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Presynaptic Glycine Receptors Increase GABAergic Neurotransmission in Rat Periaqueductal Gray Neurons

Overview
Journal Neural Plast
Specialty Neurology
Date 2013 Oct 1
PMID 24078885
Citations 7
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Abstract

The periaqueductal gray (PAG) is involved in the central regulation of nociceptive transmission by affecting the descending inhibitory pathway. In the present study, we have addressed the functional role of presynaptic glycine receptors in spontaneous glutamatergic transmission. Spontaneous EPSCs (sEPSCs) were recorded in mechanically dissociated rat PAG neurons using a conventional whole-cell patch recording technique under voltage-clamp conditions. The application of glycine (100 µM) significantly increased the frequency of sEPSCs, without affecting the amplitude of sEPSCs. The glycine-induced increase in sEPSC frequency was blocked by 1 µM strychnine, a specific glycine receptor antagonist. The results suggest that glycine acts on presynaptic glycine receptors to increase the probability of glutamate release from excitatory nerve terminals. The glycine-induced increase in sEPSC frequency completely disappeared either in the presence of tetrodotoxin or Cd(2+), voltage-gated Na(+), or Ca(2+) channel blockers, suggesting that the activation of presynaptic glycine receptors might depolarize excitatory nerve terminals. The present results suggest that presynaptic glycine receptors can regulate the excitability of PAG neurons by enhancing glutamatergic transmission and therefore play an important role in the regulation of various physiological functions mediated by the PAG.

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References
1.
Wang F, Xiao C, Ye J . Taurine activates excitatory non-synaptic glycine receptors on dopamine neurones in ventral tegmental area of young rats. J Physiol. 2005; 565(Pt 2):503-16. PMC: 1464534. DOI: 10.1113/jphysiol.2005.085423. View

2.
Depaulis A, Morgan M, LIEBESKIND J . GABAergic modulation of the analgesic effects of morphine microinjected in the ventral periaqueductal gray matter of the rat. Brain Res. 1987; 436(2):223-8. DOI: 10.1016/0006-8993(87)91665-9. View

3.
Ye J, Wang F, Krnjevic K, Wang W, Xiong Z, Zhang J . Presynaptic glycine receptors on GABAergic terminals facilitate discharge of dopaminergic neurons in ventral tegmental area. J Neurosci. 2004; 24(41):8961-74. PMC: 6730073. DOI: 10.1523/JNEUROSCI.2016-04.2004. View

4.
Millan M . Descending control of pain. Prog Neurobiol. 2002; 66(6):355-474. DOI: 10.1016/s0301-0082(02)00009-6. View

5.
de Novellis V, Marabese I, Uliano R, Palazzo E, Scafuro A, Sca Rossi F . Type I and II metabotropic glutamate receptors modulate periaqueductal grey glycine release: interaction between mGlu2/3 and A1 adenosine receptors. Neuropharmacology. 2002; 43(7):1061-9. DOI: 10.1016/s0028-3908(02)00227-7. View