title: Cholinergic and glutamatergic agonists induce gamma frequency activity in dorsal subcoeruleus nucleus neurons.
abstract: The dorsal subcoeruleus nucleus (SubCD) is involved in generating two signs of rapid eye movement (REM) sleep: muscle atonia and ponto-geniculo-occipital (PGO) waves. We tested the hypothesis that single cell and/or population responses of SubCD neurons are capable of generating gamma frequency activity in response to intracellular stimulation or receptor agonist activation. Whole cell patch clamp recordings (immersion chamber) and population responses (interface chamber) were conducted on 9- to 20-day-old rat brain stem slices. All SubCD neurons (n = 103) fired at gamma frequency when subjected to depolarizing steps. Two statistically distinct populations of neurons were observed, which were distinguished by their high (>80 Hz, n = 24) versus low (35-80 Hz, n = 16) initial firing frequencies. Both cell types exhibited subthreshold oscillations in the gamma range (n = 43), which may underlie the gamma band firing properties of these neurons. The subthreshold oscillations were blocked by the sodium channel blockers tetrodotoxin (TTX, n = 21) extracellularly and N-(2,6-dimethylphenylcarbamoylmethyl)triethylammonium bromide (QX-314) intracellularly (n = 5), indicating they were sodium channel dependent. Gamma frequency subthreshold oscillations were observed in response to the nonspecific cholinergic receptor agonist carbachol (CAR, n = 11, d = 1.08) and the glutamate receptor agonists N-methyl-d-aspartic acid (NMDA, n = 12, d = 1.09) and kainic acid (KA, n = 13, d = 0.96), indicating that cholinergic and glutamatergic inputs may be involved in the activation of these subthreshold currents. Gamma band activity also was observed in population responses following application of CAR (n = 4, P < 0.05), NMDA (n = 4, P < 0.05) and KA (n = 4, P < 0.05). Voltage-sensitive, sodium channel-dependent gamma band activity appears to be a part of the intrinsic membrane properties of SubCD neurons.
authors.affiliation: Center for Translational Neuroscience, Department of Neurobiology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.
authors.forename: Christen
authors.initials: C
authors.lastname: Simon
authors.forename: Nebojsa
authors.initials: N
authors.lastname: Kezunovic
authors.forename: D Keith
authors.initials: DK
authors.lastname: Williams
authors.forename: Francisco J
authors.initials: FJ
authors.lastname: Urbano
authors.forename: E
authors.initials: E
authors.lastname: Garcia-Rill
mesh_terms: D000200:Action Potentials; D000704:Analysis of Variance; D000818:Animals; D058256:Brain Waves / Q000187:drug effects*; D018679:Cholinergic Agonists / Q000494:pharmacology*; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology*; D066298:In Vitro Techniques; D007700:Kinetics; D016014:Linear Models; D009474:Neurons / Q000187:drug effects* / Q000502:physiology; D009991:Oscillometry; D018408:Patch-Clamp Techniques; D011149:Pons / Q000166:cytology / Q000187:drug effects* / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012895:Sleep, REM / Q000187:drug effects*; D026941:Sodium Channel Blockers / Q000494:pharmacology; D015222:Sodium Channels / Q000187:drug effects / Q000378:metabolism
chemical_list: D018679:Cholinergic Agonists; D018690:Excitatory Amino Acid Agonists; D026941:Sodium Channel Blockers; D015222:Sodium Channels