle initially attenuated the response to (+)-amphetamine, but the response returned with time. The direction of apomorphine-induced circling was reversed in these animals. The strio-nigral pathway and nigral efferents are confirmed to be involved in circling induced by dopamine agonists in rats with a unilateral lesion of the medial forebrain bundle. Both the globus pallidus and the entopeduncular nucleus also appear to be involved in this dopamine-mediated circling behaviour.

Animals↗

Subcellular localization of GABAB receptor subunits in rat globus pallidus.

The inhibitory amino acid gamma-aminobutyric acid (GABA) is the major neurotransmitter in the globus pallidus. Although electrophysiological studies have indicated that functional GABA(B) receptors exist in rat globus pallidus, the subcellular localization of GABA(B) receptor subunits and their spatial relationship to glutamatergic and GABAergic synapses are unknown. Here, we use pre-embedding immunogold labeling to study the subcellular localization of GABA(B) receptor subunits, GABA(B1) and GABA(B2), in globus pallidus neurons and identified populations of afferent terminals. Immunolabeling for GABA(B1) and GABA(B2) was observed throughout the globus pallidus, with GABA(B1) more strongly expressed in perikarya and GABA(B2) mainly expressed in the neuropil. Electron microscopic analysis revealed that the majority of GABA(B1) labeling was localized within the cytoplasm, whereas most of GABA(B2) labeling was associated with the plasma membrane. At the subcellular level, both the GABA(B1) and GABA(B2) immunogold labeling was localized at pre- and postsynaptic sites. At asymmetric, putative excitatory, synapses, GABA(B1) and GABA(B2) immunogold labeling was found at perisynaptic sites of both pre- and postsynaptic specializations. Double immunolabeling, using the vesicular glutamate transporter 2 (VGLUT2), revealed the glutamatergic nature of most immunogold-labeled asymmetric synapses. At symmetric, putative GABAergic, synapses, including those formed by anterogradely labeled striatopallidal terminals, GABA(B1) and GABA(B2) immunogold labeling was found in the main body of both pre- and postsynaptic specializations. These results demonstrate the existence of presynaptic GABA(B) auto- and heteroreceptors and postsynaptic GABA(B) receptors, which may be involved in modulating synaptic transmission in the globus pallidus.

Animals↗

Electrophysiological, behavioral and metabolical features of globus pallidus seizures induced by a microinjection of kainic acid in rats.

There has been few studies of the globus pallidus in relation to epilepsy. In this study, kainic acid (KA)-induced globus pallidus seizure was electrophysiologically, electroencephalographically, histopathologically and metabolically investigated in rats. Sixteen Wistar rats weighing 250-350 g were used. Under intraperitoneal pentobarbital anesthesia, a stainless-steel cannula was inserted stereotaxically into the left globus pallidus pars externa (GPe) for KA injection. For recording EEG, a depth electrode was inserted into the left GPe, just posterior to the tip of the injection guide cannula. Electrodes were also inserted into the right globus pallidus and bilateral sensorimotor cortex (SMC). EEG changes after KA injection were classified as follows: Continuous low-voltage spikes were observed in the left GPe on EEG at stage 1. Intermittent multiple spikes and wave complexes began to propagate to the left SMC at stage 2. Continuous spikes and wave complexes began to propagate to the bilateral SMC at stage 3. Secondary generalized seizures were observed at stage 4. Globus pallidus seizures recurred every 7-9 min and lasted for 4-6 h. However, the seizures gradually subsided and became normal within 18 h. No spontaneous seizure was detected for the next 30 days. Histopathological study revealed a small gliotic lesion with neuronal cell loss around the cannula tip. Neither degeneration nor neuronal cell loss in the ipsilateral hippocampus were observed. The autoradiogram using [14C]2-deoxyglucose during seizure status demonstrated a remarkable increase of local cerebral glucose utilization not only in the GPe but also in the GPi. An increase glucose metabolism was also found in the follows: the medial and lateral septal nucleus, substantia nigra, hippocampus, frontal cortex, parietal cortex, piriform cortex, entorhinal cortex, accumbens nucleus, ventral and lateral nucleus of the thalamus, amygdala, and ventral nucleus of hypothalamus. KA injection into the unilateral GPe evoked not only epileptic excitation of the cortex but also transient enhancement of the globus pallidus-substantia nigra circuit.

Action Potentials↗

Dopaminergic innervation of the rat globus pallidus characterized by microdialysis and immunohistochemistry.

The present study examined the dopaminergic innervation of the rat globus pallidus by in vivo microdialysis and immunohistochemistry in more detail. Using tyrosine hydroxylase immunohistochemistry, two classes of dopaminergic fibers were distinguished morphologically in the globus pallidus. Unilateral infusion of 6-hydroxydopamine into the substantia nigra produced a loss of dopaminergic fiber density in the globus pallidus which was correlated with the nigral extent of the lesion. These findings are in line with the notion that a degenerative loss of nigral dopaminergic cell bodies might also affect the dopamine input of extrastriatal structures such as the globus pallidus. Using in vivo microdialysis, we tested whether dopamine measured in the globus pallidus is of neuronal origin. Perfusion of tetrodotoxin induced a strong and transient decrease of pallidal dopamine. The tetrodotoxin-sensitivity of pallidal dopamine demonstrates the functional significance of the nigropallidal dopaminergic innervation.

Animals↗

Search for PET probes for imaging the globus pallidus studied with rat brain ex vivo autoradiography.

We have evaluated the feasibility of using four positron emission tomography (PET) tracers for imaging the globus pallidus by ex vivo autoradiography in rats. The tracers investigated were [11C]KF18446, [11C]SCH 23390 and [11C]raclopride for mapping adenosine A2A, dopamine D1 and dopamine D2 receptors, respectively, and [18F]FDG. The highest uptake by the globus pallidus was found for [11C]SCH 23390, followed by [18F]FDG, [11C]KF18446 and [11C]raclopride. The receptor-specific uptake by the globus pallidus was observed in [11C]KF18446 and [11C]SCH 23390, but not in [11C]raclopride. Uptake ratios of globus pallidus to the striatum for [18F]FDG and [11C]KF18446 were approximately 0.6, which was twice as large as that for [11C]SCH 23390. In a rat model of degeneration of striatopallidal gamma-aminobutyric acid-ergic-enkephalin neurons induced by intrastriatal injection of quinolinic acid, the uptake of [11C]KF18446 by the striatum and globus pallidus was remarkably reduced. To prove the visualization of the globus pallidus by PET with [18F]FDG and [11C]KF18446, PET-MRI registration technique and advances in PET technologies providing high-resolution PET scanner will be required. The metabolic activity of the globus pallidus could then be measured by PET with [18F]FDG, and [11C]KF18446 may be a candidate tracer for imaging the pallidal terminals projecting from the striatum.

Animals↗

[Thalamic and cortical connections of the globus pallidus in the cat].

Two series of experiments have been performed on cats: the first -- with destruction of various parts in the globus pallidus, the second -- with destruction of the telencephalic cortex. The experimental material has been treated by Nauta -- Gygax's, Fink -- Heimer's, Kawamura -- Niimi's methods. Localization of the destructed focus has been proved in the preparations stained after Nissl. As demonstrated the results of the investigation, together with the medial, the lateral segment of the globus pallidus has some pallido-thalamic fibres. Both segments of the globus pallidus have direct connections with the telencephalic cortex. According to the degree of how these connections are expressed, the motor cortex occupies the first place, the sensory cortex -- the second and the temporal area cortex -- the third place. There is a definite distribution (topics) of the globus pallidus connections with the thalamus, the subthalamic nucleus and the telencephalic cortex. There is a definite correspondence of the cortico-pallidal and pallido-cortical pathways consisting in the fact that the senso-motor cortical area has the greatest number of direct connections with the globus pallidus. That the globus pallidus possesses complex connections with the thalamic structures and with the telencephalic cortex speaks in favour of its important role in the cerebral integrative activity.

Animals↗

Distribution of catecholaminergic afferent fibres in the rat globus pallidus and their relations with cholinergic neurons.

The topographical distribution of catecholaminergic nerve fibres and their anatomical relationship to cholinergic elements in the rat globus pallidus were studied. Peroxidase-antiperoxidase and two-colour immunoperoxidase staining procedures were used to demonstrate tyrosine hydroxylase (TH), dopamine beta-hydroxylase (DBH), phenylethanolamine N-methyltransferase (PNMT) and choline acetyltransferase (ChAT) immunoreactivities, combined with acetylcholinesterase (AChE) pharmacohistochemistry. TH immunoreactive nerve fibres were seen to enter the globus pallidus from the medial forebrain bundle. The greatest density of such fibres was found in the ventral region of the globus pallidus, which was also characterized by the greatest density of ChAT immunoreactive neurons. TH immunoreactive nerve fibres showed varicose arborizations and sparse boutons, which were occasionally seen in close opposition to cholinergic structures. In all regions of the globus pallidus, there were also larger, smooth TH immunoreactive nerve fibres of passage to the caudate putamen. A smaller number of DBH immunoreactive nerve fibres and terminal arborizations were found in the substantia innominata, internal capsule and in the globus pallidus bordering these structures. A few PNMT immunoreactive nerve fibres in the substantia innominata and internal capsule did not enter the globus pallidus. Electron microscopy revealed TH immunoreactive synaptic profiles in the ventromedial area of the globus pallidus corresponding to the nucleus basalis magnocellularis of Meynert (nBM). These made mainly symmetrical and only a few asymmetrical synaptic contacts with dendrites containing AChE reaction product. The results indicate that cholinergic structures in the nBM are innervated by dopaminergic fibres and terminals, with only a very small input from noradrenergic fibres.

Acetylcholinesterase↗

Alterations in local cerebral glucose utilization during electrical stimulation of the striatum and globus pallidus in rats.

Alterations in local cerebral glucose utilization (LCGU) in conscious rats during electrical stimulation of the striatum and the globus pallidus were investigated using the [14C]deoxyglucose method. Stimulation of the globus pallidus produced a marked contraversive circling behavior, while stimulation of the striatum led only to contraversive head turning. Unilateral stimulation of the striatum increased LCGU bilaterally in the globus pallidus and substantia nigra pars compacta, but only ipsilaterally in the entopeduncular nucleus, substantia nigra pars reticulata and subthalamic nucleus. Similar stimulation of the globus pallidus increased LGCU in the globus pallidus, substantia nigra pars reticulata and compacta, entopeduncular nucleus, subthalamic nucleus, lateral habenular nucleus, parafascicular nucleus of the thalamus, deep layers of the superior colliculus and pedunculopontine nucleus, exclusively on the ipsilateral side. These results indicate that the electrical stimulation induces LCGU changes in the respective structures having both monosynaptic and transsynaptic neuronal inputs. Some changes may also be mediated by antidromic activation. They also suggest that activation of a synaptic process whether excitatory or inhibitory results in increases in LCGU. The bilateral modulatory effects of striatal stimulation may cancel out the circling behavior seen during pallidal stimulation, and cause only head turning.

Animals↗

Death of neurons in the neonatal rodent and primate globus pallidus occurs by a mechanism of apoptosis.

We have examined the developing rat, mouse and marmoset globus pallidus for evidence of cells dying by a process of "naturally occurring" or programmed cell death. We have demonstrated that cells in the developing mammalian globus pallidus die by a process of apoptosis and that by day 7 after birth many of the apoptotic cells possess a neuronal phenotype. Light microscopic and ultrastructural evidence of apoptotic cell death included cell shrinkage, blebbing of the extracellular membrane and condensation of the nuclear chromatin. Additionally we used an in situ nick translation method to assess the integrity of the DNA within the dying cells. This revealed that cells with the morphological characteristics of apoptosis also possessed fragmented DNA typical of cells undergoing Type 1 programmed or apoptotic cell death. The lack of lysosomal enzyme activity within the dying cells and the frequent observations of phagocytosis by neighbouring cells also suggest that the form of programmed cell death is apoptosis and not Type 2 autophagic degeneration. We found no evidence for cells dying by Type 3 non-lysosomal degeneration since all dying cells examined under the electron microscope possessed intact intracellular organelles and cell membranes. We developed a sensitive silver stain which detected balls of condensed chromatin within the apoptotic cells. This enabled identification of apoptotic cells in the developing globus pallidus at low magnification and so allowed us to map the numbers and distribution of dying cells with time. The incidence of apoptotic cells in the neonatal globus pallidus was greatest at birth and then declined such that few cells were detected at one week and none was seen in the adult rat. Although the loss of large numbers of cells in the developing nervous system is a well documented phenomenon, there are only a limited number of reports of the mechanism by which neuronal cells die, and few of these are in the developing mammalian brain. There are at least four different morphological categories of neuronal cell death which are discriminated on morphological and biochemical criteria. Our analysis suggests that apoptotic or Type 1 cell death is the major form of programmed cell death occurring in the mammalian globus pallidus in the first week of life. This report also describes the use of two methods for the ready identification of apoptotic cells at the light microscope level. Because these methods are suitable for use on tissue sections they provide a means to assess the incidence of apoptotic cell death, in parallel with other analyses of the expression of gene products which control cell fate.

Acid Phosphatase↗

The globus pallidus and its rostroventral extension into the olfactory tubercle of the rat: a cyto- and chemoarchitectural study.

The globus pallidus is characterized by a high iron content and the distribution of the ferric iron in the rat brain provides evidence that globus pallidus extends rostroventrally below the anterior commissure and into the olfactory tubercle. The extension of the globus pallidus into the olfactory tubercle is consistent with the notion of the ventral striatum,14 in the sense that it provides for an expected close proximity between the striatum and the globus pallidus throughout the dorsoventral extent of the corpus striatum. The distribution of enkephalin, and of acetylcholinesterase- and succinate dehydrogenase-positive neurons is also consistent with an extension of the ventral part of globus pallidus to the base of the forebrain in the rat. Since part of the ventral pallidum corresponds to a region that is usually referred to as the subcommissural part of the substantia innominata, it seems reasonable to restrict the term substantia innominata to the more caudally-located sublenticular part of the substantia innominata.

Acetylcholinesterase↗

Nucleus accumbens to globus pallidus GABA projection: electrophysiological and iontophoretic investigations.

Extracellular recordings were obtained from neurons in the nucleus accumbens and globus pallidus of urethane anesthetized rats. Eight neurons in the nucleus accumbens were activated antidromically following stimulation of the globus pallidus. Calculated conduction velocities were 0.4-1.5 m/sec, indicative of small unmyelinated fibers. A total of 74 of 153 neurons in the globus pallidus responded to stimulation of the nucleus accumbens. Of these neurons 4 (2.7%) were excited only, 46 (30.1%) were inhibited only and 24 (15.7%) had sequential effects to excitation and inhibition. Iontophoretic application of picrotoxin was found to attenuate or abolish the poststimulus inhibition in one-half of the neurons examined. The 74 neurons which responded to stimulation of the nucleus accumbens had slower firing frequencies and generally more random firing patterns than neurons which did not respond to stimulation. Fifty-three per cent of all globus pallidus neurons examined had increased spontaneous firing frequencies following the iontophoretic administration of picrotoxin alone. This is indicative of the removal of a tonic GABA input onto these neurons. Most neurons examined had decreased spontaneous firing frequencies following the iontophoretic application of GABA which could be blocked by the iontophoretic application of picrotoxin. The results from antidromic activation, slow conduction velocity, sensitivity to GABA and picrotoxin, and picrotoxin attenuation of the poststimulus inhibitory effect provide evidence of a direct GABAergic projection from the nucleus accumbens to the globus pallidus in the rat.

Animals↗

[High signal intensity of globus pallidus on T1-weighted MRI in liver cirrhosis patients: clinical and pathological study].

In some patients with liver cirrhosis, the globus pallidus shows high signal intensity on T1-weighted MRI. The relationship was examined between high signal intensity on T1-weighted images and pathological conditions such as liver function, portal venous pressure and metal concentrations in brain. The signal of the globus pallidus on T1-weighted imaging became highly enhanced in accordance with prolongation of prothrombin time, deterioration of ICG R15, or decrease in choline esterase and the Fisher ratio. Furthermore, the high signal intensity was also seen in patients with high portal pressure and large varices. In histopathological study, remarkable atrophy and loss of nerve cells were observed in globus pallidus with high signal intensity on T1-weighted imaging, changes that were similar to those in with patients with manganese poisoning. The manganese concentration in autopsied globus pallidus with high signal intensity on T1-weighted imaging showed a 9.5-fold increase compared with that with normal intensity. In conclusion, the deposition of manganese in the globus pallidus, which is accompanied with the nerve cell deciduation, brings about the high signal intensity of the globus pallidus on T1-weighted MRI in patients with liver cirrhosis.

Adolescent↗