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PubMed2004

Reduced intracellular pH in the basal ganglia and whole brain measured by 31P-MRS in bipolar disorder.

The authors have previously reported that intracellular pH measured by phosphorus-31 magnetic resonance spectroscopy (31P-MRS) was decreased in the frontal lobes of patients with bipolar disorder. In the present study, phosphorus metabolism in the basal ganglia was examined in 13 patients with bipolar disorder and 10 matched controls by localized 31P-MRS. While no significant alteration of peak area ratios was found for all phosphorus metabolites, intracellular pH was significantly reduced in the basal ganglia in patients with bipolar disorder (7.014 +/- 0.045) compared with control subjects (7.066 +/- 0.047, P < 0.05). Unexpectedly, non-localized 31P-MR spectra also showed significantly lower levels of intracellular pH (6.970 +/- 0.025) than controls (6.986 +/- 0.024, P < 0.05). These results suggest that decreased intracellular pH in the brain of patients with bipolar disorder is not caused by dysfunction of the frontal lobes but reflect altered metabolism at the cellular level.

Adult↗
PubMed2001

Adenosine triphosphate and diadenosine pentaphosphate induce [Ca(2+)](i) increase in rat basal ganglia aminergic terminals.

Synaptosomal preparations from rat midbrain exhibit specific responses to both ATP and Ap(5)A, which stimulate a [Ca(2+)](i) increase in the presynaptic terminals via specific ionotropic receptors, termed P2X, and diadenosine polyphosphate receptors. Aminergic terminals from rat brain basal ganglia were characterized by immunocolocalization of synaptophysin and the vesicular monoamine transporter VMAT2 and represent 29% of the total. These aminergic terminals respond to ATP and/or Ap(5)A with an increase in the intrasynaptosomal calcium concentration as measured by a microfluorimetric technique. This technique, which allows single synaptic terminals to be studied, showed that roughly 8.2% +/- 1.6% of the aminergic terminals respond to ATP, 16.9% +/- 1.3% respond to Ap(5)A, 32.6% +/- 0.8% to both, and 42.3% +/- 1.5% of them have no response. Immunological studies performed with antibodies against ionotropic ATP receptor subunits showed positive labelling with anti-P2X(3) antibodies in 39% of the terminals. However, colocalization studies of VMAT and P2X(3) receptor subunit indicate that only 25% of the aminergic terminals also contain this receptor subtype. These results demonstrate that the aminergic terminals from the rat brain basal ganglia are to a large extent under the modulation of presynaptic nucleotide and dinucleotide receptors.

Adenosine Triphosphate↗
PubMed1997

HIV dementia and the basal ganglia.

Infection with the human immunodeficiency virus frequently results in a dementing illness which manifests predominantly as a subcortical dementia. Parkinsonian features may be prominent in these patients and may on occasion be the presenting manifestation. These patients are exquisitely sensitive to dopaminergic blocking agents. Radiological studies, metabolic uptake studies and pathological examination of the brain suggest that the basal ganglia are the major target of this infection. Although further studies are necessary to determine appropriate treatment for this condition and to develop an understanding of the underlying pathophysiological mechanisms, available evidence suggests that the response to dopamine agonists may be variable and that viral strains and viral products may specifically target cells within the basal ganglia.

AIDS Dementia Complex↗
PubMed1998

[Meige's syndrome associated with basal ganglia and thalamic functional disorders].

Magnetic resonance imaging (MRI) or single positron emission computed tomography (SPECT) or both were performed and the responses of surface electromyography (EMG) were examined in seven cases of Meige's syndrome. MRI or SPECT or both demonstrated lesions of the basal ganglia, the thalamus, or both in five of the cases. Surface EMG revealed abnormal burst discharges in the orbicularis oculi and a failure of reciprocal muscular activity between the frontalis and orbicularis oculi in all the cases. These findings suggest that voluntary motor control and reciprocal activity in the basal ganglia-thalamocortical circuits are impaired in Meige's syndrome. In addition, good responses were seen to clonazepam, tiapride and trihexyphenidyl in these cases. Therefore, we conclude that dopaminergic, cholinergic, and gamma-aminobutyric acid (GABA) ergic imbalances in the disorders of the basal ganglia and thalamus in Meige's syndrome cause control in the excitatory and inhibitory pathways to be lost, resulting in the failure of integration in reciprocal muscular activity and voluntary motor control. This failure subsequently causes the symptoms of Meige's syndrome.

Aged↗
PubMed2005

Basal ganglia infarction mimicking glioblastoma.

Modern brain imaging techniques usually allow a very good differential diagnosis of intracerebral lesions, but in some cases the differential diagnosis is difficult. We report the case of a 52 year old male with acute brachiofacial paresis and a hyperintense lesion with mass effect and ring-enhancement in basal ganglia suspiciously to a tumor. The neurosurgeons recommend stereotactical brain biopsy for diagnosis, but the patient recovered in following time gradually and in repeated computer tomographic images contrast enhancement disappeared and a hypodense zone in the basal ganglia remains. Our case demonstrates that brain infarctions can mimick glioblastoma in taking cystic appearance and contrast enhancement. Stereotactic biopsy would have been a precipitated invasive procedure in this case.

Basal Ganglia↗
PubMed1975

Basal ganglia scans in the human.

Using a 64Cu complex, we obtained human basal ganglia scans in three normal volunteers and in one patient with Wilson's disease with an oral dose of 1 mCi. The method with this new radioactive compound was simple and safe and the results were very encouraging.

Basal Ganglia↗
PubMedDate not supplied

[The role of the basal ganglia in monitorization of frontal lobe function].

OBJECTIVE: To review current understanding of the mechanisms controlling the activity of the frontal lobes and consider simple explanations of hypotheses regarding this. DEVELOPMENT: We describe the basic functional anatomy of the frontal cortex and its relation to the basal ganglia by means of five parallel fronto subcortical circuits (motor, oculomotor, dorsolateral, orbitofrontal and anterior cingulate. From the functional point of view we emphasize that the frontal cortex can keep certain zones active in relation to relevant tasks, and can be very flexible. These properties form the so called anterior attention system. We describe various recent models explaining frontal cortical activity in these terms, and emphasize those based on fronto subcortical circuits. These circuits control motor, cognitive, social and emotional behaviour. CONCLUSIONS: The cortical activity of the frontal lobes is regulated by various parallel, segregated fronto subcortical circuits. These circuits permit the selection and maintenance of activity of particular cortical regions regarding relevant conduct, whilst irrelevant conduct is inhibited. In this way they constitute the basic functional mechanism of the attention system described above. For prediction of the relevance or irrelevance of the consequences of each new stimulus, the anterior cingulate cortex probably establishes comparisons with previous situations which have already been stored together with certain somatic markers which indicate their emotional significance for the organism. This cortex fulfils the anatomical conditions necessary for regulation of the activity of the basal ganglia together with the whole frontal cortex so as to permit behaviour which is orderly from the time aspect.

Basal Ganglia↗
PubMed1980

Anterograde and transsynaptic degeneration 'en cascade' in basal ganglia induced by intrastriatal injection of kainic acid: an animal analogue of Huntington's disease.

Damage of striatal neurons by kainic acid (KA) induces an anterograde and transsynaptic degeneration 'en cascade' in the globus pallidus (GP) and substantia nigra (SN). By causing only degeneration of projections arising from KA-sensitive striatal neurons while sparing the connections of KA-resistant striatal neurons, the lesion-induced alterations of the basal ganglia show a characteristic pattern which bears a close resemblance with the neuropathological changes occurring in Huntington's disease: (1) severe degeneration of small and medium-sized striatal neurons, of pallidal neurons and the neurons of the pars reticulata of the SN, and (2) sparing of large striatal neurons, 'peripallidal' (nucleus basalis) neurons and neurons of the pars compacta of the SN. The probable interconnections of both the degenerated and the spared neuronal groups are discussed with respect to the present concept of the neuronal organization and biochemical neuroanatomy of the basal ganglia.

Acetylcholinesterase↗
PubMed2003

Unilateral absence of the basal ganglia plus epilepsy without motor symptoms.

A patient with absence of the basal ganglia and refractory epilepsy without impairment of pyramidal or extrapyramidal motor function is reported. Imaging findings suggest a vascular insult as etiology. Preserved motor function could be explained by neuronal plasticity involving contralateral corticostriatal and pallidothalamic connections and points to a lesion received in early pregnancy.

Adolescent↗
PubMed2004

Down-regulation of dopamine D1 and D2 receptors in the basal ganglia of PTZ kindling model of epilepsy: effects of angiotensin IV.

The present study examined the effect of pentylenetetrazol (PTZ) induced kindling as well as the action of the hexapeptide angiotensin IV (ANG IV) on the dopamine (DA) D1 and D2 receptor binding in the basal ganglia of the mouse brain. By using quantitative receptor autoradiography, it was found that PTZ kindling led to a decrease in DA D2 receptor density (about 20%) in all regions of the neostriatum (NS) as well as in the olfactory tubercle (OT), the nucleus accumbens (NA) and the globus pallidus, which persisted 24 h and 7 days after the kindling procedure. PTZ induced kindling also elicited a decrease in DA D1 receptor binding sites (about 10%), which however was, restricted to the rostral NS (rNA) and NA. ANG IV (0.2 mg/kg), injected prior to PTZ, not only prevented the development of the kindling process but it also reversed the kindling-induced down-regulation of both DA receptors to the control levels. Furthermore ANG IV induced an area-specific increase of DA D1 receptor density above control levels in the dorsal part of rNS. These findings suggest that DA D2 receptors could mainly contribute to epileptogenesis in the PTZ kindling model, whereas the role of DA D1 receptors is limited to particular regions in the basal ganglia. The anticonvulsant effect of ANG IV pretreatment might be influenced by a DA-related mechanism and particularly by preventing D2 receptor down-regulation as well as by an adaptive area-specific increase in DA D1 receptors.

Angiotensin II↗
PubMed1981

Hemichorea-hemiballism and lacunar infarction in the basal ganglia.

We present a case of acute hemichorea-hemiballism associated with lacunar infarct documented by computerized tomography scan in the contralateral putamen and caudate nuclei. The pathoanatomic data of similar cases in the literature are reviewed with reference to the location of the responsible lesions. Acute hemichorea-hemiballism is most frequently caused by lacunar infarcts in the basal ganglia contralateral to the dyskinesia.

Basal Ganglia↗
PubMed1978

[Effect of neuroleptics on acetylcholine metabolism in the basal ganglia of the brain].

Neuroleptics (haloperidol) closapine, pimozid, chlorpromazine) diminished the level of free (functionally active) form of acetylcholine (ACh), and, to some extent, the bound form of ACh; they changed the content of the labile-bound (vesicular) form of ACh and weakly influenced the choline-acetyltranspherase activity in the basal ganglia of the rat brain 5 to 30 min after the injection. In contrast to the inhibitory action on the acetyl-cholinesterase (AChE) activity in vitro, most of the neuroleptics, except closapine, increased the AChE activity in vivo. These results indicate that the neuroleptics activate ACh-metabolism and probably stimulate the cholinergic structure in the basal ganglia of the brain; the AChE activity may serve as a criterion of such stimulating action of neuroleptics.

Acetylcholine↗
PubMed2004

Evidence for a role of basal ganglia in the regulation of rapid eye movement sleep by electrical and chemical stimulation for the pedunculopontine tegmental nucleus and the substantia nigra pars reticulata in decerebrate cats.

The present study was to determine how afferents from the substantia nigra pars reticulata (SNr) of the basal ganglia to the pedunculopontine tegmental nucleus (PPN) in the brainstem could contribute to the control of behavioral states. We used anesthetized and acutely decerebrated cats (n=22). Repetitive electrical stimulation (10-100 Hz, 20-50 microA, for 4-20 s) to the ventrolateral part of the PPN produced rapid eye movement (REM) associated with a suppression of postural muscle tone (REM with atonia). Although repetitive electrical stimuli (10-200 Hz, 10-60 microA, for 5-20 s) delivered to the dorsolateral part of the SNr did not evoke eye movements or muscular tonus in baseline conditions, it altered the PPN-induced REM with atonia. The following three types of effects were induced: (1) attenuation of the REM with atonia; (2) attenuation of muscular atonia without changes in REM (REM without atonia); and (3) attenuation of only REM. The optimal stimulus sites for these effects were intermingled within the lateral part of the SNr. The PPN-induced REM with atonia was abolished by an injection into the PPN of muscimol (1-15 mM, 0.1-0.25 microl), a GABAA receptor agonist, but not altered by an injection of baclofen (1-10 mM, 0.1-0.25 microl), a GABAB receptor agonist. Moreover, an injection of bicuculline (1-15 mM, 0.1-0.25 microl), a GABAA receptor antagonist, into the PPN, resulted in REM with atonia. On the other hand, an injection of muscimol into the dorsolateral part of the SNr (1-15 mM, 0.1-0.25 microl) induced REM with atonia, which was in turn eliminated by a further injection of muscimol into the PPN (5-10 mM, 0.2-0.25 microl). These results suggest that a GABAergic projection from the SNr to the PPN could be involved in the control of REM with atonia, signs which indicate REM sleep. An excessive GABAergic output from the basal ganglia to the PPN in parkinsonian patients may induce sleep disturbances, including a reduction of REM sleep periods and REM sleep behavioral disorders (REM without atonia).

Animals↗
PubMed1994

D2 dopamine receptor binding in the basal ganglia of antipsychotic-free schizophrenic patients. An 123I-IBZM single photon emission computerised tomography study.

We used SPECT to examine striatal D2 receptor binding in 20 antipsychotic-free DSM-III-R schizophrenic patients and 20 age- and sex-matched normal controls. Dynamic single-slice SPECT, at a slice chosen to include the basal ganglia, began immediately following intravenous injection of 185 MBq of 123I-IBZM. A semiquantitative approach was used to generate indices of specific D2 receptor binding in the basal ganglia. There was no overall elevation of D2 receptor binding between patients and controls. A male sex-specific left lateralised asymmetry of striatal D2 receptor binding was found in the patient group. Age-dependent decline of striatal D2 receptors was confirmed in controls, but not in patients. These results suggest that alterations in striatal D2 receptor distribution and density do occur in schizophrenia, and possibly reflect wider disruptions in prefrontal-striatal-limbic circuits.

Adolescent↗
PubMedDate not supplied

[Basal ganglia and behavior].

A comparative analysis of the most well known hypotheses of basal ganglia participation in organisation and control of behavioural functions, is presented.

Animals↗
PubMedDate not supplied

Basal ganglia neural mechanisms of natural movement sequences.

Natural rodent grooming and other instinctive behavior serves as a natural model of complex movement sequences. Rodent grooming has syntactic (rule-driven) sequences and more random movement patterns. Both incorporate the same movements--only the serial structure differs. Recordings of neural activity in the dorsolateral striatum and the substantia nigra pars reticulata indicate preferential activation during syntactic sequences over more random sequences. Neurons that are responsive during syntactic grooming sequences are often unresponsive or have reverse activation profiles during kinematically similar movements that occur in flexible or random grooming sequences. Few neurons could be categorized as strictly movement related--instead they were activated only in the context of particular sequential patterns of movements. Particular sequential patterns included "syntactic chain" grooming sequences of paw, head, and body movements and also "warm-up" sequences, which consist of head and body/limb movements that precede locomotion after a period of quiet resting (Golani 1992). Activation during warm-up was less intense and less frequent than during grooming sequences, but both sequences activated neurons above baseline levels, and the same neurons sometimes responded to both sequences. The fact that striatal neurons code 2 natural sequences which are made up of different constituent movements suggests that the basal ganglia may have a generalized role in sequence control. The basal ganglia are modulated by the context of the sequence and may play an executive function in the complex natural patterns of sequenced behaviour.

Animals↗
PubMed2002

Neurochemical organization of the human basal ganglia: anatomofunctional territories defined by the distributions of calcium-binding proteins and SMI-32.

The distribution of the calcium-binding proteins calbindin-D28K (CB), parvalbumin (PV) and calretinin (CR), and of the nonphosphorylated neurofilament protein (with SMI-32) was investigated in the human basal ganglia to identify anatomofunctional territories. In the striatum, gradients of neuropil immunostaining define four major territories: The first (T1) includes all but the rostroventral half of the putamen and is characterized by enhanced matriceal PV and SMI-32 immunoreactivity (-ir). The second territory (T2) encompasses most part of the caudate nucleus (Cd) and rostral putamen (PuT), which show enhanced matriceal CB-ir. The third and fourth territories (T3 and T4) comprise rostroventral parts of Cd and PuT characterized by complementary patch/matrix distributions of CB- and CR-ir, and the accumbens nucleus (Acb), respectively. The latter is separated into lateral (prominently enhanced in CB-ir) and medial (prominently enhanced in CR-ir) subdivisions. In the pallidum, parallel gradients also delimit four territories, T1 in the caudal half of external (GPe) and internal (GPi) divisions, characterized by enhanced PV- and SMI-32-ir; T2 in their rostral half, characterized by enhanced CB-ir; and T3 and T4 in their rostroventral pole and in the subpallidal area, respectively, both expressing CB- and CR-ir but with different intensities. The subthalamic nucleus (STh) shows contrasting patterns of dense PV-ir (sparing only the most medial part) and low CB-ir. Expression of CR-ir is relatively low, except in the medial, low PV-ir, part of the nucleus, whereas SMI-32-ir is moderate across the whole nucleus. The substantia nigra is characterized by complementary patterns of high neuropil CB- and SMI-32-ir in pars reticulata (SNr) and high CR-ir in pars compacta (SNc) and in the ventral tegmental area (VTA). The compartmentalization of calcium-binding proteins and SMI-32 in the human basal ganglia, in particular in the striatum and pallidum, delimits anatomofunctional territories that are of significance for functional imaging studies and target selection in stereotactic neurosurgery.

Aged↗
PubMed1984

Primate model of Parkinson's disease: alterations in multiple opioid systems in the basal ganglia.

A motor disorder similar to idiopathic Parkinson's Disease develops in rhesus monkeys after several daily repeated doses of N-methyl-4-phenyl, 1,2,3,6-tetrahydropyridine (MPTP). The concentrations of peptides derived from proenkephalin A, proenkephalin B, substance P and somatostatin were measured by specific radioimmunoassays in the basal ganglia of MPTP-treated monkeys. In MPTP-treated monkeys, dynorphin B concentration was reduced in the caudate. In the putamen, the concentrations of peptides derived from both proenkephalin A and proenkephalin B were decreased. In the globus pallidus, the concentrations of all opioid peptides tend to be increased, reaching significance only for alpha-neo-endorphin. In the substantia nigra, only Met-enkephalin concentration was reduced, while other peptides derived from either proenkephalin A or proenkephalin B were not changed. Substance P and somatostatin were not changed in any brain area examined. Some of the symptoms associated with Parkinson's Disease may be related to altered activity of endogenous opiates in basal ganglia.

Animals↗