Local group I mGluR antagonists reduce TMJ-evoked activity of trigeminal subnucleus caudalis neurons in female rats.
Group I metabotropic glutamate receptors (mGluR1 and mGluR5) are functionally linked to estrogen receptors and play a key role in the plasticity of central neurons. Estrogen status strongly influences sensory input from the temporomandibular joint (TMJ) to neurons at the spinomedullary (Vc/C1-2) region. This study tested the hypothesis that TMJ input to trigeminal subnucleus caudalis/upper cervical cord (Vc/C1-2) neurons involved group I mGluR activation and depended on estrogen status. TMJ-responsive neurons were recorded in superficial laminae at the Vc/C1-2 region in ovariectomized (OvX) female rats treated with low-dose estradiol (2 μg/day, LE) or high-dose estradiol (20 μg/day, HE) for 2 days. TMJ-responsive units were activated by adenosine triphosphate (ATP, 1mM) injected into the joint space. Receptor antagonists selective for mGluR1 (CPCCOEt) or mGluR5 (MPEP) were applied topically to the Vc/C1-2 surface at the site of recording 10 min prior to the intra-TMJ ATP stimulus. In HE rats, CPCCOEt (50 and 500 μM) markedly reduced ATP-evoked unit activity. By contrast, in LE rats, a small but significant increase in neural activity was seen after 50 μM CPCCOEt, while 500 μM caused a large reduction in activity that was similar in magnitude as that seen in HE rats. Local application of MPEP produced a significant inhibition of TMJ-evoked unit activity independent of estrogen status. Neither mGluR1 nor mGluR5 antagonism altered the spontaneous activity of TMJ units in HE or LE rats. High-dose MPEP caused a small reduction in the size of the convergent cutaneous receptive field in HE rats, while CPCCOEt had no effect. These data suggest that group I mGluRs play a key role in sensory integration of TMJ nociceptive input to the Vc/C1-2 region and are largely independent of estrogen status.
Department of Physiology, National Defense Medical College, Namiki 3-2, Tokorozawa City, Saitama 359-8513, Japan. Electronic address: tashiro@ndmc.ac.jp.
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Tashiro
Department of Physiology, National Defense Medical College, Namiki 3-2, Tokorozawa City, Saitama 359-8513, Japan.
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Nishida
Department of Diagnostic and Biological Sciences, University of Minnesota School of Dentistry, Moos Tower 18-214, 515 Delaware Street SE, Minneapolis, MN 55455, USA.
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Bereiter
D000255:Adenosine Triphosphate / Q000494:pharmacology; D000818:Animals; D002867:Chromones / Q000494:pharmacology; D004958:Estradiol / Q000008:administration & dosage / Q000502:physiology; D005260:Female; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D059225:Nociception / Q000187:drug effects / Q000502:physiology*; D011725:Pyridines / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D064529:Receptor, Metabotropic Glutamate 5 / Q000037:antagonists & inhibitors; D018094:Receptors, Metabotropic Glutamate / Q000037:antagonists & inhibitors / Q000502:physiology*; D013704:Temporomandibular Joint / Q000187:drug effects / Q000294:innervation / Q000502:physiology*; D014275:Trigeminal Caudal Nucleus / Q000187:drug effects / Q000502:physiology*
C117789:7-(hydroxyimino)cyclopropan(b)chromen-1a-carbxoylic acid ethyl ester; D002867:Chromones; C578937:Grm5 protein, rat; D011725:Pyridines; D064529:Receptor, Metabotropic Glutamate 5; D018094:Receptors, Metabotropic Glutamate; C104077:metabotropic glutamate receptor type 1; D004958:Estradiol; C121465:6-methyl-2-(phenylethynyl)pyridine; D000255:Adenosine Triphosphate
estrogen; group I metabotropic glutamate receptors; temporomandibular muscle/joint disorders; trigeminal subnucleus