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This Article Full Text Full Text (PDF) All Versions of this Article: 94/4/2867    most recent 00465.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (8) Citing Articles via Google Scholar Google Scholar Articles by Shay, B. L. Articles by Hochman, S. Search for Related Content PubMed PubMed Citation Articles by Shay, B. L. Articles by Hochman, S.

Serotonin 5-HT₂ Receptors Induce a Long-Lasting Facilitation of Spinal Reflexes Independent of Ionotropic Receptor Activity

¹Department of Physical Therapy, University of Manitoba, Winnipeg, Manitoba, Canada; and ²Department of Physiology, Emory University, Atlanta, Georgia

Submitted 6 May 2005; accepted in final form 14 July 2005

Dorsal root-evoked stimulation of sensory afferents in the hemisected in vitro rat spinal cord produces reflex output, recorded on the ventral roots. Transient spinal 5-HT_2C receptor activation induces a long-lasting facilitation of these reflexes (LLFR) by largely unknown mechanisms. Two Sprague–Dawley substrains were used to characterize network properties involved in this serotonin (5-HT) receptor–mediated reflex plasticity. Serotonin more easily produced LLFR in one substrain and a long-lasting depression of reflexes (LLDR) in the other. Interestingly, LLFR and LLDR were bidirectionally interconvertible using 5-HT_2A/2C and 5-HT_1A receptor agonists, respectively, regardless of substrain. LLFR was predominantly A afferent fiber mediated, consistent with prominent 5-HT_2C receptor expression in the A fiber projection territories (deeper spinal laminae). Reflex facilitation involved an unmasking of polysynaptic pathways and an increased receptive field size. LLFR emerged even when reflexes were evoked three to five times/h, indicating an activity independent induction. Both the NMDA and AMPA/kainate receptor–mediated components of the reflex could be facilitated, and facilitation was dependent on 5-HT receptor activation alone, not on coincident reflex activation in the presence of 5-HT. Selective blockade of GABA_A and/or glycine receptors also did not prevent reflex amplification and so are not required for LLFR. Indeed, a more robust response was seen after blockade of spinal inhibition, indicating that inhibitory processes serve to limit reflex amplification. Overall we demonstrate that the serotonergic system has the capacity to induce long-lasting bidirectional changes in reflex strength in a manner that is nonassociative and independent of evoked activity or activation of ionotropic excitatory and inhibitory receptors.

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