Proceedings of The Physiological Society

Trinity College Dublin (2003) J Physiol 551P, C56

Communications

TRH modulates electrotonic coupling between rat hypoglossal motoneurones in vitro

Vitali A. Bouryi and David I. Lewis

Neuroscience Group, School of Biomedical Sciences, University of Leeds, Leeds LS2 9NQ, UK


Thyrotropin-releasing hormone (TRH) projections to hypoglossal motoneurones originate from the raphe pallidus and obscurus (Lynn et al. 1991). TRH-evoked excitatory responses in these motoneurones are the combination of both pre- and postsynaptic actions: a direct membrane depolarisation (Bayliss et al. 1992; Bouryi & Lewis, 2002) and an increased release of glutamate from the terminals of caudal raphe projections (Bouryi & Lewis, 2002). Here we provide evidence of an additional action of TRH on hypoglossal motoneurones, the opening of gap junctions between adjacent neurones and hence electrotonic coupling.

Male Wistar rats (12-14 days) were terminally anaesthetised with sodium pentobarbitone (120 mg kg-1, I.P.) and 300 µm coronal slices of the appropriate region of the medulla oblongata prepared (Bouryi & Lewis, 2001). Whole cell voltage clamp recordings were made from visually identified hypoglossal motoneurones within the ventral region of the nucleus, with pharmacological agents being applied in the superfusate as required.

Superfusion of TRH (10 µM) resulted in the induction of oscillatory activity or spikelets, characterised as a fast inward current followed by a slower outward current in 28 hypoglossal motoneurones. These spikelets were not observed at rest or when the neurones were depolarised by increased extracellular K+ (10 mM, n = 19). They remained during the co-application (n = 12) of 2,3-dioxo-6-nitro-1,2,2,3-tetrahydrobenzo[f]quinxaline-7-sulphonamide disodium (NBQX, 20 µM), strychnine (4 µM) and bicuculline (10 µM) demonstrating that they were not synaptic potentials. They were, however, abolished by the gap junction blocker, carbenoxolone (200 µM, n = 6). With a superfusate containing high K+, NBQX, strychnine and bicuculline, inclusion of GTP-λ-S (100 µM) in the patch pipette resulted in the gradual appearance of spikelets following attainment of the whole cell configuration. These GTP-λ-S-evoked spikelets were abolished when K+ levels were reduced to 3.1 mM, reappearing when K+ was returned to 10 mM.

These data suggest that TRH, as a result of the modulation of G-protein-mediated pathways within hypoglossal motoneurones, can open gap junctions between adjacent motoneurones. The resultant electrotonic coupling would facilitate the co-ordinated activation of distinct sub-populations of hypoglossal motoneurones.

The support of The Wellcome Trust is gratefully acknowledged.

Where applicable, experiments conform with Society ethical requirements