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PubMed2006

Dopamine modulation in the basal ganglia locks the gate to working memory.

The prefrontal cortex and basal ganglia are deeply implicated in working memory. Both structures are subject to dopaminergic neuromodulation in a way that exerts a critical influence on the proper operation of working memory. We present a novel network model to elucidate the role of phasic dopamine in the interaction of these two structures in initiating and maintaining mnemonic activity. We argue that neuromodulation plays a critical role in protecting memories against both internal and external sources of noise. Increases in cortical gain engendered by prefrontal dopamine release help make memories robust against external distraction, but do not offer protection against internal noise accompanying recurrent cortical activity. Rather, the output of the basal ganglia provides the gating function of stabilization against noise and distraction by enhancing select memories through targeted disinhibition of cortex. Dopamine in the basal ganglia effectively locks this gate by influencing the stability of up and down states in the striatum. Dopamine's involvement in affective processing endows this gating with specificity to motivational salience. We model a spatial working memory task and show that these combined effects of dopamine lead to superior performance.

Action Potentials↗
PubMed2006

Effective treatment with levodopa and carbidopa for hypomyelination with atrophy of the basal ganglia and cerebellum.

Hypomyelination with atrophy of the basal ganglia and cerebellum (H-ABC) is a rare leukoencephalopathy presenting in the infantile period and characterized by diffuse cerebral hypomyelination, and atrophy of the basal ganglia and cerebellum. As patients with H-ABC lack remarkable laboratory findings, the diagnosis is based on brain magnetic resonance imaging findings alone. Only eight cases have been reported in the literature, and thus the natural course and treatment of this disease are not fully understood. We report a 35-month-old boy with H-ABC who had hemidystonia, hypomyelination, and cerebellar ataxia. We diagnosed H-ABC after considering a thorough differential diagnosis, excluding other diseases involving hemidystonia, hypomyelination, and cerebellar ataxia. Furthermore, technetium-99m ethyl cysteinate dimmer-single-photon emission computerized tomography (Tc-ECD-SPECT) and positron emission tomography with fluorodeoxyglucose (18)F (FDG-PET) revealed decreased blood flow and glucose metabolism in the bilateral lenticular nucleus, thalamus, and cerebellum. A peroral levodopa preparation containing carbidopa (levodopa-carbidopa) was effective at ameliorating and stopping the progression of the patient's dystonia (final effective doses: levodopa, 200 mg/day and carbidopa, 20 mg/day). This is the first case report of a Japanese patient with H-ABC and treatment for this disease. Levodopa-carbidopa may be an effective treatment for H-ABC.

Administration, Oral↗
PubMed2002

Natural killer cell proliferation and circulating cytokines in patients with bilateral basal ganglia calcification.

Ten adult patients with symmetrical calcifications in the bilateral basal ganglia (diagnosed as physiological calcifications) were analyzed for lymphocyte subsets and cytokines. Increased number of natural killer (NK) cells were identified in the peripheral blood of seven patients by lymphocyte subset analysis. Tumor necrosis factor-alpha was detected in the sera of five patients and interferon-gamma was detected in one patient. In summary, NK cell propagation and circulating cytokines, particularly tumor necrosis factor-alpha, may be involved in the etiology of basal ganglia calcification.

Aged↗
PubMed1982

Basal ganglia calcification in the neonate.

Calcification of the basal ganglia developed following intracranial hemorrhage in a neonate recovering from severe perinatal asphyxia. Cranial computed tomography is useful in demonstrating the anatomic distribution of dystrophic calcification in regions previously involved by hemorrhage. The demonstration of hemorrhage or hemorrhagic infarction with CT may help to verify the association of basal ganglia calcification with birth anoxia.

Adult↗
PubMed1990

Primate models of movement disorders of basal ganglia origin.

Movement disorders associated with basal ganglia dysfunction comprise a spectrum of abnormalities that range from the hypokinetic disorders (of which Parkinson's disease is the best-known example) at one extreme to the hyperkinetic disorders (exemplified by Huntington's disease and hemiballismus) at the other. Both extremes of this movement disorder spectrum can be accounted for by postulating specific disturbances within the basal ganglia-thalamocortical 'motor' circuit. In this paper, Mahlon DeLong describes the changes in neuronal activity in the motor circuit in animal models of hypo- and hyperkinetic disorders.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed2002

The basal ganglia and disorders of movement: pathophysiological mechanisms.

The basal ganglia are part of a neuronal network organized in parallel circuits. The "motor circuit" is most relevant to the pathophysiology of movement. Abnormal increment or reduction in the inhibitory output activity of basal ganglia give rise, respectively, to poverty and slowness of movement (i.e., Parkinson's disease) or dyskinesias.

Basal Ganglia↗
PubMed1999

[Functional imaging for disorders of basal ganglia].

The nigrostriatal dopaminergic function and regional glucose metabolism were evaluated in patients suffering from various disorders of basal ganglia by using positron emission tomography with 18F-dopa and 18F-FDG, respectively. The 18F-dopa uptake in the striatum (the caudate head and the putamen) decreased in patients with Parkinson's disease but was relatively unaffected in the caudate. The cerebral glucose metabolism was normal in patients with Parkinson's disease. The 18F-dopa uptake in the striatum also decreased in cases of multiple system atrophy and progressive supranuclear palsy, but there was no difference in the uptake between the caudate and the putamen. The glucose metabolism decreased in the cerebral cortices and the striatum: this finding was also different from those of Parkinson's disease. A normal 18F-dopa uptake with a markedly decreased striatal glucose metabolism was observed in cases of Huntington's disease. The 18F-dopa uptake increased and the glucose metabolism was normal in cases of idiopathic dystonia. Various patterns of 18F-dopa uptake and glucose metabolism were thus observed in the various disorders of basal ganglia. These results suggest that the measurements of the 18F-dopa uptake and glucose metabolism would be useful for evaluating the function of the basal ganglia in various disorders of basal ganglia.

Basal Ganglia↗
PubMed2003

Left and right basal ganglia and frontal activity during language generation: contributions to lexical, semantic, and phonological processes.

fMRI was used to determine the frontal, basal ganglia, and thalamic structures engaged by three facets of language generation: lexical status of generated items, the use of semantic vs. phonological information during language generation, and rate of generation. During fMRI, 21 neurologically normal subjects performed four tasks: generation of nonsense syllables given beginning and ending consonant blends, generation of words given a rhyming word, generation of words given a semantic category at a fast rate (matched to the rate of nonsense syllable generation), and generation of words given a semantic category at a slow rate (matched to the rate of generating of rhyming words). Components of a left pre-SMA-dorsal caudate nucleus-ventral anterior thalamic loop were active during word generation from rhyming or category cues but not during nonsense syllable generation. Findings indicate that this loop is involved in retrieving words from pre-existing lexical stores. Relatively diffuse activity in the right basal ganglia (caudate nucleus and putamen) also was found during word-generation tasks but not during nonsense syllable generation. Given the relative absence of right frontal activity during the word generation tasks, we suggest that the right basal ganglia activity serves to suppress right frontal activity, preventing right frontal structures from interfering with language production. Current findings establish roles for the left and the right basal ganglia in word generation. Hypotheses are discussed for future research to help refine our understanding of basal ganglia functions in language generation.

Adolescent↗
PubMed1997

Patients with stroke confined to basal ganglia have diminished response to rehabilitation efforts.

Prediction of the functional outcome for patients with stroke has depended on the severity of impairment, location of brain injury, age, and general medical condition. This study compared admission and discharge functional outcome (Functional Independence Measure, FIM) and deficit severity (Fugl-Meyer, F-M) scores in a retrospective study of patients with similar neurologic impairments: homonymous hemianopia, hemisensory loss, and hemiparesis. CT-verified stroke location was the independent variable: cortical (n = 11), basal ganglia and internal capsule (normal cortex and thalamus, n = 13), or combined (cortical, basal ganglia, and internal capsule, n = 22). By 3 months on average after stroke, all groups demonstrated significantly improved motor function as measured by F-M scores. Patients with cortical lesions had the least CT-imaged damage and the best outcome. Patients with combined lesions and more extensive brain injury had significantly higher FIM scores (P < 0.05) than patients with injury restricted to the basal ganglia/ internal capsule. Patients with basal ganglia/internal capsule injury were more likely to have hypotonia, flaccid paralysis, and persistently impaired balance and ambulation performance. While all patients had a comparable rehabilitation experience, these results suggest that patients with stroke confined to the basal ganglia and internal capsule benefited less from therapy. Isolated basal ganglia stroke may cause persistent corticothalamic-basal ganglia interactions that are dysfunctional and impede recovery.

Aged↗
PubMed2004

Evidence for a glutamatergic projection from the zona incerta to the basal ganglia of rats.

This study explores the organisation and neurochemical nature of the projections from the zona incerta (ZI) to the basal ganglia. Sprague-Dawley rats were anaesthetised with ketamine (100 mg/kg) and Rompun (10 mg/kg), and injections of cholera toxin subunit B were made into each of the following nuclei: the ZI, the substantia nigra (SN), the pedunculopontine tegmental nucleus (PpT), and the entopeduncular nucleus (Ep). Brains were aldehyde fixed, sectioned, and processed using standard methods. Tracer-labelled sections were then doubly labelled with antibodies to glutamate (Glu), nitric oxide synthase (NOS), parvalbumin (Pv), or glutamic acid decarboxylase (GAD; the latter two are markers for GABAergic cells); these neurochemicals characterise most types of ZI cells. After ZI injections, labelling was nonuniform across the different basal ganglia nuclei. The bulk of labelling, both anterograde and retrograde, was seen in the SN and PpT and, to a lesser extent, within the other nuclei of the basal ganglia (e.g., caudate-putamen, globus pallidus, subthalamus, Ep). In the SN, labelling was found in both major parts of the nucleus, the pars compacta and pars reticulata. Within the PpT, however, the bulk of labelling was limited to only one of the two sectors of the nucleus, namely, the pars dissipata (PpTd). The pars compacta of the PpT (PpTc) remained largely free of labelled profiles. After CTb injections into three basal ganglia nuclei (SN, PpT, Ep), most labelled cells in the ZI were glutamate+ and very few were NOS+ or gamma-aminobutyric acidergic. Overall, the results indicate that the ZI is in a position to influence preferentially the activity of the SN and PpTd of the basal ganglia via an excitatory, glutamatergic input.

Animals↗
PubMed2001

A computational model of action selection in the basal ganglia. I. A new functional anatomy.

We present a biologically plausible model of processing intrinsic to the basal ganglia based on the computational premise that action selection is a primary role of these central brain structures. By encoding the propensity for selecting a given action in a scalar value (the salience), it is shown that action selection may be recast in terms of signal selection. The generic properties of signal selection are defined and neural networks for this type of computation examined. A comparison between these networks and basal ganglia anatomy leads to a novel functional decomposition of the basal ganglia architecture into 'selection' and 'control' pathways. The former pathway performs the selection per se via a feedforward off-centre on-surround network. The control pathway regulates the action of the selection pathway to ensure its effective operation, and synergistically complements its dopaminergic modulation. The model contrasts with the prevailing functional segregation of basal ganglia into 'direct' and 'indirect' pathways.

Animals↗
PubMed2002

Slow oscillatory discharge in the primate basal ganglia.

Oscillations with periods in the multisecond range have previously been recorded in basal ganglia neurons of awake paralyzed rats, and in these animals were shown to be increased by systemic dopaminergic stimulation, but not altered by depletion of the nigrostriatal dopamine supply. To determine whether oscillations with frequencies below 0.5 Hz also exist in the primate basal ganglia, the spontaneous neuronal activity in the subthalamic nucleus (STN) and in the external and internal segments of the globus pallidus (GPe and GPi, respectively) was recorded with standard extracellular recording methods in two animals before and after treatment with the dopaminergic neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Oscillations with mean periods around 80 s were identified in 30% percent of GPe neurons, 36% of STN neurons, and 48% of GPi neurons. After recording in the normal state, the animals were rendered parkinsonian by intracarotid application of MPTP. This treatment resulted in a 30% reduction of the average discharge rate in GPe, a 47% increase of the average discharge rate in STN, and a 15% increase of the average discharge rate in GPi. However, there were no changes in the proportion of cells with slow oscillatory discharge. The oscillation frequencies were slightly increased in STN but remained unchanged in GPe and GPi. The results demonstrate that multisecond oscillations commonly occur in primate basal ganglia neurons and are unchanged by treatment with MPTP. The oscillations may have roles in fundamental functions of the basal ganglia-thalamocortical network, such as the regulation of the state of arousal.

Animals↗
PubMed1990

[A case of large basal ganglia AVM totally removed by staged operation].

Large basal ganglia AVMs have been deemed inoperable because of their location in critical structures. Nonetheless, the unfavorable natural history of an untreated ruptured AVM in a young patient induced us to approach these lesions. We presented a case of a large basal ganglia AVM totally removed by a three-staged operation. A 26-year-old man who had twice experienced intracranial hemorrhage was admitted for examination. On admission, mild left hemiparesis, hypesthesia and left hemianopsia were disclosed. CT scan showed the AVM was located in the posterior thalamus with the hematoma cavity laterally. Right carotid and vertebral angiograms demonstrated a large AVM, 5cm in diameter, supplied by the anterior choroidal artery (AchoA), the lateral lenticulostriate arteries (I-LSAs), the lateral posterior choroidal artery (LPchoA) and the thalamo-perforating artery. Drainage was via the internal cerebral vein and the basal vein of Rosenthal. MRI demonstrated more clearly the anatomical relationship of the nidus and surrounding structures. The patient underwent a three staged operation. At the first operation AchoA was interrupted in the inferior horn of the lateral ventricle (IHL) via the hematoma cavity using the trans-sylvian approach. The anterior part of the nidus was dissected with all except one of the I-LSAs being disconnected. At the next operation by occipital interhemispheric approach, some feeders from the posterior cerebral artery were coagulated and disconnected. The medial and posterior part of the nidus was dissected from the thalamus along with the choroid plexus of the trigone of the lateral ventricle.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2006

Developmental reflexes and 31P Magnetic Resonance Spectroscopy of basal ganglia in antipsychotic-naive schizophrenia.

The study examined the high energy-phosphate metabolism of basal ganglia in antipsychotic-naive schizophrenia patients with and without developmental reflexes in comparison to healthy subjects. Nineteen antipsychotic-naive schizophrenics of whom 11 had developmental reflexes and 26 age-sex-matched healthy subjects without developmental reflexes underwent in-vivo 2-D 31P Magnetic Resonance Spectroscopy of basal ganglia on a 1.5-T scanner. Mean age-at-onset of psychosis was significantly lower in patients with developmental reflexes. Mean PCr/Total ATP ratio in bilateral basal ganglia was lower in patients than healthy subjects. The ratio was the least in patients with developmental reflexes (F=10.7; df=2, 42; p<0.001). Schizophrenia patients with developmental reflexes had the lowest PCr/Total ATP ratio in basal ganglia indicating more severe metabolic abnormality. These patients had younger age-at-onset of psychosis. Together, this suggests neurodevelopmental etiopathogenesis in schizophrenia.

Adenosine Triphosphate↗
PubMed2000

Pre- and postsynaptic localization of GABA(B) receptors in the basal ganglia in monkeys.

GABAergic neurotransmission involves ionotropic GABA(A) and metabotropic GABA(B) receptor subtypes. Although fast inhibitory transmission through GABA(A) receptors activation is commonly found in the basal ganglia, the functions as well as the cellular and subcellular localization of GABA(B) receptors are still poorly known. Polyclonal antibodies that specifically recognize the GABA(B)R1 receptor subunit were produced and used for immunocytochemical localization of these receptors at the light and electron microscope levels in the monkey basal ganglia. Western blot analysis of monkey brain homogenates revealed that these antibodies reacted specifically with two native proteins corresponding to the size of the two splice variants GABA(B)R1a and GABA(B)R1b. Preadsorption of the purified antiserum with synthetic peptides demonstrated that these antibodies recognize specifically GABA(B)R1 receptors with no cross-reactivity with GABA(B)R2 receptors. Overall, the distribution of GABA(B)R1 immunoreactivity throughout the monkey brain correlates with previous GABA(B) ligand binding studies and in situ hybridization data as well as with recent immunocytochemical studies in rodents. GABA(B)R1-immunoreactive cell bodies were found in all basal ganglia nuclei but the intensity of immunostaining varied among neuronal populations in each nucleus. In the striatum, interneurons were more strongly stained than medium-sized projection neurons while in the substantia nigra, dopaminergic neurons of the pars compacta were much more intensely labeled than GABAergic neurons of the pars reticulata. In the subthalamic nucleus, clear immunonegative neuronal perikarya were intermingled with numerous GABA(B)R1-immunoreactive cells. Moderate GABA(B)R1 immunoreactivity was observed in neuronal perikarya and dendritic processes throughout the external and internal pallidal segments. At the electron microscope level, GABA(B)R1 immunoreactivity was commonly found in neuronal cell bodies and dendrites in every basal ganglia nuclei. Many dendritic spines also displayed GABA(B)R1 immunoreactivity in the striatum. In addition to strong postsynaptic labeling, GABA(B)R1-immunoreactive preterminal axonal segments and axon terminals were frequently encountered throughout the basal ganglia components. The majority of labeled terminals displayed the ultrastructural features of glutamatergic boutons and formed asymmetric synapses. In the striatum, GABA(B)R1-containing boutons resembled terminals of cortical origin, while in the globus pallidus and substantia nigra, subthalamic-like terminals were labeled. Overall, these findings demonstrate that GABA(B) receptors are widely distributed and located to subserve both pre- and postsynaptic roles in controlling synaptic transmission in the primate basal ganglia.

Animals↗
PubMed1984

Synaptic organization of the basal ganglia: an electroanatomical approach in the rat.

The physiological processes by which basal ganglia participate in the elaboration of movement are still poorly understood. In particular, lack of information about the synaptic organization of the output pathways of the basal ganglia impedes functional analysis of this system. To bridge this gap electroanatomical studies have been undertaken of one of the major output systems of the basal ganglia: the substantia nigra pars reticulata (SNr). This paper reviews recent results and proposes functional perspectives. The findings reported clearly establish that SNr exerts a tonic inhibitory influence on its collicular and thalamic targets. It is suggested that the striatum may achieve a complex-spatial pattern of facilitation in a large spectrum of structures related to ocular and cephalic motor activity by inhibiting the inhibitory nigrothalamic and nigrocollicular branched neurons.

Animals↗
PubMed1998

Differential modulation of dopamine D1-receptor binding and mRNA expression in the basal ganglia by the D1-receptor antagonist, SCH-23390.

Dopamine D1-receptor binding in the basal ganglia is differentially regulated by subtype nonspecific dopamine antagonists such as the antipsychotic, Fluphenazine. The purpose of the present study was to determine the relative contributions of D1 and D2 receptor systems in the regulation of basal ganglia D1-receptor binding. Rats were injected twice daily for 21 days with saline, the D1-receptor antagonist, SCH-23390, the D2-receptor antagonist, Raclopride, or both SCH-23390 and Raclopride. Dopamine D1-receptor levels (as indicated by [125I]SCH-23982 binding) and mRNA expression were measured using receptor autoradiographic and in situ hybridization histochemical techniques. [125I]NCQ-298 binding to D2-receptors was also measured as a positive control for the effects of Raclopride. SCH-23390 administration independently increased [125I]SCH-23982 binding in a region-dependent manner with the greatest increases occurring in the entopeduncular nucleus. SCH-23390 also increased D1-receptor mRNA expression in specific striatal subregions suggesting that increases in binding were related to changes in receptor synthesis. In addition, Raclopride independently enhanced D2 binding with comparable increases observed in extrastriatal regions and increases of a lesser magnitude in the striatum. These data show that the modulation of basal ganglia D1-receptor binding observed in animals treated with nonselective antagonists is due primarily to the blockade of D1-receptors. The differential enhancement in basal ganglia D1 binding observed after D1-receptor blockade may be due to anatomical or phenotypic heterogeneity within the population of striatal D1-receptor synthesizing neurons. Similarly, the differential enhancement in striatal and extrastriatal D2-receptor binding may be due to differences in the regulation of striatal and extrastriatal D2-receptor synthesizing neurons.

Animals↗
PubMed1998

Temporal processing in the basal ganglia.

This study investigated the role of the basal ganglia in timing operations. Nondemented, medicated Parkinson's disease (PD) patients and controls were tested on 2 motor-timing tasks (paced finger tapping at a 300- or 600-ms target interval), 2 time perception tasks (duration perception wherein the interval between the standard tone pair was 300 or 600 ms), and 2 tasks that controlled for the auditory processing (frequency perception) demands of the time perception task and the movement rate (rapid tapping) in the motor-timing task. Using A.M. Wing and A.B. Kristofferson's (1973) model, the total variability in motor timing was partitioned into a clock component, which reflects central timekeeping operations, and a motor delay component, which estimates random variability due to response implementation processes. The PD group was impaired at both target intervals of the time perception and motor-timing tasks. Impaired motor timing was due to elevated clock but not motor delay variability. The findings implicate the basal ganglia and its thalamocortical connections in timing operations.

Aged↗