Bisphenol A depresses monosynaptic and polysynaptic reflexes in neonatal XXXX spinal cord in vitro involving estrogen receptor-dependent NO-mediated mechanisms.

@entity35 @entity717 @entity30921 @entity308
UNASSIGNED: Bisphenol A (BPA), a toxic chemical from plastics, is known to produce @entity717 which may imply the alteration in synaptic activity at Ia-a motoneuron synapse also. However the effect of BPA on this synapse is not known. Therefore, this study was undertaken to examine the effect of BPA on reflexes originating at Ia-a motoneuron synapse in the spinal cord. The experiments were performed on isolated hemisected spinal cords from 4 to 6d @entity35 . Stimulation of a dorsal root evoked segmental monosynaptic ( @entity30921 ) and polysynaptic (PSR) reflex potentials in the corresponding ventral root. Nitrite content (indicator of NO activity) of cords was estimated in the presence of BPA with/without antagonists. Superfusion of BPA (3-100 M) depressed the reflexes in a concentration- and time-dependent manner. The @entity308 was    20,    50 and    70% at 10, 30 and 100 M of BPA, respectively. The 50% @entity308 occurred around 15min at 30 M of BPA. Pretreatment with estrogen receptor (ERa) antagonist, tamoxifen, blocked the BPA-induced @entity308 of reflexes, whereas, 17b-estradiol, ER agonist, did not depress the reflexes even up to 10 M. Further, pretreatment with N  -Nitro-l-arginine methyl ester hydrochloride (l-NAME) or hemoglobin (Hb) blocked the BPA-induced @entity308 of spinal reflexes. Nitric oxide (NO) donor sodium-nitroprusside depressed the @entity30921 and PSR in a concentration-dependent manner. The nitrite concentration of the cords exposed to BPA was 733 M/gm of tissue (three times the saline group). Pretreatment with tamoxifen/l-NAME/Hb blocked the BPA-induced increase of nitrite levels. The present observations indicate that BPA depressed spinal synaptic transmission through ERa-dependent NO-mediated mechanisms. The altered synaptic activity may implicate for @entity717 after exposure to BPA.
