Response characteristics of subthalamic neurons to the stimulation of the sensorimotor cortex in the rat

Fujimoto, Ken’ichi; Kita, Hitoshi

doi:10.1016/0006-8993(93)90872-k

Cited by 201 publications

(170 citation statements)

References 26 publications

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“…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. However, preliminary studies from this laboratory found that the glutamatergic antagonists (5R,10S)-(ϩ)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]-cyclohepten-5,10-imine and 1,2,3,4-tetrahydro-6-nitro-2 ,3-dioxo-benzo[ f ]quinoxaline-7-sulfonamide, did not alter average neuronal firing rates in the subthalamus of either the intact or lesioned rat (Thompson and Walters, 1993;Allers et al, 1996).…”

Section: Discussionmentioning

confidence: 71%

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: 71%

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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“…( Figure 7D), a latency very close to the lower margin of subthalamic firing triggered by cortico-subthalamic transmission based on intracellular and single-unit recordings in normal rats (29,30,35) and much faster than the modulation traveling via the indirect pathway (30,(36)(37)(38). The time-dependent spike distribution was also abolished by local infusion of AP5 into the STN ( Figure 7, C and D), lending strong support to the notion that the cortico-subthalamic pathway profoundly alters STN firing via the NMDA receptor.…”

Section: Subthalamic Nmda Receptor Blocker Remedies Hypokinetic Movemmentioning

confidence: 84%

“…Normal rats showed a typical 2-peak distribution in the spike histogram ( Figure 7C). The first and second peaks, which are located at 15 to 25 ms and 55 to 65 ms, are related to cortico-subthalamic input (29,30,35) and separated by an interpeak suppression period ascribable to the indirect pathway (30,36). In contrast, parkinsonian rats showed only a single, strictly time-locked peak at approximately 9 ms Quantitative measurement of burst-firing (in burst mode) and spike-firing (in spike mode) frequencies.…”

Section: Subthalamic Nmda Receptor Blocker Remedies Hypokinetic Movemmentioning

confidence: 99%

Deranged NMDAergic cortico-subthalamic transmission underlies parkinsonian motor deficits

Pan¹,

Tai²,

Liu³

et al. 2014

J. Clin. Invest.

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“…In our model, we consider the existence of a transmission delay between STN and GPe neurons. We were unable to find experimental studies investigating the delay in transmission from GPe to STN in monkeys, and hence used the value from an analogous study in rat (Fujimoto and Kita, 1993). We were also unable to find studies investigating transmission delays between two GPe neurons.…”

Section: Determining Model Parameters From Experimental Studiesmentioning

confidence: 99%

Conditions for the Generation of Beta Oscillations in the Subthalamic Nucleus–Globus Pallidus Network

Nevado‐Holgado¹,

Terry²,

Bogacz³

2010

J. Neurosci.

238

292

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The advance of Parkinson's disease is associated with the existence of abnormal oscillations within the basal ganglia with frequencies in the beta band (13-30 Hz). While the origin of these oscillations remains unknown, there is some evidence suggesting that oscillations observed in the basalgangliaariseduetointeractionsoftwonuclei:thesubthalamicnucleus(STN)andtheglobuspallidusparsexterna(GPe).Toinvestigatethis hypothesis, we develop a computational model of the STN-GPe network based upon anatomical and electrophysiological studies. Significantly, our study shows that for certain parameter regimes, the model intrinsically oscillates in the beta range. Through an analytical study of the model, we identify a simple set of necessary conditions on model parameters that guarantees the existence of beta oscillations. These conditions for generation of oscillations are described by a set of simple inequalities and can be summarized as follows: (1) The excitatory connections from STN to GPe and the inhibitory connections from GPe to STN need to be sufficiently strong. (2) The time required by neurons to react to their inputs needs to be short relative to synaptic transmission delays. (3) The excitatory input from the cortex to STN needs to be high relative to the inhibition from striatum to GPe. We confirmed the validity of these conditions via numerical simulation. These conditions describe changes in parameters that are consistent with those expected as a result of the development of Parkinson's disease, and predict manipulations that could inhibit the pathological oscillations.

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Response characteristics of subthalamic neurons to the stimulation of the sensorimotor cortex in the rat

Cited by 201 publications

References 26 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

Deranged NMDAergic cortico-subthalamic transmission underlies parkinsonian motor deficits

Conditions for the Generation of Beta Oscillations in the Subthalamic Nucleus–Globus Pallidus Network

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