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PubMed1995

Functional anatomy of the basal ganglia. II. The place of subthalamic nucleus and external pallidum in basal ganglia circuitry.

The subthalamic nucleus and the external pallidum (GPe) are classically viewed as part of the so-called indirect pathway, which acts in concert with the direct pathway. The direct and indirect pathways form the conceptual framework of the anatomical and functional organization of the basal ganglia. A review of recent data regarding the connections of the subthalamic nucleus and the GPe has revealed a lack of firm anatomical support for the existence of the indirect pathway. However, newly recognized projections of the subthalamic nucleus and the GPe place these structures on various novel routes that change the conceptual architecture of the basal ganglia circuitry. These new findings force us to modify our view of the functional identity of the subthalamic nucleus and the GPe. In this new perspective, the GPe stands as an additional integrative station, together with the striatum and the internal pallidum and substantia nigra pars reticulata (GPi/SNr), along the main steam of information processing within the basal ganglia circuitry. Because of its crucial position between the input and output stations of the basal ganglia, the GPe can markedly influence the neuronal computation that occurs at GPi/SNr levels. The subthalamic nucleus can still be regarded as a 'control structure' lying alongside the main stream of information processing. However, because of its widespread efferent projections, the subthalamic nucleus exerts its driving effect on most components of the basal ganglia. Its action is mediated not only by the indirect pathway, but by a multitude of mono- and polysynaptic projections that ultimately reach the basal ganglia output cells.

Afferent Pathways↗
PubMed2002

Atrophy of the basal ganglia as the initial diagnostic sign of germinoma in the basal ganglia.

Germ-cell tumors of the central nervous system generally develop in the midline, but the tumors can also occur in the basal ganglia and/or thalamus. However, MR images have rarely been documented in the early stage of the tumor in these regions. We retrospectively reviewed MR images obtained on admission and approximately 3 years earlier in two patients with germinoma in the basal ganglia, and compared them with CT. In addition to hyperdensity on CT, both hyperintensity on T1-weighted images and a small hyperintense lesion on T2-weighted images were commonly seen in the basal ganglia. These findings may be early MRI signs of germinoma in this region, and the earliest and most characteristic diagnostic feature on MRI was atrophy of the basal ganglia, which was recognizable before development of hemiparesis.

Adolescent↗
PubMed1992

Mobius syndrome with basal ganglia calcification.

Basal ganglia calcification has not been described in Mobius syndrome. A family with two children with Mobius syndrome are reported. Bilateral basal ganglia calcification was seen on computed tomography in both. This is the first family where cerebral involvement has been clearly documented in this syndrome.

Abducens Nerve↗
PubMed1995

Functional anatomy of the basal ganglia. I. The cortico-basal ganglia-thalamo-cortical loop.

This paper reviews some of the recent findings on different aspects of the anatomical organization of the basal ganglia. Attempts have been made to delineate the anatomical substrate of information processing along the cortico-basal ganglia-thalamo-cortical loop. Emphasis has been placed on data obtained with highly sensitive anterograde tract-tracing methods applied to the study of the main axis of the loop, which is composed of the striatum, the pallidum, and the substantia nigra. These findings have highlighted the complexities of the organization of the intrinsic basal ganglia circuitry, which comprises multiple modular units that are distributed according to highly ordered and repetitive patterns. Such an arrangement is well suited to convey cortical information in a highly specific manner throughout the basal ganglia. The basal ganglia circuitry is also designed so as to modulate in a precise manner the neuronal activity of several brain functional systems, which are involved in the direct control of different aspects of psychomotor behavior. Of utmost importance is the action of the basal ganglia on thalamocortical premotor neurons. It is through these neurons, which can be considered as a sort of final common pathway, that the basal ganglia ultimately influence the complex neuronal computation that goes on at cortical level.

Afferent Pathways↗
PubMed1990

Neurotransmitters and neuromodulators in the basal ganglia.

The basal ganglia have become a focus for work on neurotransmitter interactions in the brain. These structures contain a remarkable diversity of neuroactive substances, organized into functional subsystems that have unique developmental histories and vulnerabilities in neurodegenerative diseases. A new view of the basal ganglia is emerging on the basis of this neurochemical heterogeneity, suggesting that dynamic regulation of transmitter expression may be a key to extrapyramidal function.

Animals↗
PubMed2001

[Sensory-motor disintegration in the basal ganglia disorders].

Basal ganglia lie between the cerebral cortex and the thalamus, and have dense fiber connections between them. These connections form 4-5 distinct loops to allow parallel processing of information. Among them, the most intensively studied is the motor loop, which comprises 2 distinct direct and indirect pathways. The direct pathway disinhibits the powerful inhibition of Gpi/SNr upon the thalamic VL nuclei with a net result of facilitatory influence upon the motor cortex. By contrast, the indirect pathway exerts an inhibitory effect. Overall this dual system provides a center-surround mechanism to focus its effect on selected cortical neurons. The functional role of the loop in motor control has not been precisely understood. Several lines of evidence have recently been presented to support the view that this mechanism is used to focus the output to a specific group of muscles required for performing a specific task. Recent observations in dystonia and Parkinsonism suggest that this operation is made possible through opening the sensory channel for the expected sensory feed-back afferents during movement. Thus one of the important functions of basal ganglia seems to be the gating of sensory input for motor control.

Basal Ganglia↗
PubMed2005

Abnormal sensory gating in basal ganglia disorders.

Basal ganglia encompass four to five distinct loops to allow parallel processing of information. Among them, the most intensively studied is the motor loop, which includes two distinct direct and indirect pathways. The direct pathway exerts facilitatory influence upon the motor cortex, whereas the indirect pathway exerts an inhibitory effect. Overall, this dual system provides a center(excitatory)-surround-(inhibitory) mechanism to focus its effect on selected cortical neurons, and several lines of evidence suggest that this center-surround mechanism is used to focus the output on a specific group of muscles required for performing a specific task. This operation is made possible through opening the sensory channel for the expected sensory feed-back afferents during movement. Thus, one of the important functions of basal ganglia seems to be the gating of sensory input for motor control. Dystonia may be caused by a mismatch between sensory input versus motor output, and parkinsonism may be viewed as a disorder of gain control of this sensorimotor integration.

Animals↗
PubMed2003

Basal ganglia efferents to the brainstem centers controlling postural muscle tone and locomotion: a new concept for understanding motor disorders in basal ganglia dysfunction.

The present study is designed to elucidate how basal ganglia afferents from the substantia nigra pars reticulata (SNr) to the mesopontine tegmental area of the brainstem contribute to gait control and muscle-tone regulation. We used unanesthetized and acutely decerebrated cats (n=27) in which the striatum, thalamus and cerebral cortex were removed but the SNr was preserved. Repetitive stimulation (50 Hz, 10-60 microA, for 5-20 s) applied to a mesencephalic locomotor region (MLR), which corresponded to the cuneiform nucleus, and adjacent areas, evoked locomotor movements. On the other hand, stimulation of a muscle-tone inhibitory region in the pedunculopontine tegmental nucleus (PPN) suppressed postural muscle tone. An injection of either glutamatergic agonists (N-methyl-D-aspartic acid and kainic acid) or GABA antagonists (bicuculline and picrotoxin) into the MLR and PPN also induced locomotion and muscle-tone suppression, respectively. Repetitive electrical stimuli (50-100 Hz, 20-60 microA for 5-20 s) delivered to the SNr alone did not alter muscular activity. However stimulating the lateral part of the SNr attenuated and blocked PPN-induced muscle-tone suppression. Moreover, weaker stimulation of the medial part of the SNr reduced the number of step cycles and disturbed the rhythmic alternation of limb movements of MLR-induced locomotion. The onset of locomotion was delayed as the stimulus intensity was increased. At a higher strength SNr stimulation abolished the locomotion. An injection of bicuculline into either the PPN or the MLR diminished the SNr effects noted above. These results suggest that locomotion and postural muscle tone are subject to modulation by GABAergic nigrotegmental projections which have a partial functional topography: a lateral and medial SNr, for regulation of postural muscle tone and locomotion, respectively. We conclude that disorders of the basal ganglia may include dysfunction of the nigrotegmental (basal ganglia-brainstem) systems, which consequently leads to the production of abnormal muscle tone and gait disturbance.

Animals↗
PubMed2000

Functional anatomy of the basal ganglia.

The basal ganglia are a series of interconnected nuclei located deep within the cerebral hemispheres. These structures play an important role in movement. Complex feedback loops form direct and indirect pathways that balance excitatory and inhibitory activities through neurotransmitter activity.

Basal Ganglia↗
PubMed2006

A physiologically plausible model of action selection and oscillatory activity in the basal ganglia.

The basal ganglia (BG) have long been implicated in both motor function and dysfunction. It has been proposed that the BG form a centralized action selection circuit, resolving conflict between multiple neural systems competing for access to the final common motor pathway. We present a new spiking neuron model of the BG circuitry to test this proposal, incorporating all major features and many physiologically plausible details. We include the following: effects of dopamine in the subthalamic nucleus (STN) and globus pallidus (GP), transmission delays between neurons, and specific distributions of synaptic inputs over dendrites. All main parameters were derived from experimental studies. We find that the BG circuitry supports motor program selection and switching, which deteriorates under dopamine-depleted and dopamine-excessive conditions in a manner consistent with some pathologies associated with those dopamine states. We also validated the model against data describing oscillatory properties of BG. We find that the same model displayed detailed features of both gamma-band (30-80 Hz) and slow (approximately 1 Hz) oscillatory phenomena reported by Brown et al. (2002) and Magill et al. (2001), respectively. Only the parameters required to mimic experimental conditions (e.g., anesthetic) or manipulations (e.g., lesions) were changed. From the results, we derive the following novel predictions about the STN-GP feedback loop: (1) the loop is functionally decoupled by tonic dopamine under normal conditions and recoupled by dopamine depletion; (2) the loop does not show pacemaking activity under normal conditions in vivo (but does after combined dopamine depletion and cortical lesion); (3) the loop has a resonant frequency in the gamma-band.

Action Potentials↗
PubMed2001

Electrophysiological and behavioral output of the rat basal ganglia after intrastriatal infusion of d-amphetamine: lack of support for the basal ganglia model.

Dopamine, by acting upon D1 and D2 dopamine receptors located on striatonigral and striatopallidal neurons, respectively, has been postulated to inhibit output from the substantia nigra pars reticulata (SNpr) and internal pallidal segment (GPi). The inhibition of the SNpr/GPi should, in turn, disinhibit the thalamus to facilitate movement. The present study tests this prediction in intact (unlesioned) rats by attempting to correlate changes in the single unit activities of SNpr neurons with motor (i.e. behavioral) responses in the 20-30 min after infusions of d-amphetamine into the striatum. Unilateral injections of amphetamine (20 microg/microl) into either the dorsal-rostral, central, or ventral-lateral striatum failed to appreciably alter behavior and, in parallel electrophysiological studies, failed to consistently or significantly alter the activities of SNpr neurons in either chloral hydrate-anesthetized rats or awake locally anesthetized rats. However, when amphetamine was infused bilaterally into the ventral-lateral striatum (VLS; 20 microg/microl per side), a robust behavioral activation ensued (increased locomotor activity, oral movements, and sniffing) with an onset ranging from immediate to 20 min post-infusion and persisting for at least 40 min. In parallel studies, bilateral amphetamine infusions into VLS also caused changes in the firing frequency of a majority of SNpr neurons. However, the changes in firing were extremely variable and, contrary to expectation, the net population response of SNpr neurons was an increase in firing which corresponded in time with the period of peak behavioral activation. These results show that (i) bilateral but not unilateral activation of striatal dopamine receptors is needed to elicit behavioral and electrophysiological output from the basal ganglia, and (ii) motor activation is apparently not signaled by a generalized inhibition of SNpr firing, as is predicted by the basal ganglia model.

Animals↗
PubMed1982

Basal ganglia.

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Basal Ganglia Diseases↗
PubMed1995

Balance of transmitter activities in the basal ganglia loops.

The basal ganglia of mammals are interconnected with the cortex in multiple loops. The main input station of the basal ganglia, the striatum, receives projections from the cortex and gives rise to two main pathways projecting back to the cortex by way of the thalamus: A direct pathway projecting to the thalamus via two GABAergic neurons and an indirect pathway that projects to the thalamus via three GABAergic neurons. Thus an excitatory cortical input to the striatum is either facilitatory (by the direct pathway) or inhibitory (by the indirect pathway) upon thalamic nuclei and on behaviour. It is speculated that by virtue of this, the basal ganglia are involved in a process of evaluation that results in suppression of "unwanted" and in facilitation of "wanted" behaviour. With decreasing dopamine activity in the striatum and in turn increasing inhibition of the thalamus, arbitrary switching of behaviours is suppressed, then externally guided behaviours predominate over internally guided behaviours and finally akinesia occurs. A loss of dopamine results in a relative overactivity of glutamate in the striatum and in an absolute glutamatergic overactivity in the medial segment of the globus pallidus and the substantia nigra pars reticulata. Reducing the glutamatergic overactivity at these sites by local injection of glutamate receptor-antagonists or by lesions reverses akinesia and rigidity. Systemically given, NMDA receptor-antagonists, either competitive-, non-competitive- or glycine-site-antagonists, are able to reverse parkinsonian symptoms in the rat.

Animals↗
PubMed2003

Information processing, dimensionality reduction and reinforcement learning in the basal ganglia.

Modeling of the basal ganglia has played a major role in our understanding of this elusive group of nuclei. Models of the basal ganglia have undergone evolutionary and revolutionary changes over the last 20 years, as new research in the fields of anatomy, physiology and biochemistry of these nuclei has yielded new information. Early models dealt with a single pathway through the nuclei and focused on the nature of the processing performed within it, convergence of information versus parallel processing of information. Later, the Albin-DeLong "box-and-arrow" model characterized the inter-nuclei interaction as multiple pathways while maintaining a simplistic scalar representation of the nuclei themselves. This model made a breakthrough by providing key insights into the behavior of these nuclei in hypo- and hyper-kinetic movement disorders. The next generation of models elaborated the intra-nuclei interactions and focused on the role of the basal ganglia in action selection and sequence generation which form the most current consensus regarding basal ganglia function in both normal and pathological conditions. However, new findings challenge these models and point to a different neural network approach to information processing in the basal ganglia. Here, we take an in-depth look at the reinforcement driven dimensionality reduction (RDDR) model which postulates that the basal ganglia compress cortical information according to a reinforcement signal using optimal extraction methods. The model provides new insights and experimental predictions on the computational capacity of the basal ganglia and their role in health and disease.

Animals↗
PubMed2002

Learning and memory functions of the Basal Ganglia.

Although the mammalian basal ganglia have long been implicated in motor behavior, it is generally recognized that the behavioral functions of this subcortical group of structures are not exclusively motoric in nature. Extensive evidence now indicates a role for the basal ganglia, in particular the dorsal striatum, in learning and memory. One prominent hypothesis is that this brain region mediates a form of learning in which stimulus-response (S-R) associations or habits are incrementally acquired. Support for this hypothesis is provided by numerous neurobehavioral studies in different mammalian species, including rats, monkeys, and humans. In rats and monkeys, localized brain lesion and pharmacological approaches have been used to examine the role of the basal ganglia in S-R learning. In humans, study of patients with neurodegenerative diseases that compromise the basal ganglia, as well as research using brain neuroimaging techniques, also provide evidence of a role for the basal ganglia in habit learning. Several of these studies have dissociated the role of the basal ganglia in S-R learning from those of a cognitive or declarative medial temporal lobe memory system that includes the hippocampus as a primary component. Evidence suggests that during learning, basal ganglia and medial temporal lobe memory systems are activated simultaneously and that in some learning situations competitive interference exists between these two systems.

Animals↗
PubMed1987

Anatomy and pathology of the basal ganglia.

Neurotransmitters of the basal ganglia are of three types: I, amino acids; II, amines; and III, peptides. The amino acids generally act ionotropically while the amines and peptides generally act metabotropically. There are many examples of neurotransmitter coexistence in basal ganglia neurons. Diseases of the basal ganglia are characterized by selective neuronal degeneration. Lesions of the caudate, putamen, subthalamus and substantia nigra pars compacta occur, respectively, in chorea, dystonia, hemiballismus and parkinsonism. The differing signs and symptoms of these diseases constitute strong evidence of the functions of these various nuclei. Basal ganglia diseases can be of genetic origin, as in Huntington's chorea and Wilson's disease, of infectious origin as in Sydenham's chorea and postencephalitic parkinsonism, or of toxic origin as in MPTP poisoning. Regardless of the etiology, the pathogenesis is often regionally concentrated for reasons that are poorly understood. From studies on Parkinson and Huntington disease brains, evidence is presented that a common feature may be the expression of HLA-DR antigen on reactive microglia in the region where pathological neuronal dropout is occurring.

Basal Ganglia↗