Intraspinal amino acid neurotransmitter activities are involved in the generation of rhythmic sympathetic nerve discharge in newborn rat spinal cord.
Endogenous neurotransmitter activities underlying the sympathetic nerve discharge (SND) generated by newborn rat spinal cord in vitro were investigated using glutamatergic, glycinergic, and GABAergic antagonists. Under control conditions, the SND power spectrum had two major frequency components: synchronous bursting SND (bSND) with power dominant at < 0.1 Hz and quasiperiodic SND (qSND) oscillating at 1-2 Hz. Using high Mg2+ solution (12-24 mM) to block Ca2+-dependent synaptic transmission reversibly abolished SND. An interruption of glutamatergic neurotransmission by CNQX (non-NMDA receptor blocker) or L-AP4 (reducing the synaptic release of glutamate) failed to affect qSND, but consistently reduced bSND. Application of kynurenate, a broad-spectrum ionotropic glutamate receptor blocker, only caused an unstable SND but did not reduce SND. In contrast, strychnine (Stry, glycine receptor antagonist) consistently reduced qSND in a dose-dependent manner. Bicuculline (Bic, GABA(A) receptor antagonist) induced a synchronous bSND of irregular rhythm, which could be further regularized by adding Stry. Bic-induced bSND was reversibly abolished by CNQX or L-AP4. In conclusion, intraspinal glycinergic, GABAergic, and glutamatergic activities are involved in the generation of the spinal cord-derived SND in newborn rats. Intraspinal GABAergic interneurons may tonically inhibit the glutamatergic bursting neurons that generate a synchronous bSND. Activities of these glutamatergic bursting neurons may also be modulated by intraspinal glycinergic interneurons.
Su
C K
CK
Institute of Biomedical Sciences, Academia Sinica, 11529, Taipei, Taiwan. csu@ibms.sinica.edu.tw
D018750:6-Cyano-7-nitroquinoxaline-2,3-dione / Q000494:pharmacology; D000200:Action Potentials / Q000502:physiology*; D000818:Animals; D000831:Animals, Newborn / Q000033:anatomy & histology / Q000254:growth & development* / Q000378:metabolism; D001640:Bicuculline / Q000494:pharmacology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D018756:GABA Antagonists / Q000494:pharmacology; D018698:Glutamic Acid / Q000378:metabolism; D005998:Glycine / Q000378:metabolism; D018684:Glycine Agents / Q000494:pharmacology; D007395:Interneurons / Q000166:cytology / Q000378:metabolism; D008274:Magnesium / Q000494:pharmacology; D009474:Neurons / Q000166:cytology / Q000378:metabolism*; D018377:Neurotransmitter Agents / Q000378:metabolism*; D009924:Organ Culture Techniques; D010507:Periodicity; D051381:Rats; D013116:Spinal Cord / Q000187:drug effects / Q000254:growth & development* / Q000378:metabolism; D013331:Strychnine / Q000494:pharmacology; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000254:growth & development* / Q000378:metabolism; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D018691:Excitatory Amino Acid Antagonists; D018756:GABA Antagonists; D018684:Glycine Agents; D018377:Neurotransmitter Agents; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid; D018750:6-Cyano-7-nitroquinoxaline-2,3-dione; D013331:Strychnine; D008274:Magnesium; D005998:Glycine; D001640:Bicuculline