Topographical projections of the cerebral cortex to the subthalamic nucleus

Afsharpour, Salman

doi:10.1002/cne.902360103

Cited by 162 publications

(89 citation statements)

References 31 publications

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“…However, this hypothesis implies that dopamine receptors in the STN exert an inhibitory effect on STN neuronal activity, which is at odds with results from this laboratory that demonstrate that locally infused dopaminergic agonists excite STN neurons in the intact rat . Another factor that could contribute to the increased activity of STN neurons in the lesioned rat is an enhancement of excitatory input (Overton and Greenfield, 1995;Hassani et al, 1996), putatively from the cortex that is a major source of glutamatergic afferents (Afsharpour, 1985;Rouzaire-Dubois and Scarnati, 1987;Canteras et al, 1990). Observations that stimulation of cortical neurons increased bursting activity (Kitai and Deniau, 1981;Fujimoto and Kita, 1993) and c-fos expression in the STN (Wan et al, 1992) are supportive of this hypothesis.…”

Section: Discussionmentioning

confidence: 99%

“…One explanation for these unpredicted observations is that dopamine receptor stimulation at extrastriatal sites predominately influences the STN. For instance, the STN is modulated by afferents from cortical areas (Afsharpour, 1985;Campbell et al, 1985;Canteras et al, 1990) that are innervated by midbrain dopamine cells (Björklund and Lindvall, 1984;Descarries et al, 1987;Van Eden et al, 1987). In addition, the STN itself receives direct input from dopamine neurons (Meibach and Katzman, 1979;Campbell et al, 1985;Canteras et al, 1990;Hassani et al, 1997).…”

Section: Analysis; Firing Patternmentioning

confidence: 99%

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The Response of Subthalamic Nucleus Neurons to Dopamine Receptor Stimulation in a Rodent Model of Parkinson’s Disease

et al. 1997

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Overactivity in the subthalamic nucleus (STN) is believed to contribute to the pathophysiology of Parkinson's disease. It is hypothesized that dopamine receptor agonists reduce neuronal output from the STN. The present study tests this hypothesis by using in vivo extracellular single unit recording techniques to measure neuronal activity in the STN of rats with 6-hydroxydopamineinduced lesions of the nigrostriatal pathway (a model of Parkinson's disease). As predicted, firing rates of STN neurons in lesioned rats were tonically elevated under basal conditions and were decreased by the nonselective dopamine receptor agonists apomorphine and L-3,4-dihydroxyphenylalanine (L-DOPA). STN firing rates were also decreased by the D2 receptor agonist quinpirole when administered after the D1 receptor agonist (Ϯ)-1-phenyl-2,3,4,5-tetrahydro-(1H)-3-benzazepine-7,8-diol (SKF 38393). Results of the present study challenge the prediction that dopaminergic agonists reduce STN activity predominantly through actions at striatal dopamine D2 receptors. Firing rates of STN neurons were not altered by selective stimulation of D2 receptors and were increased by selective stimulation of D1 receptors. Moreover, there was a striking difference between the responses of the STN to D1/D2 receptor stimulation in the lesioned and intact rat; apomorphine inhibited STN firing in the lesioned rat and increased STN firing in the intact rat. These findings support the premise that therapeutic efficacy in the treatment of Parkinson's disease is associated with a decrease in the activity of the STN, but challenge assumptions about the roles of D1 and D2 receptors in the regulation of neuronal activity of the STN in both the intact and dopamine-depleted states.

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Section: Discussionmentioning

confidence: 99%

Section: Analysis; Firing Patternmentioning

confidence: 99%

The Response of Subthalamic Nucleus Neurons to Dopamine Receptor Stimulation in a Rodent Model of Parkinson’s Disease

et al. 1997

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“…The asymmetries observed in the motor cortex were the same in both control and experimental groups, reflecting a non specific effect of the electrode that passes through the same structures in all stimulated and sham operated animals. Given the well established ros trocortical projections to the STH (Afsharpour, 1985;Rouzaire-Dubois and Scarnati, 1985;Can teras et aI., 1988;Ryan and Clark, 1991), the failure …”

Section: Effects Elicited In Motor Areasmentioning

confidence: 99%

“…the cerebral cortex (Hartmann-Von Monakow et ai., 1978;Romansky et ai., 1979;Kitai and Deniau, 1981;Afsharpour 1985;Rouzaire-Dubois and Scar nati, 1985;Canteras et ai., 1988). It also receives moderate projections from the parafascicular tha lamic nucleus (Sugimoto et ai., 1983;Canteras et ai., 1990;Groenewegen and Berendse, 1990) and the pedunculopontine tegmental nucleus (Nomura et ai.…”

mentioning

confidence: 99%

Functional Metabolic Mapping of the Rat Brain during Unilateral Electrical Stimulation of the Subthalamic Nucleus

Tzagournissakis

Dermon

Savaki

1994

J Cereb Blood Flow Metab

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Summary:The alterations in local metabolic activity of several anatomically distinct brain areas were investi gated by means of the quantitative autoradiographic 2-deoxY-D-[l-14C]glucose method in awake rats during uni lateral electrical stimulation of the subthalamic nucleus (STH). Unilateral electrical stimulation of the STH in duced local metabolic activation (by 70% as compared with the control group), as well as distal metabolic acti vations in the substantia nigra reticulata (by 34%), globus pallidus (by 19%), entopeduncular nucleus (by 18%), deep layers of the superior colliculi (by 15%), and para fascicular thalamic nucleus (by 18%), ipsilaterally to the stimulated side. The ventrolateral motor thalamic nucleus as well as the limbic components, posterior cingulate cor tex, and anteroventral thalamic nucleus displayed bilat eral metabolic activations (by 20--28%). These results in dicate that, in addition to its known ipsilateral motor conThe subthalamic nucleus (STH) is generally con sidered to exert control over motor functions. The association of STH hypoactivity with the clinical syndrome of hemiballismus has long been docu mented (Whittier, 1947;Whittier and Mettler, 1949;Carpenter and Carpenter, 1951; Hammond et ai., 1979; Mitchel et ai., 1985a; Crossman, 1987 132nections, each STH is functionally related to the limbic system bilaterally. It is suggested that the STH is a site where the central motor information is accessible to the limbic system. Quantitative image analysis of individual serial sections in the STH, substantia nigra, and globus pallidus revealed a consistent dorsoventral pattern of to pographic interrelations. Stimulation of either the dorsal or the ventral subdivision of the STH induced always stronger activation in the dorsal compartment of the sub stantia nigra and in the ventral compartment of the globus pallidus. These results suggest that the earlier-described inversion of the dorsoventral functional correspondence between the substantia nigra and globus pallidus may be partly mediated via the subthalamic nerve cells projecting collateral axons to both these areas.

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“…STN neurons integrate powerful monosynaptic glutamatergic inputs originating from corticosubthalamic (CSth) neurons and relay these excitatory signals to the SNr and the globus pallidus (GP) (Deniau et al, 1978;Van Der Kooy and Hattori, 1980;Kitai and Deniau, 1981;Afsharpour, 1985;Rouzaire-Dubois and Scarnati, 1987;Maurice et al, 1998;Magill et al, 2000). GABAergic neurons of the GP shape the activity of STN neurons by a disinhibitory mechanism involving corticostriatal and striatopallidal pathways (Maurice et al, 1998;Bevan et al, 2002b) and via reciprocal connections with the STN Bevan et al, 2002b).…”

Section: Introductionmentioning

confidence: 99%

Rhythmic Bursting in the Cortico-Subthalamo-Pallidal Network during Spontaneous Genetically Determined Spike and Wave Discharges

Paz¹,

Deniau²,

Charpier³

2005

J. Neurosci.

110

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Absence seizures are characterized by impairment of consciousness associated with bilaterally synchronous spike-and-wave discharges (SWDs) in the electroencephalogram (EEG), which reflect paroxysmal oscillations in thalamocortical networks. Although recent studies suggest that the subthalamic nucleus (STN) provides an endogenous control system that influences the occurrence of absence seizures, the mechanisms of propagation of cortical epileptic discharges in the STN have never been explored. The present study provides the first description of the electrophysiological activity in the cortico-subthalamo-pallidal network during absence seizures in the genetic absence epilepsy rats from Strasbourg, a well established model of absence epilepsy. In corticosubthalamic neurons, the SWDs were associated with repetitive suprathreshold depolarizations correlated with EEG spikes. These cortical paroxysms were reflected in the STN by synchronized, rhythmic, high-frequency bursts of action potentials. Intracellular recordings revealed that the intraburst pattern in STN neurons was sculpted by an early depolarizing synaptic potential, followed by a short hyperpolarization and a rebound of excitation. The rhythmic hyperpolarizations in STN neurons during SWDs likely originate from a subpopulation of pallidal neurons exhibiting rhythmic bursting temporally correlated with the EEG spikes. The repetitive discharges in STN neurons accompanying absence seizures might convey powerful excitation to basal ganglia output nuclei and, consequently, may participate in the control of thalamocortical SWDs.

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Topographical projections of the cerebral cortex to the subthalamic nucleus

Cited by 162 publications

References 31 publications

The Response of Subthalamic Nucleus Neurons to Dopamine Receptor Stimulation in a Rodent Model of Parkinson’s Disease

The Response of Subthalamic Nucleus Neurons to Dopamine Receptor Stimulation in a Rodent Model of Parkinson’s Disease

Functional Metabolic Mapping of the Rat Brain during Unilateral Electrical Stimulation of the Subthalamic Nucleus

Rhythmic Bursting in the Cortico-Subthalamo-Pallidal Network during Spontaneous Genetically Determined Spike and Wave Discharges

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