Serotonin1A facilitation of frog motoneuron responses to afferent stimuli and to N-methyl-D-aspartate.
The effects of serotonin and excitatory amino acids on motoneurons were examined by sucrose gap recordings from the ventral root of the isolated, hemisected frog spinal cord superfused with magnesium-free, carbonate-buffered Ringer solution. Low concentrations of serotonin (0.1 microM) and the serotonin1A agonist 8-hydroxy-2-(n-dipropylamino)tetralin (8-OH-DPAT; 0.01 microM) significantly increased the duration and amplitude of the polysynaptic components of ventral root potentials produced by dorsal root stimulation. The facilitations of the ventral root potentials were blocked by the serotonin1A antagonist spiroxatrine, but were unaffected by the serotonin2 antagonist ketanserin or the serotonin3 antagonist 1 alpha H,3 alpha,5 alpha H-tropan-3-yl-3,-dichlorobenzoate (MDL 72222). The actions of 0.1 microM serotonin on motoneuron depolarizations evoked by the putative excitatory amino acid transmitters L-glutamate and L-aspartate were quite variable, but in the presence of ketanserin (20 microM), small consistent increases in amino acid-induced motoneuron depolarizations were observed. 8-OH-DPAT significantly enhanced motoneuron depolarizations elicited by the selective excitatory amino acid agonist N-methyl-D-aspartate in both normal and tetrodotoxin-containing Ringer solution. Quisqualate-induced motoneuron depolarizations were also facilitated by 8-OH-DPAT in normal Ringer solution, but these increases were eliminated by addition of either tetrodotoxin or the N-methyl-D-aspartate antagonist D(-)-2-amino-5-phosphonovalerate to the Ringer superfusate. Kainate-depolarizations were not altered by low concentrations of serotonin or 8-OH-DPAT. Prior exposure of the cord to spiperone, but not ketanserin or MDL 72222 blocked the enhancement of N-methyl-D-aspartate-induced motoneuron depolarizations by 8-OH-DPAT.(ABSTRACT TRUNCATED AT 250 WORDS)
Neurophysiology and Spinal Cord Pharmacology Laboratories, Veterans Affairs Medical Center, Miami.
A M
AM
Holohean
J C
JC
Hackman
S B
SB
Shope
R A
RA
Davidoff
D015763:2-Amino-5-phosphonovalerate / Q000494:pharmacology; D017371:8-Hydroxy-2-(di-n-propylamino)tetralin; D000344:Afferent Pathways / Q000502:physiology*; D000818:Animals; D004558:Electric Stimulation; D005071:Evoked Potentials / Q000187:drug effects; D005998:Glycine / Q000494:pharmacology; D066298:In Vitro Techniques; D007608:Kainic Acid / Q000494:pharmacology; D008564:Membrane Potentials / Q000187:drug effects; D009046:Motor Neurons / Q000187:drug effects / Q000502:physiology*; D016202:N-Methylaspartate / Q000494:pharmacology*; D009412:Nerve Fibers / Q000187:drug effects / Q000502:physiology; D016318:Quisqualic Acid / Q000494:pharmacology; D011894:Rana pipiens; D012701:Serotonin / Q000494:pharmacology*; D013116:Spinal Cord / Q000187:drug effects / Q000502:physiology*; D013126:Spinal Nerve Roots / Q000187:drug effects / Q000502:physiology; D013764:Tetrahydronaphthalenes / Q000494:pharmacology*; D013779:Tetrodotoxin / Q000494:pharmacology; D014326:Tropanes / Q000494:pharmacology
D013764:Tetrahydronaphthalenes; D014326:Tropanes; D012701:Serotonin; D013779:Tetrodotoxin; D016202:N-Methylaspartate; D015763:2-Amino-5-phosphonovalerate; D017371:8-Hydroxy-2-(di-n-propylamino)tetralin; D016318:Quisqualic Acid; C042253:bemesetron; D007608:Kainic Acid; D005998:Glycine