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GABA_A Receptor Activation Modulates Corneal Unit Activity in Rostral and Caudal Portions of Trigeminal Subnucleus Caudalis

¹ Department of Surgery, Brown Medical School, Rhode Island Hospital, Providence, Rhode Island 02903 ² Department of Neuroscience, Brown Medical School, Rhode Island Hospital, Providence, Rhode Island 02903

Submitted 4 June 2003; accepted in final form 21 July 2003

Corneal nociceptors terminate at the trigeminal subnucleus interpolaris/caudalis (Vi/Vc) transition and subnucleus caudalis/upper cervical spinal cord (Vc/C1) junction regions of the lower brain stem. The aims of this study were to determine if local GABA_A receptor activation modifies corneal input to second-order neurons at these regions and if GABA_A receptor activation in one region affects corneal input to the other region. In barbiturate-anesthetized male rats, corneal nociceptors were excited by pulses of CO₂ gas, and GABA_A receptors were activated by microinjections of the selective agonist muscimol. Local muscimol injection at the site of recording inhibited all Vi/Vc and Vc/C1 units tested and was reversed partially by bicuculline. To test for ascending intersubnuclear communication, muscimol injection into the caudal Vc/C1 junction, remote from the recording site at the Vi/Vc transition, inhibited the evoked response of most corneal units, although some neurons were enhanced. Injection of the nonselective synaptic blocking agent, CoCl₂, remotely into the Vc/C1 region inhibited the evoked response of all Vi/Vc units tested. To test for descending intersubnuclear communication, muscimol was injected remotely into the rostral Vi/Vc transition and enhanced the evoked activity of all corneal units tested at the caudal Vc/C1 junction. These results suggest that GABA_A receptor mechanisms play a significant role in corneal nociceptive processing by second-order trigeminal brain stem neurons. GABA_A receptor mechanisms act locally at both the Vi/Vc transition and Vc/C1 junction regions to inhibit corneal input and act through polysynaptic pathways to modify corneal input at multiple levels of the trigeminal brain stem complex.

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