1. Intracellular recordings were made from locus coeruleus neurones in a slice of tissue cut from the rat pons. A depolarizing postsynaptic potential (PSP) followed electrical stimulation of the slice surface; the latency was 1‐3 ms and the duration was 50‐200 ms. 2. The reversal potential of the PSP (estimated by extrapolation from potentials between ‐60 and ‐90 mV) was ‐27 mV when the recording electrodes contained potassium chloride, and ‐36 mV when electrodes contained potassium acetate or methylsulphate. 3. Kynurenic acid depressed the PSP amplitude by up to 60%. The residual PSP reversed polarity at ‐50 mV (extrapolated, potassium chloride in electrodes) or ‐70 mV (observed, potassium methylsulphate in electrodes): it was blocked by bicuculline (10 microM). 4. Exogenously applied gamma‐aminobutyric acid (GABA) depolarized cells when the recording electrode contained potassium chloride (reversal potential was ‐45 mV) and hyperpolarized cells when the recording electrode contained potassium methylsulphate (reversal potential was ‐70 mV). 5. In the presence of bicuculline, the residual PSP was blocked by kynurenic acid, whereas DL‐2‐amino‐5‐phosphonovaleric acid (2‐APV) reduced its amplitude to 80% of control. 6. Exogenously applied glutamate, quisqualate and N‐methyl‐D‐aspartate (NMDA) all caused a membrane depolarization (or an inward current under voltage clamp) which reversed polarity at about 0 mV. These effects were blocked by kynurenic acid (500 microM); 2‐APV (50 microM) selectively blocked the effect of NMDA. 7. The results indicate that the PSP evoked by focal stimulation within the nucleus locus coeruleus results from an excitatory amino acid acting predominantly at non‐NMDA receptors, and from GABA acting at GABAA receptors.
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