title: Alteration of GABAergic neurotransmission by pulsed infrared laser stimulation.
abstract: Transient electrical impulses are conventionally used to elicit physiological responses in excitable tissues. While electrical stimulation has many advantages, it requires an electrode-tissue interface, exhibits relatively low spatial selectivity and always produces a "stimulus artifact". Recently, it has been shown that pulsed, low-energy infrared laser light can evoke nerve, muscle and sensory responses similar to those induced by traditional electrical stimulation in a contact-free, damage-free, artifact-free and spatially selective manner. However, the effect of transient infrared laser light on neurotransmission in the CNS is still largely unknown. Here, we tested the effect of infrared laser light on GABAergic neurotransmission. We recorded spontaneous inhibitory postsynaptic currents (sIPSCs) from cultured rat cortical neurons prior to and after infrared laser stimulation. Using transient infrared laser light, we either stimulated the neuronal soma that had axonal projections to the recorded neuron or directly stimulated the axons that projected to the recorded neuron. Optical stimulation led to enhanced amplitude, decreased decay time constant and increased frequency of sIPSCs. These alterations of sIPSC properties produced by optical stimulation were specifically mediated by GABA(A) receptors and caused by the transient laser light per se since no exogenous substances such as caged compounds were used. These data show that optical stimulation using transient infrared laser light can alter GABAergic neurotransmission and demonstrate that it may be an alternative approach to electrical stimulation in studying GABAergic function.
authors.affiliation: Department of Neurology, Vanderbilt University Medical Center, 6140 MRB III, 465 21st Ave South, Nashville, TN 37232-8552, United States.
authors.forename: Hua-Jun
authors.initials: HJ
authors.lastname: Feng
authors.forename: Chris
authors.initials: C
authors.lastname: Kao
authors.forename: Martin J
authors.initials: MJ
authors.lastname: Gallagher
authors.forename: E Duco
authors.initials: ED
authors.lastname: Jansen
authors.forename: Anita
authors.initials: A
authors.lastname: Mahadevan-Jansen
authors.forename: Peter E
authors.initials: PE
authors.lastname: Konrad
authors.forename: Robert L
authors.initials: RL
authors.lastname: Macdonald
mesh_terms: D018750:6-Cyano-7-nitroquinoxaline-2,3-dione / Q000494:pharmacology; D000818:Animals; D001596:Benzylamines / Q000494:pharmacology; D001640:Bicuculline / Q000031:analogs & derivatives; D002478:Cells, Cultured; D002540:Cerebral Cortex / Q000166:cytology; D004307:Dose-Response Relationship, Radiation; D004622:Embryo, Mammalian; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D005260:Female; D058787:GABA-A Receptor Antagonists / Q000494:pharmacology; D053444:Inhibitory Postsynaptic Potentials / Q000187:drug effects / Q000528:radiation effects; D007834:Lasers; D009474:Neurons / Q000378:metabolism* / Q000528:radiation effects*; D018408:Patch-Clamp Techniques / Q000379:methods; D010721:Phosphinic Acids / Q000494:pharmacology; D011247:Pregnancy; D051381:Rats; D009435:Synaptic Transmission / Q000502:physiology / Q000528:radiation effects*; D013696:Temperature; D014633:Valine / Q000031:analogs & derivatives / Q000494:pharmacology
chemical_list: D001596:Benzylamines; D018691:Excitatory Amino Acid Antagonists; D058787:GABA-A Receptor Antagonists; D010721:Phosphinic Acids; C083008:CGP 52432; C017069:bicuculline methiodide; D018750:6-Cyano-7-nitroquinoxaline-2,3-dione; C056639:2-amino-5-phosphopentanoic acid; D014633:Valine; D001640:Bicuculline