Noradrenaline‐mediated synaptic inhibition in rat locus coeruleus neurones.

Intracellular recordings were made from neurones in the nucleus locus coeruleus (l.c.) in slices of rat pons maintained in vitro. Focal electrical stimulation to the slice surface within the region of the l.c. evoked a synaptic depolarization followed by a hyperpolarization. These potentials were graded with stimulus intensity and were abolished in calcium‐free and/or high‐magnesium solutions. The nature of the hyperpolarizing synaptic potential (i.p.s.p.) was investigated. The i.p.s.p. amplitude decreased as the membrane was artificially made more negative and reversed at ‐114 mV. This reversal potential shifted to less negative potentials in solutions of elevated potassium ion content as predicted by the Nernst equation. The i.p.s.p. was potentiated in amplitude and its time course was prolonged by desmethylimipramine (DMI). Yohimbine (100 nM) and phentolamine (100 nM) reversibly abolished the i.p.s.p. and did not change the synaptic depolarization. Noradrenaline hyperpolarized all l.c. neurones tested, whether applied by perfusion (1‐30 microM) or by pressure ejection from a micropipette placed in the solution near the recording site. The noradrenaline‐induced hyperpolarization was accompanied by an increase in conductance and it reversed in polarity at ‐104 mV. The reversal potential of the noradrenaline hyperpolarization became less negative when the potassium ion content was increased. The noradrenaline‐induced hyperpolarization was potentiated by DMI and was antagonized by yohimbine and phentolamine in the same concentrations which blocked the i.p.s.p. The results support the notion that l.c. neurones can release noradrenaline onto the somadendritic membrane of other l.c. neurones and thereby provide local feed‐back inhibition.