Temporal shaping of phasic neuronal responses by GABA- and non-GABA-mediated mechanisms in the somatosensory thalamus of the rat.
Trapezoidal mechanical movement of whiskers was used to study the responses of 44 single thalamic ventral posteromedial (VPM) neurons to dynamic and static stimulus components in urethane-anesthetized rats. The effects of local administration of the GABAA receptor antagonist, bicuculline, and the GABAB receptor antagonist, 2-hydroxysaclofen, were tested to determine whether and to what extent the responses altered when GABA-mediated inhibitory synaptic transmission was blocked. Two classes of phasically responding neurons were identified, ON/OFF and movement-sensitive types. Bicuculline enhanced the magnitudes of the responses from both types by 2.5-fold and ON/OFF responses were converted to movement-sensitive ones in 17 (43%) of the 40 ON/OFF neurons. 2-hydroxysaclofen either had no effect or appeared to act like a GABA agonist. In 21 (48%) neurons, a significantly reduced responsiveness was observed during a 100-ms period following the ON and OFF responses. This discharge suppression was especially prominent during the plateau phase of the stimulus, and in some cases extended for several 100 ms following its onset. This suppression was overcome neither by the GABA receptor antagonists, nor by ejection of AMPA or glutamate at currents that otherwise produced vigorous excitation. These results suggest that one functional role for GABAA-receptor-mediated synaptic inhibition in the somatosensory thalamus is the intramodal regulation of the form of expression of phasically responding neurons. Other thalamic inhibitory processes not mediated by GABAA or GABAB receptors that help to shape the expression of the responses of certain phasic neurons to maintained stimulation may exist. Overall, these mechanisms appear to mediate the precision of timing of thalamic neuronal firing in response to the rat's tactile environment.
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000344:Afferent Pathways / Q000502:physiology*; D000818:Animals; D005260:Female; D018756:GABA Antagonists / Q000494:pharmacology; D058787:GABA-A Receptor Antagonists; D058788:GABA-B Receptor Antagonists; D018698:Glutamic Acid / Q000494:pharmacology; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology; D009474:Neurons / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D011930:Reaction Time / Q000187:drug effects / Q000502:physiology; D011963:Receptors, GABA-A / Q000378:metabolism; D018080:Receptors, GABA-B / Q000378:metabolism; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*; D014110:Touch / Q000187:drug effects / Q000502:physiology; D020651:Ventral Thalamic Nuclei / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D014738:Vibrissae / Q000502:physiology; D018350:alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid / Q000494:pharmacology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
D018756:GABA Antagonists; D058787:GABA-A Receptor Antagonists; D058788:GABA-B Receptor Antagonists; D011963:Receptors, GABA-A; D018080:Receptors, GABA-B; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid; D018350:alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid