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Paul D Shilling - One of the best experts on this subject based on the ideXlab platform.
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A Systemically Administered Neurotensin Agonist Blocks Disruption of Prepulse Inhibition Produced by a Serotonin-2A Agonist
2003Co-Authors: David Feifel, Gilia Melendez, Paul D ShillingAbstract:Prepulse inhibition (PPI) of the startle reflex can be disrupted by drugs that act as Agonists at the Serotonin (5-HT) 2A receptor, such as DOI, and this effect is blocked by drugs that inhibit 5-HT2A transmission. We tested the effects of systemic administration of PD149163, a neurotensin Agonist, on DOI-induced disruption of PPI in Sprague–Dawley rats. PD149163 completely and dose dependently blocked the PPI deficits produced by DOI. These findings suggest that, in addition to their established ability to inhibit dopamine transmission, neurotensin Agonists may also inhibit 5-HT2A transmission, a pharmacological feature associated with atypical antipsychotic drugs.
David Feifel - One of the best experts on this subject based on the ideXlab platform.
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A Systemically Administered Neurotensin Agonist Blocks Disruption of Prepulse Inhibition Produced by a Serotonin-2A Agonist
2003Co-Authors: David Feifel, Gilia Melendez, Paul D ShillingAbstract:Prepulse inhibition (PPI) of the startle reflex can be disrupted by drugs that act as Agonists at the Serotonin (5-HT) 2A receptor, such as DOI, and this effect is blocked by drugs that inhibit 5-HT2A transmission. We tested the effects of systemic administration of PD149163, a neurotensin Agonist, on DOI-induced disruption of PPI in Sprague–Dawley rats. PD149163 completely and dose dependently blocked the PPI deficits produced by DOI. These findings suggest that, in addition to their established ability to inhibit dopamine transmission, neurotensin Agonists may also inhibit 5-HT2A transmission, a pharmacological feature associated with atypical antipsychotic drugs.
Gilia Melendez - One of the best experts on this subject based on the ideXlab platform.
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A Systemically Administered Neurotensin Agonist Blocks Disruption of Prepulse Inhibition Produced by a Serotonin-2A Agonist
2003Co-Authors: David Feifel, Gilia Melendez, Paul D ShillingAbstract:Prepulse inhibition (PPI) of the startle reflex can be disrupted by drugs that act as Agonists at the Serotonin (5-HT) 2A receptor, such as DOI, and this effect is blocked by drugs that inhibit 5-HT2A transmission. We tested the effects of systemic administration of PD149163, a neurotensin Agonist, on DOI-induced disruption of PPI in Sprague–Dawley rats. PD149163 completely and dose dependently blocked the PPI deficits produced by DOI. These findings suggest that, in addition to their established ability to inhibit dopamine transmission, neurotensin Agonists may also inhibit 5-HT2A transmission, a pharmacological feature associated with atypical antipsychotic drugs.
A.z. Hassan - One of the best experts on this subject based on the ideXlab platform.
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Calcium-mediated intracellular messengers modulate the serotonergic effects on axonal excitability
1997Co-Authors: Yasuo Saruhashi, Wise Young, A.z. HassanAbstract:Abstract We carried out experiments to investigate the mechanisms of Serotonin-induced axonal excitability changes using isolated dorsal columns from young (seven to 11-day-old) Long–Evan's hooded rats. Conducting action potentials were activated by submaximal (50%) and supramaximal constant current electrical stimuli and recorded with glass micropipette electrodes. In experiment 1, to study Ca 2+ -mediated mechanisms, we superfused the preparations with Ringer solutions containing varying Ca 2+ concentrations. Following superfusion with Ca 2+ -free Ringer solution for 4 h, we tested initial responses to Serotonin Agonists. Studies then were repeated after preparations had been washed for 1 h with Ringer solution containing 1.5 mM Ca 2+ and 1.5 mM Mg 2+ . After 4 h superfusion of Ca 2+ -free Ringer solution, quipazine (a Serotonin 2A Agonist, 100 μ M) did not induce significant axonal excitability changes (amplitude change of 1.4±1.3%, percentage of predrug control level, ±S.D., n =6). A 100 μ M concentration of 8-hydroxy-dipropylaminotetralin (a Serotonin 1A Agonist) reduced response amplitudes by 36.3±4.2% (±S.D., P n =7) and prolonged latencies by 22.3±4.3% (±S.D., P n =7). Application of Serotonin (100 μ M) decreased amplitudes by 6.6±5.0% (±S.D., P n =6). Extracellular calcium concentration ([Ca 2+ ] e ) was measured at various depths in the dorsal column with ion-selective microelectrodes. Four hours' superfusion with Ca 2+ -free Ringer solution reduced [Ca 2+ ] e to less than 0.1 mM in dorsal columns. In 1.5 mM Ca 2+ Ringer solution, quipazine increased the amplitudes by 38.3±5.8% ( P n =6). Likewise, Serotonin increased the amplitudes by 13.8±4.9% ( P n =6). In contrast however, 8-hydroxy-dipropylaminotetralin still reduced amplitudes by 35.0±6.4% ( P n =7) and prolonged latencies by 24.1±4.5% ( P n =7). In experiment 2, we investigated calcium-dependent and cAMP-mediated protein kinase signalling pathways to evaluate their role as intracellular messengers for Serotonin 2A receptor activation. Two protein kinase inhibitors, 50 μ M H7 (an inhibitor of protein kinase C and c-AMP dependent protein kinase) and 100 μ M d -sphingosine (an inhibitor of protein kinase A and C) effectively eliminated the excitatory effects of the Serotonin 2A Agonist. 100 μ M cadmium (a Ca 2+ channel blocker) also blocked the effects of quipazine. Neither these protein kinase inhibitors nor cadmium alone affected action potential amplitudes. These results suggest that replacing Ca 2+ with Mg 2+ blocks the excitatory effects of quipazine but does not prevent the inhibitory effects of 8-hydroxy-dipropylaminotetralin, and calcium-mediated protein kinase mechanisms modulate axonal excitability changes induced by Serotonin and its Agonist.
Yasuo Saruhashi - One of the best experts on this subject based on the ideXlab platform.
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Calcium-mediated intracellular messengers modulate the serotonergic effects on axonal excitability
1997Co-Authors: Yasuo Saruhashi, Wise Young, A.z. HassanAbstract:Abstract We carried out experiments to investigate the mechanisms of Serotonin-induced axonal excitability changes using isolated dorsal columns from young (seven to 11-day-old) Long–Evan's hooded rats. Conducting action potentials were activated by submaximal (50%) and supramaximal constant current electrical stimuli and recorded with glass micropipette electrodes. In experiment 1, to study Ca 2+ -mediated mechanisms, we superfused the preparations with Ringer solutions containing varying Ca 2+ concentrations. Following superfusion with Ca 2+ -free Ringer solution for 4 h, we tested initial responses to Serotonin Agonists. Studies then were repeated after preparations had been washed for 1 h with Ringer solution containing 1.5 mM Ca 2+ and 1.5 mM Mg 2+ . After 4 h superfusion of Ca 2+ -free Ringer solution, quipazine (a Serotonin 2A Agonist, 100 μ M) did not induce significant axonal excitability changes (amplitude change of 1.4±1.3%, percentage of predrug control level, ±S.D., n =6). A 100 μ M concentration of 8-hydroxy-dipropylaminotetralin (a Serotonin 1A Agonist) reduced response amplitudes by 36.3±4.2% (±S.D., P n =7) and prolonged latencies by 22.3±4.3% (±S.D., P n =7). Application of Serotonin (100 μ M) decreased amplitudes by 6.6±5.0% (±S.D., P n =6). Extracellular calcium concentration ([Ca 2+ ] e ) was measured at various depths in the dorsal column with ion-selective microelectrodes. Four hours' superfusion with Ca 2+ -free Ringer solution reduced [Ca 2+ ] e to less than 0.1 mM in dorsal columns. In 1.5 mM Ca 2+ Ringer solution, quipazine increased the amplitudes by 38.3±5.8% ( P n =6). Likewise, Serotonin increased the amplitudes by 13.8±4.9% ( P n =6). In contrast however, 8-hydroxy-dipropylaminotetralin still reduced amplitudes by 35.0±6.4% ( P n =7) and prolonged latencies by 24.1±4.5% ( P n =7). In experiment 2, we investigated calcium-dependent and cAMP-mediated protein kinase signalling pathways to evaluate their role as intracellular messengers for Serotonin 2A receptor activation. Two protein kinase inhibitors, 50 μ M H7 (an inhibitor of protein kinase C and c-AMP dependent protein kinase) and 100 μ M d -sphingosine (an inhibitor of protein kinase A and C) effectively eliminated the excitatory effects of the Serotonin 2A Agonist. 100 μ M cadmium (a Ca 2+ channel blocker) also blocked the effects of quipazine. Neither these protein kinase inhibitors nor cadmium alone affected action potential amplitudes. These results suggest that replacing Ca 2+ with Mg 2+ blocks the excitatory effects of quipazine but does not prevent the inhibitory effects of 8-hydroxy-dipropylaminotetralin, and calcium-mediated protein kinase mechanisms modulate axonal excitability changes induced by Serotonin and its Agonist.
