title: 3-Nitropropionic acid-induced depression of spinal reflexes does not involve 5-hydroxytryptaminergic system in contrast to ischemia-induced depression in neonatal rat spinal cord in vitro.
abstract: The involvement of 5-hydroxytryptaminergic (5-HTergic) system for the 3-nitropropionic acid (3-NPA)-induced depression of spinal reflexes was evaluated and compared with other energy deficiency condition (ischemia; glucose-free and O2-free). The monosynaptic (MSR) and polysynaptic reflex (PSR) potentials were recorded at ventral root by stimulating the corresponding dorsal root in neonatal rat spinal cord in vitro. Superfusion of 3-NPA (3.4 mM) or ischemic solution depressed the reflexes in a time-dependent manner abolishing them by 35 min. Pretreatment with pindolol (1 microM), ketanserin (10 microM) or ondansetron (0.1 microM); 5-HT1, 5-HT2, or 5-HT3 receptor antagonist, respectively, did not block the 3-NPA-induced depression of reflexes whereas, ischemia-induced depression was blocked by ondansetron. 5-HT content of the spinal cords incubated with 3-NPA (3.4 mM) for 30 min was decreased significantly (33 ng/g tissue) while increased (286 ng/g) in cords exposed to ischemic solution as compared to saline-treated cords (161 ng/g). Thus, 3-NPA-induced depression of spinal reflexes does not involve 5-HTergic pathway unlike ischemia-induced depression.
authors.affiliation: Department of Physiology, Institute of Medical Sciences, Banaras Hindu University, Varanasi 221005, UP, India.
authors.forename: Rajesh
authors.initials: R
authors.lastname: Gupta
authors.forename: Archana
authors.initials: A
authors.lastname: Jha
authors.forename: Shripad B
authors.initials: SB
authors.lastname: Deshpande
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001928:Brain Diseases, Metabolic / Q000139:chemically induced / Q000378:metabolism* / Q000503:physiopathology; D004195:Disease Models, Animal; D004558:Electric Stimulation; D042963:Electron Transport Complex II / Q000187:drug effects / Q000378:metabolism; D004734:Energy Metabolism / Q000187:drug effects / Q000502:physiology*; D004791:Enzyme Inhibitors / Q000633:toxicity; D005260:Female; D008297:Male; D009434:Neural Pathways / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology; D009474:Neurons / Q000187:drug effects / Q000378:metabolism; D009574:Nitro Compounds / Q000633:toxicity; D011422:Propionates / Q000633:toxicity; D051381:Rats; D012021:Reflex, Abnormal / Q000187:drug effects / Q000502:physiology*; D012701:Serotonin / Q000378:metabolism*; D012702:Serotonin Antagonists / Q000633:toxicity; D013116:Spinal Cord / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology; D020760:Spinal Cord Ischemia / Q000378:metabolism* / Q000503:physiopathology; D013126:Spinal Nerve Roots / Q000187:drug effects / Q000503:physiopathology; D013385:Succinate Dehydrogenase / Q000037:antagonists & inhibitors / Q000378:metabolism; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology
chemical_list: D004791:Enzyme Inhibitors; D009574:Nitro Compounds; D011422:Propionates; D012702:Serotonin Antagonists; C478189:respiratory complex II; D012701:Serotonin; D042963:Electron Transport Complex II; D013385:Succinate Dehydrogenase; C015392:3-nitropropionic acid