Proceedings of The Physiological Society

University of Leeds (2002) J Physiol 544P, S008

Communications

TRH potentiates excitatory inputs from the raphe pallidus to rat hypoglossal motoneurones, in vitro

Vitali A. Bouryi and David I. Lewis

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


Thyrotropin-releasing hormone (TRH) is co-localised with 5-hydroxytryptamine (5-HT) and glutamate in raphe pallidus projections to rat hypoglossal motoneurones (Kachidan et al. 1991; Nicholas et al. 1992), with this peptide having been shown to have an excitatory action on these latter neurones (Bayliss et al. 1992). Since we have previously demonstrated that 5-HT inhibits glutamatergic inputs from the raphe pallidus to hypoglossal motoneurones via an action at presynaptic terminals (Bouryi & Lewis, 2001), the aim of the present study was to determine whether TRH could also modulate glutamate release via an action at this site.

Male Wistar rats (12-14 days) were terminally anaesthetised with sodium pentobarbitone (120 mg kg-1, I.P.) and 300 mm coronal slices of the medulla prepared (Lewis, 1994). Whole-cell voltage-clamp recordings were made from identified hypoglossal motoneurones. Synaptic pathways from the raphe pallidus were activated utilising a stimulating electrode placed within this region, with pharmacological agents being applied in the superfusate as required.

Recordings were made from 21 hypoglossal motoneurones located within the ventral region of the nucleus. TRH (10 mM) evoked a membrane depolarisation of 6.53 ± 4.7 mV (mean ± S.D., P < 0.001, Student's paired t test, n = 15), an increase in cell input resistance of 34.0 ± 33 % (P < 0.001, n = 15) and an increase in spontaneous excitatory postsynaptic currents (EPSCs) in the majority of neurones. TRH increased the amplitude of EPSCs (120 ± 16 %, n = 7) evoked by stimulation within the raphe pallidus whilst decreasing the paired pulse ratio from 1.22 ± 0.13 to 1.14 ± 0.09 (P < 0.05, n = 4). In seven neurones, TRH also evoked spikelets. The spontaneous EPSCs, but not the spikelets, were abolished by 2,3-dioxo-6-nitro-1,2,3,4-tetrahydrobenzo[f]quinoxaline-7-sulphonamide disodium (NBQX, 10 mM). The amplitudes of the spikelets were unaffected by membrane voltage in the recorded cell.

These data demonstrate that TRH has multiple actions on hypoglossal motoneurones including a postsynaptic excitatory action, potentiation of excitatory glutamatergic inputs from the raphe pallidus via an action at presynaptic terminals and the synchronisation of activity in adjacent neurones following the opening of gap junctions.

The support of The Wellcome Trust is gratefully acknowledged.

All procedures accord with current UK legislation.

Where applicable, experiments conform with Society ethical requirements