Abstract: In rats and primates, (±)3,4-Methylenedioxymethamphetamine (MDMA, ecstasy) produces both long-lasting damage to serotonergic axons and memory impairment. Our objective was to determine effects of neurotoxic dose of MDMA on long-term potentiation (LTP) in hippocampal area CA1 in Dark–Agouti (DA) rats. One week after neurotoxic MDMA treatment in vivo (12.5 mg/kg i.p., once a week, per three weeks), serotonergic deficit was evident in hippocampal slices as 56.3% reduction in 5-HT content (p = 0.04) and as 68.4% reduction in the effect of endogenous 5-HT release on synaptic neurotransmission (p < 0.01). In hippocampal slices from the same animals, LTP was on average 46% greater than that observed in sham-treated controls (42.9 ± 3.5%; n = 12 vs. 29.2 ± 3.2%; n = 12; p < 0.01). Non-neurotoxic dose of MDMA (12.5 mg/kg, i.p., one time) did not change LTP one week after the treatment, suggesting correlation between serotonergic deficit and enhanced synaptic plasticity. We conclude that MDMA-induced impairment of learning and memory is not a consequence of hippocampal LTP inhibition.

Enhanced hippocampal long-term potentiation following repeated MDMA treatment in Dark-Agouti rats / R.Morini; B.Mlinar; G.Baccini; R.Corradetti. - In: EUROPEAN NEUROPSYCHOPHARMACOLOGY. - ISSN 0924-977X. - STAMPA. - 21(2011), pp. 80-91. [10.1016/j.euroneuro.2010.07.007]

Enhanced hippocampal long-term potentiation following repeated MDMA treatment in Dark-Agouti rats.

MORINI, RAFFAELLA;MLINAR, BORIS;BACCINI, GILDA;CORRADETTI, RENATO
2011

Abstract

Abstract: In rats and primates, (±)3,4-Methylenedioxymethamphetamine (MDMA, ecstasy) produces both long-lasting damage to serotonergic axons and memory impairment. Our objective was to determine effects of neurotoxic dose of MDMA on long-term potentiation (LTP) in hippocampal area CA1 in Dark–Agouti (DA) rats. One week after neurotoxic MDMA treatment in vivo (12.5 mg/kg i.p., once a week, per three weeks), serotonergic deficit was evident in hippocampal slices as 56.3% reduction in 5-HT content (p = 0.04) and as 68.4% reduction in the effect of endogenous 5-HT release on synaptic neurotransmission (p < 0.01). In hippocampal slices from the same animals, LTP was on average 46% greater than that observed in sham-treated controls (42.9 ± 3.5%; n = 12 vs. 29.2 ± 3.2%; n = 12; p < 0.01). Non-neurotoxic dose of MDMA (12.5 mg/kg, i.p., one time) did not change LTP one week after the treatment, suggesting correlation between serotonergic deficit and enhanced synaptic plasticity. We conclude that MDMA-induced impairment of learning and memory is not a consequence of hippocampal LTP inhibition.
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80
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R.Morini; B.Mlinar; G.Baccini; R.Corradetti
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/2158/391992
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