Calbindin Essay

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Anti-Calbindin binds to Calbindin (CB) and labels GABAergic neurons

In our immunohistochemistry (IHC) experiment, we used anti-Calbindin as our primary antibody, Goat anti-Rabbit 488 IgG as our secondary antibody (“488” meaning that the fluorescent dye is excited at a wavelength of 488nm, fluorescing green), and DAPI-mounting serum as a DNA (nucleus) marker with blue fluorescence for reference against anti-Calbindin-marked GABAergic neurons (Lammel, 2016). While GABAergic-neuron-expressing anti-Calbindin labeled various regions of the brain such as, midbrain reticular nucleus (MRN), Red nucleus (RN), Substantia Nigra pars reticulate (SNr), and Interpeduncular nucleus (IPN), our region of study was focused on the ventral tegmentum area (VTA) and the prefrontal cortex (PFC).

Role of Calbindin (CB)

Calbindin (CB) has four active calcium-binding sites (with two sites that lost their capacity to bind to calcium), called EF hands
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PFC maintains its functional role as a “mental sketchpad” through regulating the outputs of pyramidal cells, and inhibition is crucial in this regulation. In a research review article by D.W. Eyles and his colleagues, the malfunctioning of CB-containing double bouquet neurons in the PFC was a feature of schizophrenia (2002). However, contradictory research findings – one experiment reporting increased CB-neuron density in schizophrenic patients compared to control patients, and another reporting reduced or disordered CB neurons in schizophrenic patients – suggest the need to shift our attention from the number of CBP-containing neurons to the CBP intracellular content itself, in order to verify the significance of CBPs in neuronal function and the potential consequences of reduced intracellular CBP content in PFC GABAergic inhibitory function. (Eyles et al,

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