Neuronal basis of the slow (<1 Hz) oscillation in neurons of the nucleus reticularis thalami in vitro.
During deep sleep and anesthesia, the EEG of humans and animals exhibits a distinctive slow (<1 Hz) rhythm. In inhibitory neurons of the nucleus reticularis thalami (NRT), this rhythm is reflected as a slow (<1 Hz) oscillation of the membrane potential comprising stereotypical, recurring "up" and "down" states. Here we show that reducing the leak current through the activation of group I metabotropic glutamate receptors (mGluRs) with either trans-ACPD [(+/-)-1-aminocyclopentane-trans-1,3-dicarboxylic acid] (50-100 microM) or DHPG [(S)-3,5-dihydroxyphenylglycine] (100 microM) instates an intrinsic slow oscillation in NRT neurons in vitro that is qualitatively equivalent to that observed in vivo. A slow oscillation could also be evoked by synaptically activating mGluRs on NRT neurons via the tetanic stimulation of corticothalamic fibers. Through a combination of experiments and computational modeling we show that the up state of the slow oscillation is predominantly generated by the "window" component of the T-type Ca2+ current, with an additional supportive role for a Ca2+-activated nonselective cation current. The slow oscillation is also fundamentally reliant on an Ih current and is extensively shaped by both Ca2+- and Na+-activated K+ currents. In combination with previous work in thalamocortical neurons, this study suggests that the thalamus plays an important and active role in shaping the slow (<1 Hz) rhythm during deep sleep.
Blethyn
Kate L
KL
School of Biosciences, Cardiff University, Cardiff CF10 3US, United Kingdom.
Hughes
Stuart W
SW
Tóth
Tibor I
TI
Cope
David W
DW
Crunelli
Vincenzo
V
D000200:Action Potentials / Q000187:drug effects / Q000528:radiation effects; D000818:Animals; D001030:Apamin / Q000494:pharmacology; D002104:Cadmium / Q000494:pharmacology; D002415:Cats; D003198:Computer Simulation; D003515:Cycloleucine / Q000031:analogs & derivatives / Q000494:pharmacology; D004307:Dose-Response Relationship, Radiation; D004347:Drug Interactions; D025802:Electric Capacitance; D004558:Electric Stimulation / Q000379:methods; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D018756:GABA Antagonists / Q000494:pharmacology; D066298:In Vitro Techniques; D020646:Intralaminar Thalamic Nuclei / Q000166:cytology*; D008959:Models, Neurological; D009434:Neural Pathways / Q000187:drug effects / Q000528:radiation effects; D009474:Neurons / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D018696:Neuroprotective Agents / Q000494:pharmacology; D009532:Nickel / Q000494:pharmacology; D009943:Organophosphorus Compounds / Q000494:pharmacology; D010507:Periodicity; D011724:Pyridazines / Q000494:pharmacology; D011743:Pyrimidines / Q000494:pharmacology; D026941:Sodium Channel Blockers / Q000494:pharmacology; D013779:Tetrodotoxin / Q000494:pharmacology; D013997:Time Factors
D018691:Excitatory Amino Acid Antagonists; D018756:GABA Antagonists; D018696:Neuroprotective Agents; D009943:Organophosphorus Compounds; D011724:Pyridazines; D011743:Pyrimidines; D026941:Sodium Channel Blockers; D002104:Cadmium; D003515:Cycloleucine; C036361:1-amino-1,3-dicarboxycyclopentane; C082246:ICI D2788; C107353:CGP 54626; D001030:Apamin; D013779:Tetrodotoxin; D009532:Nickel; C049853:gabazine