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Title: The endogenous agonist, β-alanine, activates glycine receptors in rat spinal dorsal neurons

Journal Article · · Biochemical and Biophysical Research Communications
;  [1];  [2]
  1. Division of Anesthesiology, Niigata University Graduate School of Medical and Dental Sciences, Asahimachi 1-757, Niigata, 951-8510 (Japan)
  2. Department of Anesthesiology, Tohoku Medical and Pharmaceutical University, Fukumuro 1-15-1, Sendai, 983-8536 (Japan)

Highlights: • Activation of glycine receptors by β-alanine in substantia gelatinosa neurons. • β-alanine opens Cl{sup −} channels on postsynaptic substantia gelatinosa neurons. • β-alanine acts as a inhibitory neurotransmitter in sunstantia gelatinosa neurons. • β-alanine may be involved in antinociception. β-alanine is a structural analog of glycine and γ-aminobutyric acid (GABA) and is thought to be involved in the modulation of nociceptive information at the spinal cord. However, it is not known whether β-alanine exerts its effect in substantia gelatinosa (SG) neurons of the spinal dorsal horn, where glycine and GABA play an important role in regulating nociceptive transmission from the periphery. Here, we investigated the effects of β-alanine on inhibitory synaptic transmission in adult rat SG neurons using whole-cell patch-clamp. β-alanine dose-dependently induced outward currents in SG neurons. Current-voltage plots revealed a reversal potential at approximately −70 mV, which was close to the equilibrium potential of Cl{sup −}. Pharmacological analysis revealed that β-alanine activates glycine receptors, but not GABA{sub A} receptors. These results suggest that β-alanine hyperpolarizes the membrane potential of SG neurons by activating Cl{sup −} channels through glycine receptors. Our findings raise the possibility that β-alanine may modulate pain sensation through glycine receptors.

OSTI ID:
23125158
Journal Information:
Biochemical and Biophysical Research Communications, Vol. 500, Issue 4; Other Information: Copyright (c) 2018 Elsevier Inc. All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
Country of Publication:
United States
Language:
English

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