Hippocampus Synthesis

The hippocampus is a neural component of cognitive function as it has the α4β2 nicotinic receptor that was discovered to be involved in memory functioning (8). Owing to the fact that chronic systemic nicotine infusion fails to block the ventral hippocampal MLA-induced memory damage on the same radial-arm maze, it is known that nicotine’s positive effects on memory function is due to the hippocampal α7 nicotinic receptors (9).

Nicotinic changes in the hippocampal function could produce enduring functional changes in the hippocampal pathways as the hippocampus strengthens synaptic connections in areas involved in addiction (9). It was found that nAChRs might facilitate effects of nicotine on memory and learning (10). Acute administration of

It was discovered that nicotine interferes with the catecholamine (neurotransmitters) and the brainstem autonomic nuclei growth throughout the prenatal phase of rodents, which also applies to humans as the first and second trimesters are equivalent (14). The neocortex, hippocampus and the cerebellum during the early postnal period can be altered, as well as the late monoamine maturation during adolescence and the limbic system

Consequently, prenatal nicotine exposure also triggers programmed apoptosis, changes in cellular maturation and perturbed cellular replication and differentiation (5,14). Rodents that were exposed to nicotine via maternal infusions throughout gestation show persistent postnatal elevated levels of ornithine decarboxylase activity (associated with cell damage and even cell death) (5). The DNA content within the cerebellum and the cerebral cortex can be reduced due to gestational nicotine exposure, decreasing the total number of brain cells (5). Furthermore, serotonin and glutamate can be impacted by prenatal nicotine exposure, especially the reduction of serotonin turnover in the midbrain, forebrain, pons and cerebellum