Metabolic effects of nigrostriatal denervation in basal ganglia

Hirsch, Étienne C.; Perier, Céline; Orieux, Gaël; François, Chantal; Féger, J.; Yelnik, Jérôme; Vila, Miquel; Lévy, Richard; Tolosa, Eduardo; Marı́n, Concepció; Herrero, María Trinidad; Obeso, José A.; Agid, Yves

doi:10.1016/s1471-1931(00)00021-5

Cited by 92 publications

(59 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Neuronal activity of the pedunculopontine and STN as well as the cortico-striatal afferents is known to be increased in the parkinsonian state. 29 It was therefore conceivable that the CM glutamatergic interconnections with the basal ganglia could be engaged in a network self-perpetuating the hyperactive state. Blockade or lesion of the STN and PPN improves parkinsonian features in animal models.…”

Section: Discussionmentioning

confidence: 99%

“…[23][24][25] In recent years, a number of studies have suggested a possible role for the CM-Pf complex on the pathophysiology of movement disorders. 26,27 In rats, Pf neurons that innervate the STN 28,29 and the striatum 25 are known to be hyperactive after unilateral midbrain dopaminergic lesion with 6-hydroxydopamine (6-OHDA). Indeed, the chemical ablation of Pf in rodents is highly effective in reversing the increases on STN metabolic activity typically observed after dopamine depletion.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Lesion of the centromedian thalamic nucleus in MPTP‐treated monkeys

et al. 2008

View full text Add to dashboard Cite

The caudal intralaminar nuclei are a major source of glutamatergic afferents to the basal ganglia. Experiments in the 6-hydroxydopamine rat model have shown that the parafascicular nucleus is overactive and its lesion alleviates basal ganglia neurochemical abnormalities associated with dopamine depletion. Accordingly, removal of this excitatory innervation of the basal ganglia could have a beneficial value in the parkinsonian state. To test this hypothesis, unilateral kainate-induced chemical ablation of the centromedian thalamic nucleus (CM) has been performed in MPTPtreated monkeys. Successful lesions restricted to the CM boundaries (n = 2) without spreading over other neighboring thalamic nuclei showed an initial, short-lasting, and mild change in the parkinsonian motor scale but no effect against levodopa-induced dyskinesias. The lack of significant and persistent motor improvement leads us to conclude that unilateral selective lesion of the CM alone cannot be considered as a suitable surgical approach for the treatment of PD or levo-dopa-induced dyskinesias. The role of the caudal intralaminar nuclei in the pathophysiology of movement disorders of basal ganglia origin remains to be clarified. HHS Public Access Author Manuscript Author ManuscriptAuthor Manuscript Author ManuscriptThe centromedian-parafascicular thalamic complex (CM-Pf) is one major source of glutamatergic innervation of several basal ganglia nuclei, including the striatum, 1-15 the subthalamic nucleus (STN), 4,7,[12][13][14][15][16][17][18][19][20][21] the globus pallidus, and the substantia nigra. 15,21,22 Projections arising from the caudal intralaminar nuclei are excitatory and use glutamate as neurotransmitter. [23][24][25] In recent years, a number of studies have suggested a possible role for the CM-Pf complex on the pathophysiology of movement disorders. 26,27 In rats, Pf neurons that innervate the STN 28,29 and the striatum 25 are known to be hyperactive after unilateral midbrain dopaminergic lesion with 6-hydroxydopamine (6-OHDA). Indeed, the chemical ablation of Pf in rodents is highly effective in reversing the increases on STN metabolic activity typically observed after dopamine depletion. 30 Interestingly, early observations considered the CM/Pf as a target by deep brain stimulation (DBS) for the treatment of levodopainduced dyskinesias in Parkinson's disease, [31][32][33] and this has recently been proposed in combination with DBS of the globus pallidus pars interna (GPi). 34 On the other hand, important cell loss has been described in the CM-Pf of PD patients 35 as well as in rodents after nigrostriatal damage. 25,36 To further assess the relevance of the CM/Pf as a potential therapeutic target for parkinsonism and levodopa-induced dyskinesias, we have performed chemical ablation of the caudal intralaminar nuclei in MPTP-treated monkeys and determined its impact on parkinsonian motor signs and dyskinesias. SUBJECTS AND METHODSA total number of five young adult male Macaca fascicularis primates (body weight ranging fr...

show abstract

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Lesion of the centromedian thalamic nucleus in MPTP‐treated monkeys

et al. 2008

View full text Add to dashboard Cite

show abstract

“…Both CO-I protein levels and mRNA coding for the subunits of CO-I are responsive to changes in neuronal activity, allowing analyses of regional, cellular, and subcellular functional levels Wong-Riley 1990, 1991;Wong-Riley 1989). Expression of CO-I correlated with neuronal firing in the basal ganglia after chronic nigrostriatal lesions (Hirsch et al 2000;Vila et al 2000). In addition, the anatomical resolution of CO-I histochemistry is better than that of 2-deoxyglucose autoradiography (Hevner et al 1995;Wong-Riley 1989).…”

Section: Discussionmentioning

confidence: 99%

“…Thus, by assessing cytochrome oxidase I (CO-I) histochemistry, we investigated whether ventral tegmental area (VTA) stimulation affects PFC metabolic levels and how these changes become altered in NVHL animals. This method was preferred because CO-I levels are tightly coupled to neuronal firing (Hirsch et al 2000;Wong-Riley 1989) and provide a better anatomical resolution than that obtained from 2-deoxyglucose autoradiography (Hevner et al 1995).…”

mentioning

confidence: 99%

Altered Prefrontal Cortical Metabolic Response to Mesocortical Activation in Adult Animals with a Neonatal Ventral Hippocampal Lesion

Tseng

Amin

Lewis

et al. 2006

Biological Psychiatry

View full text Add to dashboard Cite

Background-Adult animals with a neonatal ventral hippocampal lesion (NVHL) exhibit deficits in working memory and sensorimotor gating similar to those observed in schizophrenia. As cognitive deficits in this disorder are typically associated with changes in cortical metabolic levels, we investigated here whether an NVHL affects metabolic responses to ventral tegmental area (VTA) activation, a procedure that elicits abnormal cell firing in the prefrontal cortex (PFC) of NVHL animals.

show abstract

“…The STN represents the only excitatory drive in the basal ganglia since it sends glutamatergic projections to the SNr and the GPe. DA denervation causes overactivity and metabolic changes in the STN and its target areas (for a recent review, see Hirsch et al 2000) which can be prevented by STN lesion (Bergman et al 1990;Delfs et al 1995) and by glutamate antagonists (Vila et al 1999). Remarkably, surgical lesion as well as functional impairment (with deep brain stimulation) of STN improves parkinsonism and reduces levodopa-induced dyskinesias in humans (Fraix et al 2000;Obeso et al 2000).…”

mentioning

confidence: 99%

Striatal dopamine–NMDA receptor interactions in the modulation of glutamate release in the substantia nigra pars reticulata in vivo: opposite role for D₁ and D₂ receptors

Marti

Mela

Bianchi

et al. 2002

Journal of Neurochemistry

View full text Add to dashboard Cite

Dual probe microdialysis was employed in conscious rats to investigate whether endogenous dopamine is involved in the stimulation of glutamate release in the substantia nigra pars reticulata following striatal NMDA receptor activation. Intrastriatal perfusion with NMDA (1 and 10 lM) facilitated nigral glutamate release (dizocilpine-and tetrodotoxin-sensitive). The D 2 dopamine receptor antagonist raclopride increased spontaneous nigral glutamate release and caused a leftward shift in the NMDA sensitivity, lowering NMDA effective concentrations to submicromolar levels. Conversely, the D 1 antagonist SCH23390 prevented the effect of NMDA (1 lM) and caused a rightward shift in the NMDA sensitivity. It was tested whether the antagonist effects were due to dopamine receptor blockade or increased tone on D 1 /D 2 receptors. SCH23390 prevented the raclopride-induced enhancement of spontaneous but not NMDA-evoked glutamate release while raclopride left unchanged the SCH23390-induced inhibition. The physiopathological relevance of the dopaminergic modulation was strengthened by perfusing NMDA in the dopaminedepleted striatum of hemiparkinsonian rats. Nigral glutamate responsiveness to NMDA was enhanced as with raclopride. We conclude that endogenous striatal dopamine regulates both spontaneous and NMDA-induced nigral glutamate release via an opposite control mediated by D 1 facilitatory and D 2 inhibitory receptors. Alterations of this control may subserve the motor symptoms of Parkinson's disease.

show abstract

Metabolic effects of nigrostriatal denervation in basal ganglia

Cited by 92 publications

References 46 publications

Lesion of the centromedian thalamic nucleus in MPTP‐treated monkeys

Lesion of the centromedian thalamic nucleus in MPTP‐treated monkeys

Altered Prefrontal Cortical Metabolic Response to Mesocortical Activation in Adult Animals with a Neonatal Ventral Hippocampal Lesion

Striatal dopamine–NMDA receptor interactions in the modulation of glutamate release in the substantia nigra pars reticulata in vivo: opposite role for D₁ and D₂ receptors

Contact Info

Product

Resources

About

Metabolic effects of nigrostriatal denervation in basal ganglia

Cited by 92 publications

References 46 publications

Lesion of the centromedian thalamic nucleus in MPTP‐treated monkeys

Lesion of the centromedian thalamic nucleus in MPTP‐treated monkeys

Altered Prefrontal Cortical Metabolic Response to Mesocortical Activation in Adult Animals with a Neonatal Ventral Hippocampal Lesion

Striatal dopamine–NMDA receptor interactions in the modulation of glutamate release in the substantia nigra pars reticulata in vivo: opposite role for D1 and D2 receptors

Contact Info

Product

Resources

About

Striatal dopamine–NMDA receptor interactions in the modulation of glutamate release in the substantia nigra pars reticulata in vivo: opposite role for D₁ and D₂ receptors