{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,8]],"date-time":"2025-10-08T15:29:51Z","timestamp":1759937391717},"reference-count":48,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurophysiology"],"published-print":{"date-parts":[[1997,10,1]]},"abstract":"<jats:p> Wang, Xueyong and Donald Robertson. Two types of actions of norepinephrine on identified auditory efferent neurons in rat brain stem slices. J. Neurophysiol. 78: 1800\u20131810, 1997. Whole cell voltage-clamp recordings were performed on auditory olivocochlear neurons in the ventral nucleus of the trapezoid body (VNTB) of brain stem slices from neonatal rats. Each neuron was identified by retrograde labeling with Fast Blue injected into the cochlea. Bath application of norepinephrine (NE; 1\u201310 \u03bcM) reversibly induced an inward current in 26 of 38 labeled neurons that were voltage clamped at \u221275 mV. This was responsible for the membrane depolarization to NE observed in current-clamp mode. The NE-induced inward current appeared to be more prominent at \u221255 mV than at \u221275 mV and reversed at around \u2212100 mV. It was attenuated but not prevented by 20 mM tetraethylammonium, and it persisted when the perfusate contained 2 mM Cs<jats:sup>+<\/jats:sup> or 100 \u03bcM Cd<jats:sup>2+<\/jats:sup>. However, the NE-induced inward current was attenuated to varying degrees in a zero-Ca<jats:sup>2+<\/jats:sup> solution. Current-voltage plots revealed that NE caused a decrease in membrane K<jats:sup>+<\/jats:sup> conductance. A suppression of voltage-gated Ca<jats:sup>2+<\/jats:sup> currents by NE was also observed. The excitatory action of NE was blocked by the \u03b1-adrenoreceptor antagonist phentolamine. The \u03b1<jats:sub>1<\/jats:sub>-adrenoreceptor agonist phenylephrine had an effect similar to that of NE. In 6 of 38 labeled neurons, an inhibitory action of NE (1\u201310 \u03bcM) was observed that appeared to be due to an activation of an inwardly rectified K<jats:sup>+<\/jats:sup> current, which caused hyperpolarization of resting membrane potentials in current-clamp mode. This inhibitory response was independent of external Ca<jats:sup>2+<\/jats:sup> and was abolished by 2\u20135 mM Cs<jats:sup>+<\/jats:sup> or 0.5 mM Ba<jats:sup>2+<\/jats:sup> applied in the perfusate. The receptors involved in the inhibitory actions of NE are not clear. The effect was partially and reversibly blocked by propranolol (10 \u03bcM), a \u03b2-adrenoreceptor antagonist. However, isoprenaline (10 \u03bcM), a \u03b2-adrenoreceptor agonist, failed to induce any effect. On the other hand, the inhibitory effect was irreversibly blocked by pretreatment with phentolamine (5\u201310 \u03bcM). 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