The effects of pain-producing agents on the voltage-dependent ionic channels of rat trigeminal ganglion

ABSTRACT

Ion channels of the sensory neurons play a pivotal role in the generation and transmission of sensory information. Generally the Na+ channels are involved in the rapid generation of action potentials. Calcium influx triggers a number of cellular processes, including muscle contraction, second-messenger activation cascade, the regulation of axonal guidance, control of neurotransmitter release. There are some pain-producing agents such as bradykinin, prostaglandin E2, hydrogen ions, histamine and acetylcholine. The precise mechanisms of the agents producing pain are not fully understood yet. This experiment was performed to elucidate the electrophysiological effects of pain producing agents It is concluded that (1) bradykinin inhibited ICa of acutely isolated TRG neurons. This result suggests that bradykinin may inhibit or block the synaptic transmission of primary afferents of TRG and (2) in the presence of the prostaglandin the peak inward current was increased by about 2 nA, and this was associated with a hyperpolarizing shift in the I-V relationship for this cell. Therefore facilitation of the TTX-resistant voltage-gated sodium channel in TRG neurons underlies the increased excitability in response to PGE2.