Inhibition suppresses transmission of tonic vibrissa-evoked activity in the rat ventrobasal thalamus.
Previous studies have demonstrated that tonic responses of trigeminal ganglion neurons to maintained whisker deflections are transformed to mainly phasic responses in thalamocortical neurons. The high tonic responsiveness of thalamic reticular neurons suggests that thalamic inhibition may contribute to this suppression of tonic activity. To test this hypothesis we recorded responses of thalamocortical neurons in the ventroposterior medial (VPm) nucleus to 200 and 400 msec sustained whisker deflections during simultaneous microiontophoresis of the GABA receptor antagonists bicuculline and phaclofen. Under control conditions, VPm units responded to deflection plateaus with mean activities of only 18 spikes/sec, compared with 16 spikes/sec spontaneous firing. A minority of cells (5/19) had significantly greater plateau than spontaneous activity, and these cells were classified as tonic; the other 14/19 were considered phasic. Under GABA receptor antagonism, however, mean plateau activity increased to 53 spikes/sec compared with 30 spikes/sec spontaneous activity, and 7 of the 14 phasic units became tonically responsive. Increases in plateau activity were significantly greater, by both absolute and relative measures, than increases in spontaneous activity. Transient responses to stimulus onsets and offsets also increased in magnitude 4.0- and 2. 9-fold, attributable mainly to their increased duration. These data indicate that VPm neurons receive tonic excitatory inputs that under normal conditions are masked by inhibition. Suppression of tonic activity in VPm by inhibitory thalamic reticular neurons may reduce tonic inhibition in cortical layer IV circuits, preserving their responsiveness to transient signals.
Hartings
J A
JA
Department of Neurobiology, University of Pittsburgh, Pittsburgh, Pennsylvania 15261, USA.
Simons
D J
DJ
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001418:Baclofen / Q000008:administration & dosage / Q000031:analogs & derivatives*; D001640:Bicuculline / Q000008:administration & dosage / Q000031:analogs & derivatives*; D018756:GABA Antagonists / Q000008:administration & dosage; D058787:GABA-A Receptor Antagonists; D058788:GABA-B Receptor Antagonists; D020646:Intralaminar Thalamic Nuclei / Q000166:cytology / Q000187:drug effects / Q000502:physiology; D007478:Iontophoresis; D009433:Neural Inhibition / Q000502:physiology*; D009474:Neurons / Q000187:drug effects / Q000378:metabolism; D010812:Physical Stimulation; D051381:Rats; D017207:Rats, Sprague-Dawley; D011963:Receptors, GABA-A / Q000378:metabolism; D018080:Receptors, GABA-B / Q000378:metabolism; D009435:Synaptic Transmission / Q000502:physiology*; D013788:Thalamus / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D014738:Vibrissae / Q000294:innervation*
D018756:GABA Antagonists; D058787:GABA-A Receptor Antagonists; D058788:GABA-B Receptor Antagonists; D011963:Receptors, GABA-A; D018080:Receptors, GABA-B; C052329:phaclofen; C017069:bicuculline methiodide; D001418:Baclofen; D001640:Bicuculline