actions of Norepinephrine on Rat hypoglossal motoneurons. Parkis, Marjorie A., Douglas A. Bayliss, and Albert J. Berger. Department of Physiology and Biophysics SJ-40, University of Washington School of Medicine, Seattle Washington 98195.
APStracts 2:0198N, 1995.
SUMMARY AND CONCLUSIONS
1. We used conventional intracellular recording techniques in 400 [mu] m thick slices from the brainstem of juvenile rats to investigate the action of norepinephrine (NE) on subthreshold and firing properties of hypoglossal motoneurons (HMs). 2. Recorded in current-clamp mode, 50 or 100 [mu] M NE elicited a reversible depolarization accompanied by an increase in input resistance (R N ) in all HMs tested (n = 74). Recorded in single electrode voltage-clamp mode, NE induced a reversible inward current accompanied by a reduction in input conductance. The average reversal potential for I NE was - 104 mV. The NE responses could be elicited in a Ca 2+ -free solution containing TTX, indicating that they were postsynaptic. 3. The NE response could be blocked by the [alpha] -adrenoceptor antagonist prazosin, but not by the [beta] -adrenoceptor antagonist propranolol, and could be mimicked by the [alpha] 1 -adrenoceptor agonist phenylephrine, but not by the [alpha] 2 - adrenoceptor agonist UK 14,304, nor by the [beta] -adrenoceptor agonist isoproterenol when [alpha] -adrenoceptors were blocked. 4. Substitution of barium for calcium in the perfusing solution blocked the increase in R N in response to NE without blocking completely the depolarization. Replacement of sodium chloride with choline chloride in the barium-substituted perfusing solution blocked the remaining depolarization. 5. The neuropeptide thyrotropin-releasing hormone (TRH), which also depolarizes and increases the R N of HMs, occluded the response of HMs to NE. 6. NE altered HM firing properties in three ways: it always lowered the minimum amount of injected current needed to elicit repetitive firing, it increased the slope of the firing frequency vs. injected current relation in 8 out of 14 cells tested, and it increased the delay from the onset of the depolarizing current pulse to the first evoked spike in all cells tested. 7. We conclude that NE acts directly on [alpha] 1 -adrenoceptors to increase the excitability of HMs. It does this by reducing a barium-sensitive resting potassium current, and activating a barium-insensitive inward current carried primarily by sodium ions. A portion of the intracellular pathway for these actions is shared by TRH. In addition, there is evidence that NE alters HM firing patterns by affecting currents that are activated following depolarization. 

Received 4 April 1995; accepted in final form 20 June 1995.
APS Manuscript Number J221-5.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 July 1995.