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Serotonin Depletion Attenuates AY‐9944–Mediated Atypical Absence Seizures
Author(s) -
Bercovici Eduard,
Cortez Miguel A.,
Wang Xiaomei,
Snead O. Carter
Publication year - 2006
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1111/j.1528-1167.2006.00415.x
Subject(s) - serotonergic , serotonin , medicine , endocrinology , hippocampus , neurotransmitter , thalamus , metabolite , chemistry , biology , central nervous system , neuroscience , receptor
Summary: Purpose: To test the hypothesis that serotonin (5‐HT) plays a role in the modulation of experimental atypical absence seizures. Methods: Male Long‐Evans hooded rats were treated from postnatal day (P) 2 to P20 with the cholesterol inhibitor AY‐9944 (AY). Epidural electrodes were implanted for electrocorticography (ECoG) followed by serotonin depletion by using para ‐cholorophenylalanine (PCPA). High‐performance liquid chromatography (HPLC) was used to measure the levels of serotonin and its metabolite (5‐HIAA) in various brain regions. Serotonin metabolism was computed by using the 5‐HIAA/5‐HT ratio and used to ascertain differences between groups. Results : PCPA treatment was associated with a significant decrease in the total slow spike‐and‐wave discharge (SSWD) duration in AY‐treated rats compared with controls (p < 0.01). HPLC data confirmed the PCPA depletion of 5‐HT and 5‐HIAA in cortex, thalamus, hippocampus, and brainstem compared with naïve rats. AY‐treated rats showed higher levels of 5‐HIAA and 5‐HT in the same brain regions, with a concomitant decrease in rates of serotonin turnover. Conclusions : The data indicate that serotonin depletion protects against experimental atypical absence seizures. The increased levels of 5‐HIAA and 5‐HT and altered rates of serotonin turnover suggest that the serotonergic neurotransmission may be perturbed in the AY rat.