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Background: fourth generation antipsychotics have been implicated in the blockade of calcium\udsignalling through inhibition of dopamine receptive sites on dopaminergic D2 Receptor (D2R). As a\udresult of the abnormal calcium signalling associated with D2R inhibition, changes occur in the motor\udand memory neural axis leading to the observed behavioural deficits after prolonged haloperidol.\udThus, Vitamin D3 receptor (VD3R), a calcium controlling receptor in the striatum can be targeted\udto relief the neurological symptoms associated with haloperidol (−D2R) induced PD. Aim:\udThis study sets to investigate the role of VD3R activation in vitro and in vivo after haloperidolinduced\udDopaminergic (D2R) blockade. In addition, we examined the associated neural activity\udand behavioural changes in parkinsonian and VDRA intervention mice. Methods: Dopaminergic\udD2R inhibition was investigated in vitro using Melanocytes isolated from the scale of a Tilapia. In\udfour separate set ups, the cells were cultured in calcium free Ringer’s solution as follows; 300 µM\udhaloperidol, 100 µM VD3, 100 mM calcium chloride and a combination of 300 µM haloperidol\udand 100 µM VD3. Subsequently, dopaminergic vesicle accumulation and calcium signalling were observed in bright field microscopy using blue and green fluorescence probes. In the second phase,\udPD was induced in adult BALB/c mice (−D2; n = 8) after 14 days of intraperitoneal haloperidol\udtreatment (10 mg/Kg). A set of n = 4 mice were untreated (−D2) while the other group (n = 4) received\ud100 mg/Kg of VD3 for 7 days (−D2/+VDR). The control groups (n = 4 each) were treated with\udnormal saline (NS) and VD3 (+VDR) for 14 days. At the end of the treatment phase, the animals\udwere assessed in Rotarod, parallel bar-, cylinder-, Y-Maze-, one trial place recognition- and novel\udobject recognition-(NOR) tests. Neural activity was measured using chronic electrode implants\udplaced in the M1 (motor cortex), CPu (striatum), CA1 (hippocampus) and PFC (prefrontal cortex).\udNeural activity was compared with the outcomes of behavioural tests for memory and motor functions\udand data was expressed as mean ± SEM (analysed using ANOVA with Tukey post-hoc test,\udsignificant level was set at 0.05). Results/Discussion: in vitro outcomes show that VDR increase\udcalcium signalling and reverses the effect of haloperidol; specifically by reducing dopaminergic\udvesicle accumulation in the cell body. Similarly, in vivo neural recordings suggest an increase in\udcalcium hyperpolarization currents in the CPu and PFC of intervention mice (−D2/+VDR) when\udcompared with the parkinsonian mice (−D2). These animals (−D2/+VDR) also recorded an improvement\udin spatial working memory and motor function versus the Parkinsonian mice (−D2).\udThese outcomes suggest the role of CPu-PFC corticostriatal outputs in the motor-cognitive decline\udseen in parkinsonian mice. Similarly, VDRA reduced the neural deficits through restoration of calcium\udcurrents (burst activities) in the intervention mice (−D2/+VDR). Conclusion: VDRA treatment\udreduced the motor-cognitive defects observed in haloperidol induced PD. Our findings suggest the\udrole of VDRA in restoration of calcium currents associated with PFC and CPu corticostriatal outputs\udseen as burst frequencies in in vivo neural recording

journal of biomedical science and engineering

&amp;lt;i&amp;gt;Vitamin&amp;lt;/i&amp;gt; D&amp;lt;sub&amp;gt;3&amp;lt;/sub&amp;gt; Receptor Activation Rescued Corticostriatal Neural Activity and Improved Motor-Cognitive Function in -D&amp;lt;sub&amp;gt;2&amp;lt;/sub&amp;gt;R Parkinsonian Mice Model