Aberrant Hippocampal Neuroregenerative Plasticity in Schizophrenia: Reactive Neuroblastosis as a Possible Pathocellular Mechanism of Hallucination.

Hallucination is a sensory perception that occurs in the absence of external stimuli during abnormal neurological disturbances and various mental diseases. Hallucination is recognized as a core psychotic symptom and is particularly more prevalent in individuals with schizophrenia. Strikingly, a significant number of subjects with Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and other neurological diseases like cerebral stroke and epileptic seizure also experience hallucination. While aberrant neurotransmission has been linked to the neuropathogenic events of schizophrenia, the precise cellular mechanism accounting for hallucinations remains obscure. Neurogenesis is a cellular process of producing new neurons from the neural stem cells (NSC)-derived neuroblasts in the brain that contribute to the regulation of pattern separation, mood, olfaction, learning, and memory in adulthood. Impaired neurogenesis in the hippocampus of the adult brain has been linked to stress, anxiety, depression, and dementia. Notably, many neurodegenerative disorders are characterized by the mitotic and functional activation of neuroblasts and cell cycle re-entry of mature neurons leading to a drastic alteration in neurogenic process, known as reactive neuroblastosis. Considering their neurophysiological properties, the abnormal integration of neuroblasts into the existing neural network or withdrawal of their connections can lead to abnormal synaptogenesis, and neurotransmission. Eventually, this would be expected to result in altered perception accounting for hallucination. Thus, this article emphasizes a hypothesis that aberrant neurogenic processes at the level of reactive neuroblastosis could be an underlying mechanism of hallucination in schizophrenia and other neurological diseases.

Omeprazole treatment manifests anxiolytic effects in a cysteamine hydrochloride induced mouse model of gastrointestinal disorder.

Omeprazole, a proton pump inhibitor (PPI), has widely been used to treat various gastrointestinal (GI) disorders. Notably, many clinical symptoms of GI disorders have been known to be associated with anxiety. In recent years, an exponentially increased number of subjects with abnormal ageing, neurological deficits, and psychiatric problems simultaneously exhibit GI dysfunctions as well as anxiety. Considering the fact, drugs that are used to treat GI disorders can be speculated to mitigate anxiety-related symptoms, and vice versa. Although, omeprazole treatment has been reported to result in development of anxiety and neurocognitive decline, ample reports suggest that omeprazole treatment is beneficial for the positive regulation of neuroplasticity. While underlying mechanisms of omeprazole-mediated neurological alterations remain obscure, the available scientific data on the omeprazole induced adverse effects in the brain appear to be inadequate, uncertain, and controversial. Hence, this study revisited the effect of omeprazole treatment on the degree of anxiety-like behaviours in a cysteamine hydrochloride (HCl) induced mouse model of GI disorder using open field test (OFT), light-dark box (LDB) test and elevated plus maze (EPM). Results revealed that omeprazole treatment mitigates anxiety-related behaviours in the cysteamine HCl induced animal model of GI disorder. Thus, this study assuredly supports and validates the anxiolytic properties of omeprazole. However, the adverse effects associated with inappropriate intake of omeprazole may not completely be excluded. Therefore, this study advocates the future direction in determining the long-term effects of omeprazole on the brain functions.