Differential modulation by monoamine membrane receptor agonists of reticulospinal input to lamina VIII feline spinal commissural interneurons
- PMID: 17767499
- DOI: 10.1111/j.1460-9568.2007.05764.x
Differential modulation by monoamine membrane receptor agonists of reticulospinal input to lamina VIII feline spinal commissural interneurons
Abstract
Noradrenaline and serotonin have previously been demonstrated to facilitate the transmission between descending reticulospinal tracts fibres and commissural interneurons coordinating left-right hindlimb muscle activity. The aim of the present study was to investigate the contribution of subclasses of monoaminergic membrane receptors to this facilitation. The neurons were located in Rexed lamina VIII in midlumbar segments and identified by their projections to the contralateral gastrocnemius-soleus motor nuclei and by lack of projections rostral to the lumbosacral enlargement. The effects of ionophoretically applied membrane receptor agonists [phenylephrine (noradrenergic alpha(1)), clonidine (noradrenergic alpha(2)), 8-OH-DPAT (5-HT(1A), 5-HT(7)), 2-me-5-HT (5-HT(3)), 5-me-5-HT (5-HT(2)) and alpha-me-5-HT (5-HT(2))] were examined on extracellularly recorded spikes evoked monosynaptically by electric stimulation of descending reticulospinal fibres in the medial longitudinal fascicle. Application of alpha(1) and 5-HT(2) agonists resulted in a facilitation of responses in all investigated neurons while application of alpha(2), 5-HT(1A/7) and 5-HT(3) agonists resulted in a depression. These opposite modulatory effects of different agonists suggest that the facilitatory actions of noradrenaline and serotonin on responses of commissural interneurons reported previously following ionophoretic application are the net outcome of the activation of different subclasses of monoaminergic membrane receptors. As these receptors may be distributed predominantly, or even selectively, at either pre- or postsynaptic sites their differential modulatory actions could be compatible with a presynaptically induced depression and a postsynaptically evoked enhancement of synaptic transmission between reticulospinal neurons and commissural interneurons.
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