Role of α_2-adrenoreceptor on the excitability of trigeminal root ganglion neurons : Patch-clamp and Single-cell RT-PCR analysis

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The aim of the study was to mauiine the effects of α_2-adrerioreceptar agonists on the excitability of teigeminalroot ganglion (TRG) neurons using the perforated-patch damp technique, and to deternine wither these neurons express mRNA for α_2-adrenoreceptors. In cunent-clamp mode, the testing membrane potential was -57.4 ± 1.2 mV(n=26). Most neurons (71%) were hyperpolarized by clonidine (5-50μM) in a concentration-dependent manner. The response was associated with an increase of cell input resistance. In addition, clonidine reduced the repetitive firing evoked by depolarizing current pulses. An α_2-adrenergic agonist UK14,304 (10-20μM) also hyperpolarized TRG neurons. The donidine- and UK14, 304- induced hyperpdarizatian was blocked by idazoxan (α_2-adrenoreoeptor antagonist). In voltage-damp, donidine (1-50μM) reversibly reduced the hyperpolarization- and -time dependent cationic current. The effect was mimicked by UK13,304 (10-20μM), and antagonized by idazoxan. Hyperpoiarization-activated cationic current was blocked by extracelluar Cs^+ (2mM) or a specific blocker, ZD7288 (20μM). Analysis of taii-cinrcnts revealed that a reversal potential of the clonidine sensitive component of hyperpolarization-activated cationic current was -46mV. Single cell reverse transcription-polymerase chain reaction analysis demonstrated the expression of mRNA for α_<2A> and α_<2C> adrenoreceptors.These results demonstrate that activation of α_2-adrenoreceptors can hyperpolarize TRG neurons, and that the in hibitory effect is associated with inhibition of hyperpolarization-activated cationic current. Our results suggest that activation of α_2-adrenoreceptors in the absence of nerve injury may have an inhibitory effect on nociceptive transmission in the trigeminal system at the level of both TRG neuronal cell bodies and primary afferent terminals.