Expression of glutamate (AMPA type) and γ-aminobutyric acid (GABA)A receptors in the rat caudal trigeminal spinal nucleus

Kondo, Eiji; Kiyama, Hiroshi; Yamano, Mariko; Shida, Toru; Ueda, Yutaka; Tohyama, Masaya

doi:10.1016/0304-3940(95)11316-o

Cited by 31 publications

(15 citation statements)

References 17 publications

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“…Evidence for GABA A receptor-mediated control of Vi/Vc units was strengthened by recent findings that local muscimol inhibited all Vi/Vc corneal units tested in a BMI-reversible manner (Hirata et al, 2003). GABAergic neurons (Matthews et al, 1988;Ginestal and Matute, 1993;Polgar and Antal, 1995;Wang et al, 2000) and GABA A receptors (Fritschy and Mohler, 1995;Kondo et al, 1995) are found throughout the trigeminal brainstem complex, including at the Vi/Vc transition and Vc/C1 junction regions. In addition, the results suggested that the nature of the convergent input and local GABAergic control of rostral Vi/Vc and caudal Vc/C1 corneal units was quite different.…”

Section: Discussionmentioning

confidence: 89%

A Novel Class of Neurons at the Trigeminal Subnucleus Interpolaris/Caudalis Transition Region Monitors Ocular Surface Fluid Status and Modulates Tear Production

Hirata¹,

Okamoto²,

Tashiro³

et al. 2004

J. Neurosci.

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Section: Discussionmentioning

confidence: 89%

A Novel Class of Neurons at the Trigeminal Subnucleus Interpolaris/Caudalis Transition Region Monitors Ocular Surface Fluid Status and Modulates Tear Production

Hirata¹,

Okamoto²,

Tashiro³

et al. 2004

J. Neurosci.

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“…For example, there is a presynaptic modulatory role of AMPA receptors in the GABA release (Engelman et al, 2006) and midazolam regulates excitatory transmission in spinal cord dorsal horn neurons of adult rats (Kohno et al, 2006). In addition, colocalization between GABA and AMPA receptors has been demonstrated in several spinal and supraspinal regions (Kondo et al, 1995;Kerr et al, 1998;Bergersen et al, 2003), and ionotropic glutamate receptors are expressed in GABAergic terminals in the rat superficial dorsal horn (Lu et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

Intrathecal midazolam regulates spinal AMPA receptor expression and function after nerve injury in rats

Lim

Sung

et al. 2006

Brain Research

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Spinal γ-aminobutyric acid (GABA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors have been implicated in the mechanisms of neuropathic pain after nerve injury; however, how these two receptors interact at the spinal level remains unclear. Here we show that intrathecal midazolam through activation of spinal GABAA receptors attenuated the expression and function of spinal AMPA receptors in rats following peripheral nerve injury. Thermal hyperalgesia and mechanical allodynia induced by chronic constriction nerve injury (CCI) in rats were attenuated by the short-acting benzodiazepine midazolam (20=10>5 μg > vehicle) administered intrathecally once daily for seven postoperative days. CCI-induced upregulation of AMPA receptors within the spinal cord dorsal horn was also significantly reduced by the intrathecal midazolam (10, 20 μg) treatment. The inhibitory effects of midazolam (10, 20 μg) on neuropathic pain behaviors and AMPA receptor expression were prevented by co-administration of midazolam with the GABAA receptor antagonist bicuculline (3 μg), whereas intrathecal treatment with bicuculline (1 or 3 μg) alone in naive rats induced the upregulation of spinal AMPA receptor expression and nociceptive responses, indicating a tonic regulatory effect from endogenous GABAergic activity on the AMPA receptor expression and spinal nociceptive processing. These results indicate that modulation of spinal AMPA receptor expression and function by the GABAergic activity may serve as a mechanism contributory to the spinal nociceptive processing.

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“…The inhibitory neurochemical GABA appears to modulate the excitability of nociceptive neurons through its local release from interneurons which, in the VBSNC, may principally occur in the substantia gelatinosa of subnucleus caudalis (Matthews et al, 1989;DiFiglia and Aronin, 1990;Fromm et al, 1992;Ginestal and Matute, 1993;Kondo et al, 1995;Almond et al, 1996;Chiang et al, 1999;and see Dubner and Bennett, 1983;Sessle, 1987;Yaksh and Malmberg, 1994). Different subtypes of the GABA receptor have been discovered, and while the specific roles of these subtypes in the VBSNC have so far received only limited attention, they might be differentially involved in V nociceptive transmission.…”

Section: Associated Neurochemical Mechanismsmentioning

confidence: 99%

Acute and Chronic Craniofacial Pain: Brainstem Mechanisms of Nociceptive Transmission and Neuroplasticity, and Their Clinical Correlates

Sessle

2000

Critical Reviews in Oral Biology & Medicine

614

541

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This paper reviews the recent advances in knowledge of brainstem mechanisms related to craniofacial pain. It also draws attention to their clinical implications, and concludes with a brief overview and suggestions for future research directions. It first describes the general organizational features of the trigeminal brainstem sensory nuclear complex (VBSNC), including its input and output properties and intrinsic characteristics that are commensurate with its strategic role as the major brainstem relay of many types of somatosensory information derived from the face and mouth. The VBSNC plays a crucial role in craniofacial nociceptive transmission, as evidenced by clinical, behavioral, morphological, and electrophysiological data that have been especially derived from studies of the relay of cutaneous nociceptive afferent inputs through the subnucleus caudalis of the VBSNC. The recent literature, however, indicates that some fundamental differences exist in the processing of cutaneous vs. other craniofacial nociceptive inputs to the VBSNC, and that rostral components of the VBSNC may also play important roles in some of these processes. Modulatory mechanisms are also highlighted, including the neurochemical substrate by which nociceptive transmission in the VBSNC can be modulated. In addition, the long-term consequences of peripheral injury and inflammation and, in particular, the neuroplastic changes that can be induced in the VBSNC are emphasized in view of the likely role that central sensitization, as well as peripheral sensitization, can play in acute and chronic pain. The recent findings also provide new insights into craniofacial pain behavior and are particularly relevant to many approaches currently in use for the management of pain and to the development of new diagnostic and therapeutic procedures aimed at manipulating peripheral inputs and central processes underlying nociceptive transmission and its control within the VBSNC.

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Expression of glutamate (AMPA type) and γ-aminobutyric acid (GABA)A receptors in the rat caudal trigeminal spinal nucleus

Cited by 31 publications

References 17 publications

A Novel Class of Neurons at the Trigeminal Subnucleus Interpolaris/Caudalis Transition Region Monitors Ocular Surface Fluid Status and Modulates Tear Production

A Novel Class of Neurons at the Trigeminal Subnucleus Interpolaris/Caudalis Transition Region Monitors Ocular Surface Fluid Status and Modulates Tear Production

Intrathecal midazolam regulates spinal AMPA receptor expression and function after nerve injury in rats

Acute and Chronic Craniofacial Pain: Brainstem Mechanisms of Nociceptive Transmission and Neuroplasticity, and Their Clinical Correlates

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