NMDA receptor activation induces long-term potentiation of glycine synapses

English version

Autoři: Michelle L. Kloc ^aff001; Bruno Pradier ^aff001; Anda M. Chirila ^aff001; Julie A. Kauer ^aff001
Působiště autorů: Dept. of Pharmacology, Physiology and Biotechnology, Brown Institute for Brain Science, Brown University, Providence, RI, United States of America ^aff001
Vyšlo v časopise: PLoS ONE 14(9)
Kategorie: Research Article
doi: https://doi.org/10.1371/journal.pone.0222066

Souhrn

Of the fast ionotropic synapses, glycinergic synapses are the least well understood, but are vital for the maintenance of inhibitory signaling in the brain and spinal cord. Glycinergic signaling comprises half of the inhibitory signaling in the spinal cord, and glycinergic synapses are likely to regulate local nociceptive processing as well as the transmission to the brain of peripheral nociceptive information. Here we have investigated the rapid and prolonged potentiation of glycinergic synapses in the superficial dorsal horn of young male and female mice after brief activation of NMDA receptors (NMDARs). Glycinergic inhibitory postsynaptic currents (IPSCs) evoked with lamina II-III stimulation in identified GABAergic neurons in lamina II were potentiated by bath-applied Zn²⁺ and were depressed by the prostaglandin PGE₂, consistent with the presence of both GlyRα1- and GlyRα3-containing receptors. NMDA application rapidly potentiated synaptic glycinergic currents. Whole-cell currents evoked by exogenous glycine were also readily potentiated by NMDA, indicating that the potentiation results from altered numbers or conductance of postsynaptic glycine receptors. Repetitive depolarization alone of the postsynaptic GABAergic neuron also potentiated glycinergic synapses, and intracellular EGTA prevented both NMDA-induced and depolarization-induced potentiation of glycinergic IPSCs. Optogenetic activation of trpv1 lineage afferents also triggered NMDAR-dependent potentiation of glycinergic synapses. Our results suggest that during peripheral injury or inflammation, nociceptor firing during injury is likely to potentiate glycinergic synapses on GABAergic neurons. This disinhibition mechanism may be engaged rapidly, altering dorsal horn circuitry to promote the transmission of nociceptive information to the brain.

Klíčová slova:

Biology and life sciences – Cell biology – Cellular types – Animal cells – Afferent neurons – Signal transduction – Sensory receptors – Nociceptors – Neuroscience – Cellular neuroscience – Neurons – Synapses – Sensory perception – Anatomy – Nervous system – Physiology – Electrophysiology – Neurophysiology – Membrane potential – Depolarization – Biochemistry – Proteins – Amino acids – Aliphatic amino acids – Glycine – Psychology – Medicine and health sciences – Neuroanatomy – Immunology – Immune response – Inflammation – Diagnostic medicine – Signs and symptoms – Pathology and laboratory medicine – Physical sciences – Chemistry – Chemical compounds – Organic compounds – Organic chemistry – Social sciences

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NMDA receptor activation induces long-term potentiation of glycine synapses

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