Browsing by Author "Amar N. Maurya"

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5-HT-induced depression of the spinal monosynaptic reflex potential utilizes different types of 5-HT receptors depending on Mg2+ availability
(Polish Academy of Sciences, 2009) Shripad B. Deshpande; Amar N. Maurya; Jitendra N. Singh
Receptor subtypes involved in the 5-hydroxytryptamine (5-HT)-induced depression of synaptic transmission in neonatal rat spinal cords in vitro were evaluated in the absence or presence of Mg2+ in the medium. Stimulation of a dorsal root evoked monosynaptic reflex potential (MSP) and polysynaptic reflex potential (PSP) in the segmental ventral root in Mg2+-free medium where the voltage-dependent blockade of NMDA receptors is absent. The 5-HT (0.3-50 μM) in the Mg2+-free medium depressed the MSP and PSP in a concentration-dependent manner. At 30 μM of 5-HT, the depression was 57% and 95% for MSP and PSP, respectively, and no further depression was seen at 50 μM. The 5-HT-induced depression of the reflexes in the Mg2+-free medium was blocked by ondansetron (5-HT3 receptor antagonist), but not by spiperone (5-HT2A/2C antagonist). In the Mg2+-free medium, phenylbiguanide (5-HT3 agonist) also depressed the MSP and PSP in a concentration-dependent manner and was blocked by ondansetron. Addition of Mg2+ (1.3 mM) to the medium abolished the PSP and decreased the MSP by 30%. In the presence of Mg2+, 5-HT (1-50 μM) also depressed the MSP in a concentration-dependent manner. At 10 μM of 5-HT, there was approximately 20% depression and at 50 μM the depression was 100%. The 5-HT-induced depression of MSP in the Mg2+-containing medium was antagonized by spiperone (p < 0.05, two-way ANOVA), but not by ondansetron. The results indicate that the 5-HT-induced depression of MSP involves 5-HT3 receptors in the Mg2+-free medium and 5-HT2A/ 2C in the presence of Mg2+ when NMDA receptors are in the closed state. Copyright © 2009 by Institute of Pharmacology Polish Academy of Sciences.
Glutamate transporter inhibitor advances the ischemia-induced depression of spinal synaptic transmission in rats in vitro
(Association of Physiologists and Pharmacologists of India, 2016) Amar N. Maurya; Anil K. Tiwari; Archana Jha; Shripad B. Deshpande
Ischemia depresses the spinal Ia-α motoneuron synaptic transmission via NMDA dependent mechanism. We postulated that glutamate transporter inhibitor (DL-threo-β-hydroxy aspartate, THA) advances the ischemia-induced depression. The experiments were performed on isolated, hemisected spinal cord from 4-6 day old rats. The stimulation of a dorsal root (L3-5) with supramaximal strength at 0.1 Hz elicited monosynaptic (MSR) and polysynaptic reflex (PSR) potentials in the corresponding segmental ventral root. Superfusion of ischemic solution (glucose free without O2 bubbling) depressed the spinal reflexes in a time-dependent manner and abolished them within 50 min. THA alone did not alter the magnitude of MSR and PSR up to 20 min while THA+ischemia abolished the reflexes within 25 min. The abolition time was significantly advanced in THA+ischemia group as compared to ischemia only group. The results indicate that glutamate transporter inhibitor advances the ischemia-induced depression of spinal reflexes substantiating glutamatergic action at this synapse. © 2016, Association of Physiologists and Pharmacologists of India. All rights reserved.
Indian red scorpion venom depresses spinal synaptic transmission without involving NMDA receptors
(2010) Amar N. Maurya; Shripad B. Deshpande
Stings of Indian red scorpion (Mesobuthus tamulus, MBT) produce neurological abnormalities such as convulsions and paralysis. These parameters indicate the activity at α-motoneuron. The present study was therefore, undertaken to evaluate the effect of MBT-venom on spinal reflexes and the involvement of N-methyl-. d-aspartate (NMDA) receptors. The experiments were performed on isolated hemisected spinal cords from 4 to 6 days old rats. Stimulation of a dorsal root with supramaximal strength at 0.1. Hz evoked monosynaptic (MSR) and polysynaptic reflex (PSR) potentials in the corresponding segmental ventral root. Superfusion of MBT-venom depressed the spinal reflexes in a time- and a concentration-dependent (0.1-1μg/ml) manner. MBT-venom at 0.1, 0.3 and 1.0μg/ml produced maximal depression of 55, 75 and 90% at 30, 10 and 7. min, respectively. The time required to produce 50% depression (T-50) of MSR was 19.0, 8.0, and 3.6. min and for PSR was 15.0, 5.6, and 2.9. min at 0.1, 0.3 and 1μg/ml of venom, respectively. Pre-treatment with DL-α-2-amino-5-phosphonovaleric acid (APV) decreased MSR by 26% and abolished PSR. In the presence of APV, the MBT-venom-induced depression of MSR was not different from the venom only group. The results indicate that venom-induced depression of spinal reflexes did not involve NMDA receptors. © 2010 Elsevier Ireland Ltd.
Involvement of 5-hydroxytryptaminergic transmission for the Mesobuthus tamulus venom-induced depression of spinal reflexes in neonatal rat in vitro
(Elsevier Ireland Ltd, 2010) Amar N. Maurya; S.B. Deshpande Shripad B.
Mesobuthus tamulus (MBT) venom is shown to depress the spinal reflexes through a mechanism unrelated to the NMDA receptors. 5-Hydroxytryptamine (5-HT) is another excitatory transmitter in the spinal cord therefore, the present study was undertaken to examine the involvement of 5-HT in the venom-induced depression of reflexes. The experiments were performed on isolated hemisected spinal cords from 4 to 6-day-old rats. Stimulation of a dorsal root with supramaximal strength evoked monosynaptic reflex (MSR) and polysynaptic reflex (PSR) potentials in the corresponding segmental ventral root. MBT venom (0.3μg/ml) depressed the spinal reflexes in a time-dependent manner and the maximal depression was seen at 10min. The time to produce 50% depression (T-50) of MSR and PSR was 8.1±1.41 and 6.8±0.5min, respectively. Pretreatment with pindolol (1μM; 5-HT1A/1B receptor antagonist) blocked the reflexes up to 15min. On the other hand, ketanserin (10μM; 5-HT2A/2C receptor antagonist) or ondansetron (0.1μM; 5-HT3 receptor antagonist) blocked the venom-induced depression of MSR and PSR during entire exposure time (30min). The 5-HT concentration of the cords exposed to venom (1.6±0.04μg/g tissue) was significantly greater than the control group (0.98±0.08μg/g tissue). The results indicate that venom-induced depression of spinal reflexes is mediated via 5-HTergic transmission involving 5-HT1A/1B, 5-HT2A/2C and 5-HT3 receptors. © 2010 Elsevier Ireland Ltd.
Involvement of AMPA receptors for mesobuthus tamulus pocock venom-induced depression of monosynaptic reflex in neonatal rat spinal cord in vitro
(2011) Amar N. Maurya; Shripad B. Deshpande
Glutamate is a putative neurotransmitter at Ia-α motoneuron synapse in the spinal cord and mediate the action via Nmethyl- D-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazole-propionate (AMPA) receptors. Since NMDA receptors are not involved in M. tamulus Pocock (MBT) venom-induced depression of spinal monosynaptic reflex (MSR), the present study was undertaken to evaluate the role of AMPA receptors in mediating the depression of MSR by MBT venom. The experiments were performed on isolated hemisected spinal cord from 4-6 day old rats. Stimulation of a dorsal root with supramaximal voltage evoked MSR and polysynaptic reflex (PSR) potentials in the corresponding segmental ventral root. Superfusion of MBT venom (0.3 μg/ml) depressed the spinal reflexes in a time-dependent manner. The maximum depression of MSR(~ 66%) was seen at 10 min and it was 25 min for PSR (~ 75%). The time to produce 50% depression of MSR and PSR was 6.7 ± 1.5 and 10.8 ± 2.6 min, respectively. Pretreatment of the cords with 6-cyano-7- nitroquinoxaline-2, 3-dione (CNQX, 0.1 μM), an AMPA receptor antagonist, blocked the venom-induced depression of MSR but not PSR. The results indicate that venom-induced depression of MSR is mediated via AMPA receptors.
Involvement of NO-guanylyl cyclase pathway for the depression of spinal monosynaptic reflex by Mesobuthus tamulus venom in neonatal rat in vitro
(2011) Amar N. Maurya; Shripad B. Deshpande
Aims: The present study was undertaken to evaluate the role of nitric oxide (NO) in Mesobuthus tamulus (MBT) venom-induced depression of spinal reflexes. Main methods: Experiments were performed on isolated hemisected spinal cords from 4 to 6 day old rats. Stimulation of a dorsal root with supramaximal strength evoked monosynaptic (MSR) and polysynaptic reflex (PSR) potentials in the corresponding segmental ventral root. Key findings: Superfusion of MBT venom (0.3 μg/ml) depressed the spinal reflexes in a time-dependent manner and the maximum depression was seen at 10 min (MSR by 63%; PSR by 79%). The time to produce 50% depression (T-50) of MSR and PSR was 7.7 ± 1.3 and 5.7 ± 0.5 min, respectively. Pretreatment with bicuculline (1 μM; GABAA receptor antagonist) or strychnine (1 μM; glycine A receptor antagonist) did not block the venom-induced depression of spinal reflexes. However, Nω-nitro-L-arginine methyl ester (L-NAME, 100 or 300 μM; NO synthase inhibitor) or hemoglobin (Hb, 100 μM; NO scavenger) antagonized the venom-induced depression of MSR. Further, soluble guanylyl cylase inhibitors (1 H-[1,2,4]Oxadiazolo[4,3-a]quinoxalin-1-one, ODQ; 1 μM or methylene blue, 100 μM) also antagonized the venom-induced depression of MSR but not PSR. Nitrite concentration (indicator of NO activity) of the cords exposed to venom (0.3 μg/ml) was not different from the control group. Significance: The results indicate that venom-induced depression of MSR is mediated via NO-guanylyl cyclase pathway without involving GABAergic or glycinergic system. © 2011 Elsevier Inc.