ACTIONS OF NOREPINEPHRINE ON RAT HYPOGLOSSAL MOTONEURONS

1. We used conventional intracellular recording techniques in 400-mu m -thick slices from the brain stems of juvenile rats to investigate the action of norepinephrine (NE) on subthreshold and firing properties o f hypoglossal motoneurons (HMs). 2. In recordings in current-clamp mod e, 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). In recordings in single-electrode voltage-clamp mode, NE induced a rev ersible inward current (I-NE) accompanied by a reduction in input cond uctance. The average reversal potential for I-NE was -104 mV. The NE r esponses could be elicited in a Ca2+-free solution containing tetrodot oxin, 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 or by the beta-adrenoceptor agonist isoproterenol when alpha-adrenoceptors were blocked. 4. Substitution o f barium for calcium in the perfusion solution blocked the increase in R(N) in response to NE without completely blocking the depolarization . Replacement of sodium chloride with choline chloride in the barium-s ubstituted perfusion solution blocked the remaining depolarization. 5. The neuropeptide thyrotropin-releasing hormone (TRH), which also depo larizes 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 lower ed the minimum amount of injected current needed to elicit repetitive firing, it increased the slope of the firing frequency versus injected current relation in 8 of 14 cells tested, and it increased the delay from the onset of the depolarizing current pulse to the first evoked s pike in all cells tested. 7. We conclude that NE acts directly on alph a(1)-adrenoceptors to increase the excitability of HMs. It does this b y 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.