Intracellular recordings were made from substantia gelatinosa (s.g.) neurones in slices cut from adult rat spinal cord and maintained in vitro. Noradrenaline applied by superfusion (1‐50 microM), or by brief pressure ejection from a micropipette, reversibly hyperpolarized 80% of the s.g. cells. The noradrenaline induced hyperpolarization was associated with an increase in conductance and it reversed in polarity at ‐88 mV. The reversal potential changed when the external potassium concentration was changed, as predicted by the Nernst equation. The noradrenaline hyperpolarization was antagonized by phentolamine and yohimbine but not by propranolol and prazosin. The hyperpolarization was probably a direct action on the impaled cell and not due to release or block of release of other transmitters, because the effects persisted during a perfusion with a low calcium/high magnesium solution or in a solution containing cobalt and high magnesium. In 35 of 148 cells, noradrenaline caused a dose‐related increase of spontaneous excitatory post‐synaptic potentials (e.p.s.p.s). This effect was blocked by tetrodotoxin. The noradrenaline induced increase in e.p.s.p.s was blocked by phentolamine and prazosin but not by the alpha 2‐blockers yohimbine and RX 781094. A few cells were depolarized by noradrenaline, and this was blocked by prazosin but not by yohimbine. It is suggested that noradrenaline may inhibit nociceptive input to the spinal cord by increasing the potassium conductance of s.g. neurones.
The Journal of Physiology – Wiley
Published: Apr 1, 1984
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