Coexpression of GABAA receptor γ1 and γ2 subunits in the rat trigeminal ganglion

Kondo, Eiji; Kiyama, Hiroshi; Araki, Toshiyuki; Shida, Toru; Ueda, Yutaka; Tohyama, Masaya

doi:10.1016/0169-328x(94)90269-0

Cited by 26 publications

(13 citation statements)

References 19 publications

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“…Although large amplitude GABA A R mIPSCs have been recorded in adult lamina I-II neurons (Chéry and De Koninck, 1999), biexponentially decaying mIPSCs have not been observed in this structure. Differences between the two preparations might, therefore, be related to the specific expression of certain GABA A R subunits in the trigeminal nucleus (Araki and Tohyama, 1992;Kondo et al, 1994) that are not found in lamina II of the lumbar spinal cord (Bohlhalter et al, 1996).…”

Section: Properties Of Inhibitory Synaptic Transmission and Its Modulmentioning

confidence: 99%

Inflammatory Pain Upregulates Spinal Inhibition via Endogenous Neurosteroid Production

Poisbeau¹,

Patte‐Mensah²,

Keller³

et al. 2005

J. Neurosci.

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Inhibitory synaptic transmission in the dorsal horn (DH) of the spinal cord plays an important role in the modulation of nociceptive messages because pharmacological blockade of spinal GABA A receptors leads to thermal and mechanical pain symptoms. Here, we show that during the development of thermal hyperalgesia and mechanical allodynia associated with inflammatory pain, synaptic inhibition mediated by GABA A receptors in lamina II of the DH was in fact markedly increased. This phenomenon was accompanied by an upregulation of the endogenous production of 5␣-reduced neurosteroids, which, at the spinal level, led to a prolongation of GABA A receptor-mediated synaptic currents and to the appearance of a mixed GABA/glycine cotransmission. This increased inhibition was correlated with a selective limitation of the inflammation-induced thermal hyperalgesia, whereas mechanical allodynia remained unaffected. Our results show that peripheral inflammation activates an endogenous neurosteroid-based antinociceptive control, which discriminates between thermal and mechanical hyperalgesia.

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Section: Properties Of Inhibitory Synaptic Transmission and Its Modulmentioning

confidence: 99%

Inflammatory Pain Upregulates Spinal Inhibition via Endogenous Neurosteroid Production

Poisbeau¹,

Patte‐Mensah²,

Keller³

et al. 2005

J. Neurosci.

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“…GABA is contained within dorsal horn neurones (Hunt et al, 1981;Magoul et al, 1987), and receptors for it localize to many regions including dorsal root ganglion cells and dorsal horn neurones, where at least some of them are located on capsaicin-sensitive primary afferent fibres (Price et al, 1987;Persohn et al, 1991). Interestingly, in the trigeminal ganglion, a major population of sensory neurones and some of their processes are immunopositive for GABA (Szabat et al, 1992), while most trigeminal ganglion cells simultaneously express the mRNA for both the yl and y2 GABAA receptor subunits (Kondo et al, 1994). Although nerve fibres investing brain blood vessels possess the biosynthetic enzyme, glutamic acid decarboxylase (Imai et al, 1991), the functional consequences of GABA on vascular permeability have not been reported to our knowledge, and the role of GABAergic mechanisms within peripheral tissues is not well understood (Ong & Kerr, 1990;Bowery, 1993).…”

Section: Introductionmentioning

confidence: 99%

Peripheral GABA_A receptor‐mediated effects of sodium valproate on dural plasma protein extravasation to substance P and trigeminal stimulation

Lee

Limmroth

Ayata

et al. 1995

British J Pharmacology

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1 The GABA transaminase inhibitor and activator of glutamic acid decarboxylase, valproic acid is being used for the treatment of migraine. Its mechanism of action is unknown. We tested the effects of sodium valproate and GABAA-agonist muscimol on dural plasma protein ([1251] 3 Valproate (6.6 mg kg-', i.p.) or muscimol (58 jig kg-', i.p.) had no effect on mean arterial blood pressure or heart rate when measured for 30 min after i.p. administration. 4 The GABAA-antagonist bicuculline (0.01 mg kg-', i.p.) completely reversed the effect of valproate and muscimol on plasma extravasation following electrical stimulation or substance P administration, whereas the GABAB-receptor antagonist, phaclofen (0.01-1 mg kg', i.p.) did not. Bicuculline or phaclofen, given alone, did not alter the plasma extravasation response after either electrical stimulation or SP administration. 5 Valproate decreased plasma extravasation following substance P administration in adult animals, neonatally treated with capsaicin by a bicuculline-reversible mechanism. This suggests that GABAAreceptors are not found primarily on those afferent neurones or fibres which are sensitive to capsaicin treatment in neonatal rats. 6 We conclude that sodium valproate blocks plasma extravasation in the meninges through GABAAmediated postjunctional receptors probably within the meninges. The dosages required are comparable to those used clinically. Agonists and modulators at the GABAA receptor may become useful for the development of selective therapeutic agents for migraine and cluster headache.

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“…For example, spinal neurons with ascending projections may express greater numbers of γ-aminobutyric acid (GABA A ) receptors and fewer N-methyl-D-aspartate and α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors than neurons without ascending projections. 5,6 Thus, anesthetics that differ in their receptor modulating profiles would be expected to have a differential effect on these neuronal classes. Inhaled anesthetics have effects on a variety of receptors 7 whereas the primary mechanism of propofol anesthesia is thought to involve enhancement of GABA A receptors.…”

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confidence: 99%

Immobilizing Doses of Halothane, Isoflurane or Propofol, Do Not Preferentially Depress Noxious Heat-Evoked Responses of Rat Lumbar Dorsal Horn Neurons with Ascending Projections

Barter

Mark

Jinks

et al. 2008

Anesthesia &Amp; Analgesia

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BACKGROUND-The spinal cord is an important site where volatile anesthetics decrease sensation and produce immobility. Beyond this knowledge, our understanding of a site of anesthetic action is limited. Previous evidence suggests that dorsal horn neurons with ascending projections may be more susceptible to depression by general anesthetics than local spinal interneurons. In this study we evaluated the effects of volatile and injectable general anesthetics on lumbar dorsal horn neurons with and without ascending projections.

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Coexpression of GABAA receptor γ1 and γ2 subunits in the rat trigeminal ganglion

Cited by 26 publications

References 19 publications

Inflammatory Pain Upregulates Spinal Inhibition via Endogenous Neurosteroid Production

Inflammatory Pain Upregulates Spinal Inhibition via Endogenous Neurosteroid Production

Peripheral GABA_A receptor‐mediated effects of sodium valproate on dural plasma protein extravasation to substance P and trigeminal stimulation

Immobilizing Doses of Halothane, Isoflurane or Propofol, Do Not Preferentially Depress Noxious Heat-Evoked Responses of Rat Lumbar Dorsal Horn Neurons with Ascending Projections

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Coexpression of GABAA receptor γ1 and γ2 subunits in the rat trigeminal ganglion

Cited by 26 publications

References 19 publications

Inflammatory Pain Upregulates Spinal Inhibition via Endogenous Neurosteroid Production

Inflammatory Pain Upregulates Spinal Inhibition via Endogenous Neurosteroid Production

Peripheral GABAA receptor‐mediated effects of sodium valproate on dural plasma protein extravasation to substance P and trigeminal stimulation

Immobilizing Doses of Halothane, Isoflurane or Propofol, Do Not Preferentially Depress Noxious Heat-Evoked Responses of Rat Lumbar Dorsal Horn Neurons with Ascending Projections

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Peripheral GABA_A receptor‐mediated effects of sodium valproate on dural plasma protein extravasation to substance P and trigeminal stimulation