Noradrenaline‐mediated synaptic inhibition in rat locus coeruleus neurones.

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Abstract
Intracellular recordings were made from neurons in the nucleus locus coeruleus in slices of rat pons maintained in vitro. Focal electrical stimulation to the slice surface within the region of the LC evoked a synaptic depolarization followed by a hyperpolarization. These potentials were graded with stimulus intensity and were abolished in Ca-free and/or high-Mg solutions. The nature of the hyperpolarizing synaptic potential IPSP was investigated. The IPSP 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 K+ content as predicted by the Nernst equation. The IPSP was potentiated in amplitude and its time course was prolonged by desmethylimipramine (DMI). Yohimbine (100 nM) and phentolamine (100 nM) reversibly abolished the IPSP and did not change the synaptic depolarization. Noradrenaline [norepinephrine] hyperpolarized all LC neurons tested, whether applied by perfusion (1-30 .mu.M) 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 K+ 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 IPSP. LC neurons can release noradrenaline onto the somadendritic membrane of other LC neurons and thereby provide local feed-back inhibiton.