Calbindin expression changes in dentate gyrus of patients with resistant temporal lobe epilepsy and co-morbid depression who underwent epilepsy surgery

D' ALESSIO L, KONOPKA H, ACUÑA A, ESCOBAR E, SCÉVOLA L, FERNANDEZ LIMA M, SEOANE E, KOCHEN S

Vienna

Congreso; European Congress of Neuropsychopharmacology; 2016

European College of Neuropsychopharmacology

Propose Depression is the most common psychiatric co-morbidity in persons with resistant temporal lobe epilepsy (TLE), with a prevalence rate ranging between 30-50% reported in specialized epilepsy centers. Additionally population based studies has been described that a positive history of depression was more frequently between patients with epilepsy onset [1]. The complex underlying pathogenic mechanisms are still unknown but alterations in hippocampal neuroplasticity and granular cell pathology have been proposed as common factors involved in the pathogenesis of both disorders [2]. Dentate gyrus dispersion with abnormal sprouting, the reduced of neurogenesis and the loss of calbindin (CB) (expressed in postmitotic new generated cells during last phases of neurogenesis), are common pathological markers described in chronic TLE with hippocampal sclerosis (HS) [3] [4]. The reduced CB expression in dentate gyrus has been involved in memory deficits associated to TLE but there is a few data about CB expression and behavior [5]. The aim of this study was to determine the immunoreactivity for CB in dentate gyrus layers of patients with resistant TLE and HS with and without co-morbid depression who underwent epilepsy surgery (anterior temporal lobectomy).MethodsPatients with TLE were evaluated according clinical, neurological, neuropsychological and psychiatric assessment protocols before surgery and complementary studies EEG, Video EEG, RMN were determined. For psychiatric diagnoses, Structured Clinical Interview for DSM Disorders [SCID]-I / II were administered by a trained psychiatrist. After surgery coronal sections of hippocampus body were processed with immunoperoxidasa with anti-calbindin. Other sections were processed with anti-NeuN and/or anti GFAP for confirming HS and double immunostaining using anti-calretinin and anti-nestin were also determined. Archival material from normal post-mortem hippocampus was simultaneously processed. Quantitative analysis of photomicrographs (number of granular cells positive for CB and CB sprouted cells, mean gray value, and reactive area) was determined by computerized image analysis (Image J). One way ANOVA followed Bonferroni test were determined.ResultsHippocampal sections of patients with TLE and co-morbid depression (TLE+D) n=9 (2 men and 7 women, age 29.11± 10.3 years) and patients with TLE without depression n=13 (6 men and 7 women, age 33.5 ± 9.3), and 5 matched postmortem controls were included. A significant reduction in the total number of CB cells per field was found in both groups of epileptic patients comparing to controls (p