Topic: Cav1.2

Antidepressant treatment during pregnancy may endanger neurodevelopment of the offspring. Cellular parameters (hippocampal homeostasis) and physiological parameters (behavioral aspects) in the offspring of Mirtazapine treated and depressed mothers are not yet fully described. We evaluated changes in cellular calcium homeostasis (Fura2AM) and CaV1.2 expression, presence of mitochondrial superoxide radicals (MitoSOXTM) together with behavior of developing pups.As an experimental model of perinatal depression we used pre-gestational exposure to chronic unpredictable stress followed by Mirtazapine

L-type voltage-gated calcium channels (L-VGCCs) are upstream of competing pathways that promote or inhibit dendritic growth. How L-VGCCs achieve signaling specificity remains unknown. We hypothesize that modulation of ICaL determines distinct processes controlling dendritic growth. To address this issue fluorescence imaging experiments were conducted on young murine cultured hippocampal neurons. Our findings show that dihydropyridine (DHP) blockers suppress dendritic growth and overexpression of DHP-insensitive CaV1.2 mutant prevented this effect, indicating that CaV1.2 is the channel isoform

Voltage-gated calcium channels (Cav) mediate calcium influx in living cells and are necessary for essential physiological functions such as muscle contraction and excitation-transcription coupling. Channels of the Cav2 family (Cav2.1, 2.2, and 2.3) are highly expressed in the central nervous system (CNS) and are important regulators of neuronal excitability. They are involved in pre- and postsynaptic functions where they, for example, trigger neurotransmitter release. Cav2.3 (α1E) is involved in neuronal development and, when compared to other α1 subunits, shows the strongest expression in mou