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PubMed1987

[An autopsy case of progressive supranuclear palsy showing "pure akinesia without rigidity and tremor and with no effect by L-dopa therapy (Imai)"].

Eleven cases of "pure akinesia without rigidity and tremor and with no effect by L-dopa therapy" were first reported by Imai in 1980. Three cases were added by Hayashi and Hayashi (1983). However there have been so far no autopsy cases, remaining the nosological position of this syndrome uncertain. The authors have had an opportunity of observing the third case in the report by Hayashi and Hayashi for 8 years and autopsy was done as well. Case report The patient was a female farmer. On account of postural-reflex troubles, the pulsion phenomenon and feet freezing, which had progressed since the age of 54, she easily tumbled over. Eight years after the beginning of those symptoms, vertical oculomotor palsy, pseudobulbar palsy and dementia were added; she was diagnosed as a progressive supranuclear palsy. Before this diagnosis, her illness was being regarded as "pure akinesia without rigidity and tremor and with no effect by L-dopa therapy". Neck dystonia was not observed even in the terminal stage. She died at the age of 65. The total clinical course was about 11 years. Pathological observation The brain weighed 1,170 g before fixation. Marked atrophy of the subthalamic nucleus, globus pallidus and pontine tegmentum was observed. The substantia nigra was shown to be severely depigmented. Microscopically, loss of neurons and gliosis were seen in the subthalamic nucleus, globus pallidus, substantia nigra, hypothalamus, superior colliculus, central grey matter, brain stem reticular formation, cerebellar dentate nucleus, etc. The characteristic finding was the appearance of neurofibrillary tangles in these regions.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1991

The AMPA receptor antagonist NBQX has antiparkinsonian effects in monoamine-depleted rats and MPTP-treated monkeys.

Abnormally increased subthalamic nucleus output to the internal pallidal segment and the reticular part of the substantia nigra plays a critical pathophysiological role in the development of parkinsonism. Because synaptic transmission of subthalamic output is glutamatergic and mediated, in part, by the alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) subtype of glutamate receptor, AMPA receptor antagonists may possess antiparkinsonian properties. We report that in monoamine-depleted rats, 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(f)quinoxaline (NBQX) (Novo-Nordisk, Copenhagen, Denmark)--a selective antagonist of the AMPA subtype of glutamate receptor--suppressed muscular rigidity but had no effect on akinesia. NBQX microinjected into the subthalamic nucleus, internal pallidal segment, and reticular part of the substantia nigra, but not into the laterodorsal neostriatum of the rats, stimulated locomotor activity and reduced muscular rigidity. In aged Rhesus monkeys with bilateral 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced parkinsonism, intramuscular NBQX produced clinically apparent improvement in akinesia, tremor, posture, and gross motor skills. NBQX also potentiated the antiparkinsonian effects of L-3,4-dihydroxyphenylalanine in both rats and monkeys. Blockade of excitatory synaptic transmission by AMPA receptor antagonists may provide a new therapeutic strategy for Parkinson's disease (PD).

Animals↗
PubMed2001

Activation of metabotropic glutamate receptor 1 inhibits glutamatergic transmission in the substantia nigra pars reticulata.

The substantia nigra pars reticulata is a primary output nucleus of the basal ganglia motor circuit and is controlled by a fine balance between excitatory and inhibitory inputs. The major excitatory input to GABAergic neurons in the substantia nigra arises from glutamatergic neurons in the subthalamic nucleus, whereas inhibitory inputs arise mainly from the striatum and the globus pallidus. Anatomical studies revealed that metabotropic glutamate receptors (mGluRs) are highly expressed throughout the basal ganglia. Interestingly, mRNA for group I mGluRs are abundant in neurons of the subthalamic nucleus and the substantia nigra pars reticulata. Thus, it is possible that group I mGluRs play a role in the modulation of glutamatergic synaptic transmission at excitatory subthalamonigral synapses. To test this hypothesis, we investigated the effects of group I mGluR activation on excitatory synaptic transmission in putative GABAergic neurons in the substantia nigra pars reticulata using the whole cell patch clamp recording approach in slices of rat midbrain. We report that activation of group I mGluRs by the selective agonist (R,S)-3,5-dihydroxyphenylglycine (100 microM) decreases synaptic transmission at excitatory synapses in the substantia nigra pars reticulata. This effect is selectively mediated by presynaptic activation of the group I mGluR subtype, mGluR1. Consistent with these data, electron microscopic immunocytochemical studies demonstrate the localization of mGluR1a at presynaptic sites in the rat substantia nigra pars reticulata. From this finding that group I mGluRs modulate the major excitatory inputs to GABAergic neurons in the substantia nigra pars reticulata we suggest that these receptors may play an important role in basal ganglia functions. Studying this effect, therefore, provides new insights into the modulatory role of glutamate in basal ganglia output nuclei in physiological and pathophysiological conditions.

Animals↗
PubMed1993

Anatomical aspects of information processing in primate basal ganglia.

Recent studies with double-anterograde tract-tracing methods have shed new light on the organization of the basal ganglia circuitry in primates. This paper briefly reviews some of these findings and provides a personal interpretation of their possible functional significance. Emphasis is placed on the fact that the striatum and the subthalamic nucleus have multiple representations in the two major output structures of the basal ganglia, namely the internal segment of the globus pallidus and the substantia nigra pars reticulata. It is hypothesized that this multiple representation serves as a means of amplifying and diversifying the striatal and subthalamic influences upon thalamocortical neurons that is mediated through the globus pallidus and the substantia nigra. Furthermore, evidence for the highly ordered organization of the striatopallidal and subthalamopallidal projections, which converge onto single pallidal neurons according to different but highly specific patterns, is taken as an indication that the subthalamic nucleus uniformly excites a vast collection of pallidal neurons, whereas the striatum exerts a more specific inhibitory control upon selected subsets of subthalamically driven pallidal neurons.

Animals↗
PubMed1999

Systematic expression of immediate early genes and intensive astrocyte activation induced by intrastriatal ferrous iron injection.

The potential role(s) of transitional metals such as iron have been implicated in neurodegeneration through biochemical processes, particularly oxidative stress. We injected ferrous chloride (FeCl2) and ferric chloride (FeCl3) into the striatonigral system of Sprague-Dawley rats to investigate the biological and toxic effects of ferrous iron in the central nervous system. When FeCl2 was injected into the ventral midbrain, rats showed a characteristic behavior which indicated ipsilateral dopaminergic hyperactivity. FeCl2 injection into the striatum induced a dose-dependent damage, the activation of astrocytes and recruitment of macrophage/microglia at the injected site. Interestingly, the activation of astrocytes was also observed in the anatomically remote areas such as the ipsilateral subthalamic nucleus and pars reticulata of the substantia nigra after 1 week. Expression of immediate early genes (IEGs; c-fos and NGFI-A) was observed in the cortex, thalamic nuclei, subthalamic nucleus, pars reticulata of the substantia nigra, lateral and medial geniculate bodies on the ipsilateral side from 3 to 15 h after FeCl2 injection. Pre-treatment with dimethyl sulfoxide, a hydroxyl radical scavenger, prevented FeCl2-induced expression of IEGs in the thalamic nuclei and geniculate bodies, but not in the cerebral cortex. On the other hand, the effects of FeCl3 were faint and limited on IEGs expression and tissue damage. These results suggest that ferrous iron affects the nervous system vigorously, possibly yielding free radicals such as hydroxyl radicals, and could be one of the important candidates for neurodegenerative diseases under the state in which acclimating systems for iron toxicity are disrupted.

Animals↗
PubMedDate not supplied

[Conditioned motor-alimentary reflexes in cats following ablation of the body of Luys].

Alimentary conditioned motor reflexes in cats were elaborated in special chambers. Subsequently, the subthalamic nucleus was damaged, first on one and then on the other side. After its unilateral destruction, temporary disturbance in the cat behaviour was observed disappearing within 2--3 weeks. Bilateral destruction of the subthalamic nucleus led to a stable disturbance in the reaction of choice of reinforcement side in conditions of uncertainty.

Animals↗
PubMed1987

Long descending direct projection from the basal ganglia to the spinal cord: a revival of the extrapyramidal concept.

Our retrograde fluorescent labeling study shows that a distinct cell group of the subthalamic nucleus, posited in the basal ganglia, directly sends long descending axons contralaterally to the upper cervical segments (C1-C5) of the spinal cord in the rat. A large population (60-70%) of these subthalamic cells projecting to contralateral spinal levels give off axonal branches innervating the ipsilateral globus pallidus. Now, the classical concept of the 'extrapyramidal' motor system needs to be reconsidered. Furthermore, our results may provide a morphological substrate for the onset of a violent form of dyskinesia, 'hemiballism', which occurs in the contralateral limbs both clinically and experimentally following discrete lesions in the subthalamic nucleus or its fiber connections with the globus pallidus.

Animals↗
PubMed2003

Spreading of slow cortical rhythms to the basal ganglia output nuclei in rats with nigrostriatal lesions.

A high proportion of neurons in the basal ganglia display rhythmic burst firing after chronic nigrostriatal lesions. For instance, the periodic bursts exhibited by certain striatal and subthalamic nucleus neurons in 6-hydroxydopamine-lesioned rats seem to be driven by the approximately 1 Hz high-amplitude rhythm that is prevalent in the cerebral cortex of anaesthetized animals. Because the striatum and subthalamic nucleus are the main afferent structures of the substantia nigra pars reticulata, we examined the possibility that the low-frequency modulations (periodic bursts) that are evident in approximately 50% nigral pars reticulata neurons in the parkinsonian condition were also coupled to this slow cortical rhythm. By recording the frontal cortex field potential simultaneously with single-unit activity in the substantia nigra pars reticulata of anaesthetized rats, we proved the following. (i) The firing of nigral pars reticulata units from sham-lesioned rats is not coupled to the approximately 1 Hz frontal cortex slow oscillation. (ii) Approximately 50% nigral pars reticulata units from 6-hydroxydopamine-lesioned rats oscillate synchronously with the approximately 1 Hz cortical rhythm, with the cortex leading the substantia nigra by approximately 55 ms; the remaining approximately 50% nigral pars reticulata units behave as the units recorded from sham-lesioned rats. (iii) Periodic bursting in nigral pars reticulata units from 6-hydroxydopamine-lesioned rats is disrupted by episodes of desynchronization of cortical field potential activity. Our results strongly support that nigrostriatal lesions promote the spreading of low-frequency cortical rhythms to the substantia nigra pars reticulata and may be of outstanding relevance for understanding the pathophysiology of Parkinson's disease.

Action Potentials↗
PubMed2006

Criteria for deep-brain stimulation in Parkinson's disease: review and analysis.

Deep-brain stimulation is currently the most effective surgical treatment for advanced Parkinson's disease. The relevant targets to date are the subthalamic nucleus and the globus pallidus internus, although the thalamus (ventralis intermedius nucleus) is preferred in tremor-dominant, aged Parkinson's disease patients. Long-term benefit in cardinal parkinsonian signs, motor fluctuations and dyskinesia has been reported in 5-year follow-up studies of subthalamic nucleus deep-brain stimulation. However, some psychiatric consequences have raised important issues and emphasized the need for an experienced deep-brain stimulation surgical team. This team should be multidisciplinary and involve movement disorder neurologists, neurosurgeons, neuropsychologists and psychiatrists. The recent observation that deep-brain stimulation of the pedunculopontine nucleus improves axial signs, possibly even in those less responsive to levodopa, brings new hope to the management of advanced Parkinson's disease.

Deep Brain Stimulation↗
PubMedDate not supplied

A pulsed neural network model of bursting in the basal ganglia.

We present new techniques for extending the functionality of spiking neurons which allow the incorporation of several aspects of neuron function previously confined to the domain of low level ion-channel based models. These aspects include spontaneous (or endogenous) firing, the complex interaction of multiple ion-species and the spatial distribution of synaptic contacts over the cell membrane. These ideas are applied to a neural circuit consisting of the cortex and a subset of the nuclei in the basal ganglia-the subthalamic nucleus (STN) and the external segment of the globus pallidus (GPe). This circuit has been studied extensively in vitro by Plenz and Kitai [Plenz, D., & Kitai, S. T. (1999). A basal ganglia pacemaker formed by the subthalamic nucleus and external globus pallidus. Nature, 400 677-682] whose data we use to constrain our model. With respect to this circuit, we have obtained three main results. First, that its characteristic burst firing is due to a Ca2+ current mediated mechanism. Second, that noise can assist in the generation of bursting and, paradoxically, stabilise the network behaviour under synaptic weight variations. Third, that a variety of dendritic processing is necessary in order to obtain the full range of bursting behaviour.

Action Potentials↗
PubMed2006

Preservation of the direct and indirect pathways in an in vitro preparation of the mouse basal ganglia.

We have developed a slice preparation of the mouse basal ganglia which contains portions of the striatum, external pallidum, subthalamic nucleus and substantia nigra and the neocortex. This basal ganglia slice is unique in preserving functional direct and indirect connections between the striatum and the substantia nigra as well as interconnectivity between the globus pallidus and the subthalamic nucleus. We used fiber tract tracing studies and electrophysiological recordings to demonstrate the full functionality of these pathways. Deposits of 1,1'-dioctadecyl-3,3,3',3'-tetra-methylindocarbocyamine perchlorate in the different basal ganglia resulted in labeled fibers in each of their target nuclei. Confirming these results, electrical stimulation of the different nuclei elicited whole-cell recorded postsynaptic potentials in their target neurons with an appropriate pharmacological profile. Electrical and glutamate activation of the striatum evoked bursts of glutamatergic and GABAergic activities in whole-cell recorded nigral neurons indicating that the direct and indirect pathways are operative in this slice. It also showed that the responses evoked are not due to fibers en passant but to the activation of striatal cell bodies. These findings provide the first direct evidence for a preserved basal ganglia circuitry in vitro and make the basal ganglia slice a suitable preparation for analyzing the activity of the direct and indirect pathways in physiological and pathological conditions.

Animals↗
PubMed1994

Metabotropic glutamate receptor mRNA expression in the basal ganglia of the rat.

Metabotropic glutamate receptors (mGluRs) couple the actions of glutamate to intracellular second messenger systems through G-proteins. The mGluRs play an important role in the regulation of basal ganglia function. Ligand binding studies have revealed that the basal ganglia contain at least two pharmacological types of metabotropic binding sites. Agonists of mGluRs can affect both in vitro electrophysiologic responses of striatal neurons and motor behavior in vivo. Recently, cDNAs encoding five mGluRs have been cloned, each with distinct structural and pharmacological properties. In order to elucidate the function of these receptors in the biology of the extrapyramidal motor system, we have used in situ hybridization to examine the regional and cellular expression patterns of mGluR1-mGluR5 in the adult rat basal ganglia. In the striatum, all of these mGluRs were present in widely varying relative densities and cellular patterns. MGluR5 was particularly prominent, and exhibited a heterogeneous cellular distribution, with labeled and unlabeled populations of neurons. MGluR2 was expressed in a small population of large polygonal striatal neurons. The subthalamic nucleus was the only other basal ganglia structure that expressed mGluR2. Distinct cellular distributions of mGluR expression were also observed within the nucleus accumbens, globus pallidus, ventral pallidum, and substantia nigra pars reticulata. MGluR3 was expressed in glia in all basal ganglia structures, but was observed in neurons only in the striatum, substantia nigra pars reticulata, and very weakly in the subthalamic nucleus. Comparison of the restricted mGluR2 and mGluR3 mRNA distributions with that of metabotropic ligand binding sites supports a possible presynaptic location for these receptors in the basal ganglia. MGluR1 was the only mGluR message prominently expressed in the dopaminergic neurons of the substantia nigra pars compacta, suggesting the involvement of this receptor in the regulation of dopamine release from nigrostriatal terminals.

Animals↗
PubMed1989

Connectivity patterns of thalamic nuclei implicated in dyskinesia.

Thalamic nuclei implicated in the neural mechanisms of dyskinesia (1) have projections to components of the basal ganglia; (2) receive efferents from the corpus striatum, and/or (3) project fibers to regions of the cerebral cortex that generate signals which produce or modulate motor phenomenon. The neostriatum receives a major input from the intralaminar thalamic nuclei (ITN). Thalamostriate fibers projecting to the caudate nucleus (CN) and the putamen (Put) originate from different neuronal populations; clusters of cells in the rostral ITN and in the parafascicular nucleus (PF) project to the CN, while cells in the centromedian nucleus (CM) project to the Put. Smaller numbers of cells in the medial, dorsal and ventral nuclear subdivisions of the thalamus also project to the striatum. The amygdaloid nuclear complex receives afferents from the midline thalamic nuclei. Ventromedial and rostral parts of the subthalamic nucleus receive a small input from the centromedian-parafascicular nuclear complex. Segments of the globus pallidus (GP) and the substantia nigra (SN) do not receive afferents from either the cerebral cortex or the thalamus. Thalamic afferents originate ipsilaterally from the medial segment of the globus pallidus (MPS), and the pars reticulata of the substantia nigra (SNR), and contralaterally from the deep cerebellar nuclei (DCN). Each of these projections to nuclear subdivisions of the thalamus is distinctive without overlap. Projections from the MPS are to the ventral anterior pars principalis (VApc) and ventral lateralis, pars oralis (VLo) thalamic nuclei with collaterals to CM. The SNR provides projections to the ventral anterior, pars magnocellularis, the ventral lateral, pars medialis and the mediodorsal, pars paralaminaris thalamic nuclei. Output from the subthalamic nucleus (STN) projects to both the MPS and the SNR and could modulate influences upon thalamic nuclei. In the monkey the projection of STN to the GP is four times greater than to the SNR. The most massive input to the thalamus arises from the contralateral DCN and terminates in the so-called cell-sparse zone, which consists of the ventral posterolateral nucleus, pars oralis, the ventral lateral nucleus pars caudalis, and pars postrema and area x of Olszewski. Nuclear subdivisions of the thalamus receiving afferents from the MPS and the SNR have gamma-aminobutyric acid (GABA) as their major neurotransmitter; fiber systems originating from the DCN appear to have glutamate as their neurotransmitter.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMedDate not supplied

MR imaging in "lacunar" hemiballismus.

We compared cranial CT and proton magnetic resonance imaging in two patients with hemiballismus secondary to lacunar infarctions. Magnetic resonance, but not CT, showed lacunar infarctions in the subthalamic nucleus. To confirm the location of the infarctions, we measured the distance of the lacunae from the anteroposterior commissure line in three planes (sagittal, axial, and coronal) and demonstrated that the infarctions were located in the lateral part of the subthalamic nucleus.

Aged↗
PubMed1998

[A case manifested overlapping neuropathologic features of both progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD)].

A 62-year-old man developed clumsiness, vertical ophthalmoplegia, right-side dominant parkinsonism, pyramidal signs, limb-kinetic apraxia and dementia. His brain MRI and SPECT revealed mild fronto-parietal atrophy and hypoperfusion predominately on the right side. At the age of 65, the patient died of sepsis. The duration of his illness was approximately 3 years. Clinical diagnosis was corticobasal degeneration (CBD). On neuropathological examination, there was no neuronal loss and many neurofibrillary tangles (NFTs) in the cerebral cortices. Basal ganglia and substantia nigra showed moderate to severe neuronal loss. And there were many NFTs and argyrophillic threads (threads) in the subthalamic nucleus and nuclei of the brainstem. These findings were almost compatible to those of PSP. However, the following findings were atypical for PSP, 1) mild atrophy and absence of gliosis in the tegmentum of the brain stem, 2) Mild neuronal loss in the subthalamic nucleus and the dentate nucleus without grumose degeneration. Furthermore, characteristic findings were noted on modified Gallyas-Braak stain. Numerous threads and many astrocytic plaques (AP) were shown in cerebral cortices, which were particular to CBD cases. So this case demonstrated neuropathological findings of both PSP and CBD. Therefore, it was difficult to classify this case as either PSP or CBD, and we diagnosed this case as a neuropathological overlapping case of both PSP and CBD.

Aged↗
PubMed1998

Role of the subthalamo-nigral input in the control of amygdala-kindled seizures in the rat.

The substantia nigra pars reticulata (SNpr) is a critical site for the control of epileptic seizures. Potentiation of the inhibitory GABAergic input from the striatum to the SNpr suppresses primary or secondary generalized seizures in the rat. The purpose of this study was to examine the possible involvement of the excitatory glutamatergic input from the subthalamic nucleus to the SNpr in the control of both the electroencephalographic and the motor components of amygdala-kindled seizures in the rat. Microinjections of either an N-methyl-D-aspartate (NMDA) antagonist in the substantia nigra or a GABAA agonist in the subthalamic nucleus, significantly reduced motor seizures but did not modified the afterdischarges. These results provide evidence for the involvement of the subthalamo-nigral projection in the modulation and the propagation of the motor components of amygdala-kindled seizures.

Amygdala↗
PubMed2002

Current surgical treatment of Parkinson's disease.

There has been a renaissance in the surgical management of Parkinson's disease. This has been due to long-term effects of levodopa and a better understanding of the basal ganglia and its circuitry. Ablative surgery and neurostimulation are the only realistic surgical options at present. Although surgical treatments, such as ablation and stimulation are effective, they are not useful for stopping the progression or restoring the system. Neural transplantation helps restore the system by using a number of techniques. Targets mostly used are in the thalamus, globus pallidus and subthalamic nucleus. A number of factors must be considered including patient's age, disability and his wishes. Globus pallidus stimulation might be preferable for patients who suffer from dyskinesia as a major source of disability. Pallidotomy might be appropriate in cases where frequent stimulator adjustments are impractical. Subthalamic nucleus stimulation is more suitable for patients with significant off periods and in younger patients in whom it may be desirable to maintain intact circuitry. Fetal neural transplantation, stem cell transplantation, xenotransplantation, adrenal medullary transplantation and transplantation of genetically engineered cells are at various stages of development and research. Ethical issues surrounding these process are likely to arouse strong emotions and have to be carefully considered.

Cell Transplantation↗
PubMed2000

The pedunculopontine nucleus: its role in the genesis of movement disorders.

The pedunculopontine nucleus (PPN) is located in the dorso-lateral part of the ponto-mesencephalic tegmentum. The PPN is composed of two groups of neurons: one containing acetylcholine, and the other containing non-cholinergic neurotransmitters (GABA, glutamate). The PPN is connected reciprocally with the limbic system, the basal ganglia nuclei (globus pallidus, substantia nigra, subthalamic nucleus), and the brainstem reticular formation. The caudally directed corticolimbic-ventral striatal-ventral pallidal-PPN-pontomedullary reticular nuclei-spinal cord pathway seems to be involved in the initiation, acceleration, deceleration, and termination of locomotion. This pathway is under the control of the deep cerebellar and basal ganglia nuclei at the level of the PPN, particularly via potent inputs from the medial globus pallidus, substantia nigra pars reticulata and subthalamic nucleus. The PPN sends profuse ascending cholinergic efferent fibers to almost all the thalamic nuclei, to mediate phasic events in rapid-eye-movement sleep. Experimental evidence suggests that the PPN, along with other brain stem nuclei, is also involved in anti-nociception and startle reactions. In idiopathic Parkinson's disease (IPD) and parkinson plus syndrome, overactive pallidal and nigral inhibitory inputs to the PPN may cause sequential occurrences of PPN hypofunction, decreased excitatory PPN input to the substantia nigra, and aggravation of striatal dopamine deficiency. In addition, neuronal loss in the PPN itself may cause dopamine-resistant parkinsonian deficits, including gait disorders, postural instability and sleep disturbances. In patients with IPD, such deficits may improve after posteroventral pallidotomy, but not after thalamotomy. One of the possible explanations for such differences is that dopamine-resistant parkinsonian deficits are mediated to the PPN by the descending pallido-PPN inhibitory fibers, which leave the pallido-thalamic pathways before they reach the thalamic targets.

Animals↗