Dysregulation of the serotonergic system has been reported to have a significant role in several neurological disorders including depression, autism and substance abuse disorders. Changes in the expression of the serotonin transporter (SERT) through polymorphisms in the regulatory regions of the SERT gene have been associated, but not yet been conclusively linked to, neuropsychiatric disorders. In turn, dendritic spine structure and function are critical for neuronal function and the disruption of dendritic spine formation at glutamatergic synapses is a hallmark of several neuropsychiatric disorders. To understand the effect of SERT depletion on dendritic spine formation, neuronal cultures were established from the cortex of postnatal day 0–1 SERT knockout (KO) rats. Cortical neurons were subsequently allowed to mature to 21 days in vitro, and dendritic spine density was assessed using immunocytochemical co-labelling of drebrin and microtubule associated protein 2. Genetic knockout of the SERT had a gene-dose effect on dendritic spine densities of cortical neurons. The results of this paper implicate SERT function with the formation of dendritic spines at glutamatergic synapses, thereby offering insight into the aetiology of several neuropathologies.

据报道，5-羟色胺能系统的失调在几种神经系统疾病中具有重要作用，包括抑郁症、自闭症和药物滥用障碍。通过 SERT 基因调控区域中的多态性改变血清素转运蛋白 (SERT) 的表达与神经精神疾病有关，但尚未最终确定。反过来，树突棘结构和功能对神经元功能至关重要，谷氨酸能突触中树突棘形成的破坏是几种神经精神疾病的标志。为了了解 SERT 耗竭对树突棘形成的影响，从出生后第 0-1 天 SERT 敲除 (KO) 大鼠的皮层建立神经元培养物。随后允许皮层神经元在体外成熟至 21 天，使用 drebrin 和微管相关蛋白 2 的免疫细胞化学共标记评估树突棘密度。SERT 的基因敲除对皮质神经元的树突棘密度具有基因剂量效应。本文的结果将 SERT 功能与谷氨酸能突触处树突棘的形成联系起来，从而深入了解几种神经病理学的病因。