Electrophysiological demonstration of an excitatory subthalamonigral pathway in the rat

Hammond, Constance; Deniau, Jean-Michel; Rizk, Aurélien; Féger, J.

doi:10.1016/0006-8993(78)90881-8

Cited by 176 publications

(67 citation statements)

References 18 publications

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“…The high GLU sensitivity of SNr units found in anesthetized rats is also strongly supported by abundant neuroanatomical and electrophysiological data (Hammond et al, 1978;Waszczak and Walters, 1983;Robledo and Feger, 1990;Schmitt et al, 1999). Under these conditions, most of the cells tested showed large and consistent increases in firing rate during GLU applications.…”

Section: Discussionsupporting

confidence: 55%

“…Although the inhibitory and excitatory effects of GABA and GLU on SNr cells have long been known and some of their specific receptor-mediated contributions to the overall neuronal activity have been described (Hammond et al, 1978;Collingridge and Davies, 1981;Waszczak and Walters, 1983;Nakanishi et al, 1987;Robledo and Feger, 1990;Celada et al, 1999;Schmitt et al, 1999), most of these studies have been conducted on anesthetized animals. Although this approach provides stable, controlled conditions under which neurons can be studied, the influence of anesthesia as a confounding factor on neural activity and afferent responsiveness remains unclear.…”

Section: Introductionmentioning

confidence: 99%

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GABA, Not Glutamate, Controls the Activity of Substantia Nigra Reticulata Neurons in Awake, Unrestrained Rats

Windels

Kiyatkin²

2004

J. Neurosci.

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Substantia nigra pars reticulata (SNr) receives both GABAergic and glutamatergic (GLU) inputs that are believed to act together to regulate neuronal activity in this structure. To examine the role of these inputs, single-unit recording was coupled with iontophoresis of GLU and GABA in rats under two conditions: awake, unrestrained and under chloral hydrate anesthesia. Although GABA potently inhibited SNr cells in both conditions, freely moving rats showed lower sensitivity than anesthetized animals. Likewise, GLU effectively induced excitations in most SNr neurons in anesthetized animals but was much less effective in awake, unrestrained animals in terms of both the number of sensitive cells and the magnitude of GLU-induced excitation. These findings, along with consistent excitations induced by bicuculline in awake, unrestrained rats, suggest that modulation of GABA inhibitory input, not the opposing actions of GLU and GABA, is the primary factor that regulates the activity state of SNr neurons.

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Section: Discussionsupporting

confidence: 55%

Section: Introductionmentioning

confidence: 99%

GABA, Not Glutamate, Controls the Activity of Substantia Nigra Reticulata Neurons in Awake, Unrestrained Rats

Windels

Kiyatkin²

2004

J. Neurosci.

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“…The SN receives glutamatergic afferents from the cortex and the STN (Hammond et al 1978 ;Chang et al 1984 ;Smith et al 1990 ;Naito & Kita, 1994). However, behavioural changes can be induced by intranigral infusion of NMDA.…”

Section: Substantia Nigramentioning

confidence: 99%

NMDA receptors in the basal ganglia

Ravenscroft

Brotchie

2000

Journal of Anatomy

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The basal ganglia consist of several interconnected nuclei located in the telecephalon, diencephalon and mesencephalon that are involved in a variety of motor and non-motor behavioural functions. Glutamate receptors play a major role in neurotransmission within the basal ganglia and are present in all nuclei of the basal ganglia. This review focuses on the contribution of the NMDA class of glutamatergic receptors to various movement disorders whose primary pathology lies within the basal ganglia and discusses how pharmacological manipulation of such receptors may be therapeutically useful.

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“…In keeping with this, HFS in the STN has been shown to significantly decrease the frequency of extracellularly recorded STN neurons in rats in vivo (Benazzouz et al 1997). As STN neurons are glutamatergic excitatory output neurons (Hammond et al 1978;Robledo and Féger 1990;Smith and Parent 1988), the immediate consequence of their reduction of activity could be the decrease of activity in target nuclei [substantia nigra pars reticulata (SNr) and entopeduncular nucleus/globus pallidus internal part (EP/GPi)] as observed in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated monkeys and naive rats (Benazzouz et al 1995;Burbaud et al 1994;Hayase et al 1996). It has also been suggested that the consequence of clinical HFS will be to somehow counteract the abnormal bursting pattern recorded in the STN in animal models of Parkinson disease (Bergman et al 1994;Hassani et al 1996;Hollerman and Grace 1992;Vila et al 2000).…”

Section: Introductionmentioning

confidence: 99%

High-Frequency Stimulation Produces a Transient Blockade of Voltage-Gated Currents in Subthalamic Neurons

Beurrier

Bioulac

Audin

et al. 2001

Journal of Neurophysiology

472

316

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Beurrier, Corinne, Bernard Bioulac, Jacques Audin, and Constance Hammond. High-frequency stimulation produces a transient blockade of voltage-gated currents in subthalamic neurons. J Neurophysiol 85: 1351Neurophysiol 85: -1356Neurophysiol 85: , 2001. The effect of high-frequency stimulation (HFS) of the subthalamic nucleus (STN) was analyzed with patch-clamp techniques (whole cell configuration, current-and voltage-clamp modes) in rat STN slices in vitro. A brief tetanus, consisting of 100-s bipolar stimuli at a frequency of 100 -250 Hz during 1 min, produced a full blockade of ongoing STN activity whether it was in the tonic or bursting mode. This HFS-induced silence lasted around 6 min after the end of stimulation, was frequency dependent, could be repeated without alteration, and was not synaptically induced as it was still observed in the presence of blockers of ionotropic GABA and glutamate receptors or in the presence of cobalt at a concentration (2 mM) that blocks voltage-gated Ca 2ϩ channels and synaptic transmission. During HFS-induced silence, the following alterations were observed: the persistent Na ϩ current (I NaP ) was totally blocked (by 99%), the Ca 2ϩ -mediated responses were strongly reduced including the posthyperpolarization rebound (Ϫ62% in amplitude) and the plateau potential (Ϫ76% in duration), suggesting that T-and L-type Ca 2ϩ currents are transiently depressed by HFS, whereas the Cs ϩ -sensitive, hyperpolarization-activated cationic current (I h ) was little affected. Thus a high-frequency tetanus produces a blockade of the spontaneous activities of STN neurons as a result of a strong depression of intrinsic voltage-gated currents underlying single-spike and bursting modes of discharge. These effects of HFS, which are completely independent of synaptic transmission, provide a mechanism for interrupting ongoing activities of STN neurons.

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Electrophysiological demonstration of an excitatory subthalamonigral pathway in the rat

Cited by 176 publications

References 18 publications

GABA, Not Glutamate, Controls the Activity of Substantia Nigra Reticulata Neurons in Awake, Unrestrained Rats

GABA, Not Glutamate, Controls the Activity of Substantia Nigra Reticulata Neurons in Awake, Unrestrained Rats

NMDA receptors in the basal ganglia

High-Frequency Stimulation Produces a Transient Blockade of Voltage-Gated Currents in Subthalamic Neurons

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