title: Repetitive light stimulation inducing glycine receptor plasticity in the retinal neurons.
abstract: Neurotransmitter receptor plasticity is a mechanism that can regulate the temporal and intensity encoding of a synapse. While this has been extensively studied as a mechanism of learning, less is known about such processes in sensory systems. This study examines modulation of glycine receptor function at the first synapse in the retina. It was found that horizontal cells, which are postsynaptic to photoreceptors, have glycine receptor currents that are enhanced when internal calcium is elevated. This can be achieved by glutamatergic synaptic input or by activation of voltage-gated calcium channels. When the retina was maintained in a dark-adapted state, the calcium levels in horizontal cells were relatively low. After a series of brief light stimuli, the internal calcium concentration in horizontal cells was elevated, and the glycine currents were faster and greater in amplitude. The increase of internal calcium levels was caused by increased transmitter release from photoreceptors. Thus glycine receptor function is state dependent and can be rapidly altered by synaptic input from photoreceptors. Light stimulation drives glycine receptor plasticity in the retinal neural network.
authors.affiliation: Department of Biomedical Science, Florida Atlantic Univ., Bldg. BC-71, Rm. 229, 777 Glades Rd., Boca Raton, Florida 33431, USA. wshen@fau.edu
authors.forename: Wen
authors.initials: W
authors.lastname: Shen
mesh_terms: D000818:Animals; D019256:Cadmium Chloride / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002614:Chelating Agents / Q000494:pharmacology; D003035:Cobalt / Q000378:metabolism; D004347:Drug Interactions; D004533:Egtazic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D004558:Electric Stimulation / Q000379:methods; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology; D018698:Glutamic Acid / Q000494:pharmacology; D005998:Glycine / Q000494:pharmacology; D066298:In Vitro Techniques; D007608:Kainic Acid / Q000494:pharmacology; D007814:Larva; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D008959:Models, Neurological; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects*; D009474:Neurons / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects*; D009543:Nifedipine / Q000494:pharmacology; D018408:Patch-Clamp Techniques / Q000379:methods; D010775:Photic Stimulation / Q000379:methods*; D018009:Receptors, Glycine / Q000378:metabolism*; D012160:Retina / Q000166:cytology*; D013997:Time Factors; D014562:Caudata
chemical_list: D002121:Calcium Channel Blockers; D002614:Chelating Agents; D018690:Excitatory Amino Acid Agonists; D018009:Receptors, Glycine; D003035:Cobalt; D018698:Glutamic Acid; D004533:Egtazic Acid; D009543:Nifedipine; D019256:Cadmium Chloride; C025603:1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid; D007608:Kainic Acid; D005998:Glycine