Inhibition of Dopamine Receptor in Neonate Hippocampus: Immunolocalization of Post Synaptic Density Protein-95 and Dopamine Receptor in vivo

The effect of haloperidol on neonatal dopaminergic neurotransmission in the hippocampus of postnatal day 20 rats (P.20) was investigated in this study. Haloperidol blocked dopamine receptors (D2R) and inhibited D2R on the membrane of neonate neurons. For this study the 0.5 ml (20 mg/kg) of haloperidol was administered to pregnant female animals intraperitoneally a week before delivery. At day P.20, 5 control animals and 5 haloperidol treated animals were taken to the behavioral studies room for the Y maze and Novel object recognition test, which was done 7 am in the morning before mating. Electrophysiology was done with 2 control pups and 2 treated pups. Electrodes were implanted in the brain at the hippocampal region 2 mm beneath the bregma, 2 mm lateral to the midline. Anterior Posterior (AP=0), Medial Lateral (ML=2 mm). Also immunolocalization and immunofluorescence of post synaptic density protein (PSD-95), hippocampal morphology and hippocampal neurons have been done respectively. Results from this study showed a decline in memory index for the Y maze as a result of the effect of D2R blockade thereby inhibiting neurotransmission in newborns. Electrophysiology result in this study showed an increase in the root mean square (RMS) of control pups. The increase in RMS is equivalent to increase in wave burst pattern caused by neuronal excitation. Immunochemistry result showed an increase in the number of PSD-95 in the hippocampus of an increase in tyrosine hydroxylase in the hippocampus of the treated neonatal rats when compared to the control neonatal rats Immunofluorescence showed decline in the number of neurons in the haloperidol treated rats and it also caused hippocampal damage in terms of morphology. Furthermore, results from electrophysiology showed a statistical significant difference with P value 0.04229 (P<0.05) using the student t-test. These findings suggest that D2R inhibition may cause decline in memory function, impair learning in newborns and disrupt neonatal dopaminergic neurotransmission.