Abstract

We examined the effects of corticotropin-releasing factor (CRF) on plasticity of optically recorded neuronal activity in the substantia gelatinosa (lamina II) of 12–18-day-old rat spinal cord slices stained with a voltage-sensitive dye. Single-pulse test stimulation to the dorsal root that activated A and C fibres evoked prolonged (>100 ms) light-absorption change in the lamina II. This response represents the gross membrane potential change of all elements along the slice depth. After conditioning high-frequency stimulation of A-fibre-activating strength, test stimulus elicited less neuronal activity [−27±1% (7), (average±SE ( n)), P<0.01 (*) at 45–60 min after conditioning]. When CRF (1 μM, 10 min) was applied during conditioning, the neuronal activity was facilitated rather than suppressed [+20±3% (5), P<0.05]. CRF alone exhibited insignificant effect [−5±1% (4), P=0.2]. In the presence of the inhibitory amino acid antagonists bicuculline (1 μM) and strychnine (0.3 μM) in the perfusate, in contrast, the conditioning facilitated it [+27±1% (12)*], and CRF treatment during conditioning inhibited the facilitation dose-dependently [0.1 μM: +18±2% (5)*, 1 μM: +13±1% (7)*]. Although interneuronal actions might contribute, these results suggest that CRF may have dual effects on excitatory synaptic transmission within the lamina II depending upon cellular conditions: a conversion from the induction of long-term depression to long-term potentiation (LTP), and inhibition of LTP induction. Since the LTP is thought to be responsible at least in part for the persistent pain, CRF could regulate the induction.

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