PARABRACHIAL AREA - ELECTROPHYSIOLOGICAL EVIDENCE FOR AN INVOLVEMENT IN COLD NOCICEPTION

1. Thirty-five percent of 120 neurons recorded extracellularly in the parabrachial (PB) area of anesthetized rats responded to a peripheral cold stimulus (0 degrees C). The cold-sensitive neurons were located i n the lateral PB area, and most of those exhibiting a strong response to cold stimuli were inside or in close vicinity to the area receiving a high density of projections from superficial neurons of the dorsal horn. 2. The receptive fields for cold stimulation often were restrict ed to one or two parts of the body with a contralateral predominance f or the limbs. No side predominance was observed for the face. 3. From a low spontaneous activity (10th percentile < median < 90th percentile : 0.1 < 1.5 < 5 Hz), the PB neurons responded to cold noxious stimuli (0 degrees C water bath or waterjet, 20 s), without observable delay, with a sustained discharge. The mean maximal response to the stimulus was 16.1 +/- 1.2 Hz (mean +/- SE; n = 42). 4. About one-half (45%) of these cold-sensitive neurons were activated specifically by cold stimu lation and did not respond or were inhibited by noxious heat and/or pi nch. The remaining (55%) cold-sensitive neurons were also driven by he at and/or pinch. 5. The cold-sensitive neurons exhibited a clear capac ity to encode cold stimuli in the noxious range: the stimulus-response function was always positive and monotonic from 30 to 0 degrees C; th e mean curve was linear between 20 and 0 degrees C before plateauing b etween 0 to -10 degrees C; the mean threshold to cold stimulation was 17.1 +/- 1 degrees C (n = 21) and the mean t(50) was 10.7 +/- 1.1 degr ees C (n = 13). 6. The cold-sensitive neurons responded to intense tra nscutaneous electrical stimulation with an early and/or a late peak of activation, the latencies of which were in the 15-50 ms and 80-170 ms ranges (n = 8), respectively, i.e., compatible with the activation of A delta and C fibers. Interestingly, the cold-specific neurons predom inantly responded with a late peak, suggesting these neurons were prim arily driven by peripheral C fibers. 7. The intravenous injection of m orphine depressed the responses of PB neurons to cold noxious stimuli in a dose-related (1, 3, and 9 mg/kg) and naloxone reversible fashion. The ED(50) value was estimated similar to 2 mg/kg. Furthermore, two p opulations of neurons could be separated according to their morphine s ensitivity. 8. It is concluded that PB cold-nonspecific neurons could be involved in affective-emotional, autonomic and neuroendocrine react ions in response to noxious cold events. The PB cold-specific neurons could be, in addition, involved in some thermoregulatory processes.