On the reduction of spontaneous and glutamate-driven spinocerebellar and spinoreticular tract neuronal activity during active sleep.
The present study was performed to provide evidence that dynamic neural processes underlie the reduction in dorsal spinocerebellar tract and spinoreticular tract neuron activity that occurs during active sleep. To ascertain the effect of local inhibition on the spontaneous and glutamate-evoked spike discharge of sensory tract neurons, preliminary control tests were performed during the state of quiet wakefulness, where GABA or glycine was co-administered in a sustained fashion during pulsatile release of glutamate to dorsal spinocerebellar tract (n=3) or spinoreticular tract (n=2) neurons. Co-administration of GABA or glycine also resulted in a significant marked suppression of spontaneous spike activity and glutamate-evoked responses of these cells. Extracellular recording experiments combined with juxtacellular application of glutamate were then performed on 20 antidromically identified dorsal spinocerebellar tract and spinoreticular tract neurons in the chronic intact cat as a function of sleep and wakefulness. The glutamate-evoked activity of a group of 10 sensory tract neurons (seven dorsal spinocerebellar tract, three spinoreticular tract), which exhibited a significant decrease in their spontaneous spike activity during active sleep, was examined. Glutamate-evoked activity in these cells was significantly attenuated during active sleep compared with wakefulness. In contrast, the glutamate-evoked activity of a second group of eight sensory tract neurons (four dorsal spinocerebellar tract, four spinoreticular tract), which exhibited a significant increase in their spontaneous spike activity during active sleep, was not significantly altered in a state-dependent manner. These data indicate that, during natural active sleep, a dynamic neural process is engaged onto certain dorsal spinocerebellar tract and spinoreticular tract neurons, which in turn dampens sensory throughput to higher brain centers.
Soja
P J
PJ
Division of Pharmacology and Toxicology, Faculty of Pharmaceutical Sciences, The University of British Columbia, 2146 East Mall, B.C., V6T 1Z3, Vancouver, Canada. soja@interchange.ubc.ca
Pang
W
W
Taepavarapruk
N
N
Cairns
B E
BE
McErlane
S A
SA
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D002415:Cats; D018698:Glutamic Acid / Q000378:metabolism* / Q000494:pharmacology; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology; D009474:Neurons / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D012154:Reticular Formation / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D012895:Sleep, REM / Q000187:drug effects / Q000502:physiology*; D013116:Spinal Cord / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D020824:Spinocerebellar Tracts / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology
D018698:Glutamic Acid