title: Alpha-1 adrenoceptor agonists generate a "fast" NMDA receptor-independent motor rhythm in the neonatal rat spinal cord.
abstract: Noradrenaline, a potent activator of rhythmogenic networks in adult mammals has not been reported to produce functional rhythmic patterns in isolated spinal cords of newborn rats. We now show that a "fast" (cycle time: 1-4 s) transient rhythm was induced in sacrococcygeal (SC) and rostral-lumbar spinal segments of the neonatal rat by bath-applied noradrenaline. The fast rhythm was blocked by 1 microM of the alpha1-adrenoceptor antagonist prazosin but not by 1-20 microM of the alpha2-adrenoceptor blocker yohimbine, it could be initiated and maintained by alpha1-adrenoceptor agonists, and it was accompanied by a slow nonlocomotor rhythm. Transection at the lumbosacral junction abolished the fast-thoracolumbar (TL) rhythm while the fast-SC and slow-TL rhythms were unaffected. The N-methyl-d-aspartate (NMDA) receptor antagonist 2-amino-5-phosphonopentanoic acid (AP5) abolished the slow- and did not interrupt the fast rhythm. Thus alpha1-adrenoceptor agonists induce an NMDA receptor-independent rhythm in the SC cord and modulate NMDA receptor-dependent rhythmicity in TL segments. Injection of current steps into S(2) and flexor-dominated L(2) motoneurons during the fast rhythm revealed a 20-30% decrease in input-resistance (R(N)), coinciding with contralateral bursting. The R(N) of extensor-dominated L(5) motoneurons did not vary with the fast rhythm. The rhythmic fluctuations of R(N) in L(2) motoneurons were abolished, but the alternating left-right pattern of the fast rhythm was unchanged in midsagittally split TL cords. We suggest that the locomotor generators were not activated during the fast rhythm, that crossed-inhibitory pathways activated by SC projections controlled the rhythmic decrease in R(N) in L(2) motoneurons, and that the alternating pattern of the split TL cord was maintained by excitatory SC projections.
authors.affiliation: Dept. of Anatomy and Cell Biology, The Hebrew University Medical School, P.O. Box 12272, Jerusalem 91120, Israel.
authors.forename: H
authors.initials: H
authors.lastname: Gabbay
authors.forename: A
authors.initials: A
authors.lastname: Lev-Tov
mesh_terms: D015763:2-Amino-5-phosphonovalerate / Q000494:pharmacology; D058646:Adrenergic alpha-1 Receptor Agonists; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology*; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D017097:Electric Impedance; D004558:Electric Stimulation; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D066298:In Vitro Techniques; D008161:Lumbosacral Region; D008729:Methoxamine / Q000494:pharmacology; D009043:Motor Activity / Q000502:physiology*; D009046:Motor Neurons / Q000502:physiology; D009638:Norepinephrine / Q000494:pharmacology; D010507:Periodicity; D011224:Prazosin / Q000494:pharmacology; D051381:Rats; D016194:Receptors, N-Methyl-D-Aspartate / Q000502:physiology*; D012445:Sacrococcygeal Region; D013116:Spinal Cord / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D015016:Yohimbine / Q000494:pharmacology
chemical_list: D058646:Adrenergic alpha-1 Receptor Agonists; D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D018691:Excitatory Amino Acid Antagonists; D016194:Receptors, N-Methyl-D-Aspartate; D015016:Yohimbine; D015763:2-Amino-5-phosphonovalerate; D008729:Methoxamine; D009638:Norepinephrine; D011224:Prazosin