Impairment of memory is one of the most frequently reported symptoms during sudden hypoxia exposure in human. Cortical atrophy has been linked to the impaired memory function and is suggested to occur with chronic high-altitude exposure. However, the precise molecular mechanism(s) of hypoxia-induced memory impairment remains an enigma. In this work, we review hypoxia-induced learning and memory deficit in human and rat studies. Based on data from rat studies using different protocols of continuous hypoxia, we try to elicit potential mechanisms of hypobaric hypoxia–induced memory deficit.

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INTRODUCTION: A growing body of evidence indicates that hypoxia exposure causes learning and memory deficits. Effective natural therapeutic approach has, however, not been explored widely. Our previous studies found that Tualang honey administration protected learning and memory functions in ovariectomised rats. Therefore, the present study investigated its efficacy in ameliorating hypoxia-induced memory deficits in adult male Sprague-Dawley rats. METHODS: The rats were divided into four groups; i) Normoxia treated with sucrose (n=12), ii) Normoxia treated with Tualang honey (n=12), iii) Hypoxia treated with sucrose (n=12), and iv) Hypoxia treated with Tualang honey (n=12). Tualang honey (0.2 g/kg/BW) and sucrose (1 mL of 7.9%) supplementations were administered orally to the rats daily for 14 days. Then, hypoxia groups were exposed to hypoxia (~11%) for 7 days while normoxia groups were kept in normal condition. Following exposure to hypoxia, rats memory were analyzed using novel object recognition task and T-maze test. RESULTS: The data revealed that rats exposed to hypoxia showed significant impairment in short-term memory (STM), spatial memory (p<0.01) and long term memory (LTM) when compared to the normoxia group. Hypoxia rats treated with Tualang honey showed significant improvement in STM, LTM and spatial memory (p<0.05) as compared with hypoxia treated with sucrose (p<0.05). Tualang honey also reduced neuronal damage in hippocampus of adult male Sprague-Dawley rats exposed to hypoxia. DISCUSSION AND CONCLUSION: Therefore, it is suggested that Tualang honey pretreatment has protective effects against hypoxia-induced memory deficits, possibly through its antioxidant contents.

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Background: Medial prefrontal cortex (mPFC) is considered to be involved in human cognition to mPFCin terms of learning and memory. Hypoxia is one of the crucial factors causing secondary damage incerebral hemorrhage and traumatic brain injury. However, the underlying mechanisms and possibletherapeutic approach to prevent neuronal damage has not been attempted yet. Therefore, the present studyaimed to investigate the role of Tualang honey on medial prefrontal cortical neuronal morphology andcholinergic markers such as acetylcholine (ACh) and acetylcholinesterase (AChE) following exposure to normobaric hypoxia in rats. Material and methods: Adult male Sprague-Dawley rats were dividedinto four groups: (i) sucrose treated non-hypoxia, (ii) sucrose treated hypoxia, (iii) Tualang honeytreated non-hypoxia and (iv)Tualang honey treated hypoxia. Rats received sucrose (1 mL of 7.9%) andTualang honey (0.2 g/kg), respectively, for 2 weeks prior to hypoxia exposure. Morphological study wasperformed by using Nissl staining and cholinergic markers were estimated by ELISA technique. Resultsand discussion: Sucrose treated hypoxia group showed significantly lower mean ACh and higher meanAChE concentrations (P<0.05) compared to sucrose and honey treated non-hypoxia groups. Interestingly,mean ACh concentration was significantly increased and mean AChE concentration was significantlydecreased in Tualang honey treated hypoxic rats compared to sucrose treated hypoxic rats. Morphologicaldata showed that hypoxia caused neuronal damage in mPFC in sucrose treated hypoxia group whereasTualang honey treated hypoxia group significantly prevent neuronal damage. Conclusion: Tualang honeyprotects hypoxia-induced mPFC neuronal damage through improvement of the brain cholinergic markersin male rats exposed to normobaric hypoxia. Bangladesh Journal of Medical Science Vol.20(1) 2021 p.122-129

Neuroinflammation following lipopolysaccharide (LPS) administration induces locomotor deficits and anxiety-like behaviour. In this study, minocycline was compared to memantine, an NMDA receptor antagonist, for its effects on LPS-induced locomotor deficits and anxiety-like behaviour in rats. Adult male Sprague Dawley rats were administered either two different doses of minocycline (25 or 50 mg/kg/day, i.p.) or 10 mg/kg/day of memantine (i.p.) for 14 days four days prior to an LPS (5 mg/kg, i.p.) injection. Locomotor activity and anxiety-like behaviour were assessed using the open-field test (OFT). The phosphorylated tau protein level was measured using ELISA, while the expression and density of brain-derived neurotrophic factor (BDNF) and cAMP response element-binding (CREB) protein in the medial prefrontal cortex (mPFC) were measured using immunohistochemistry and Western blot, respectively. Minocycline treatment reduced locomotor deficits and anxiety-like behaviour associated with reduced phosphorylated tau protein levels, but it upregulated BDNF/CREB protein expressions in the mPFC in a comparable manner to memantine, with a higher dose of minocycline having better benefits. Minocycline treatment attenuated LPS-induced locomotor deficits and anxiety-like behaviour in rats and decreased phosphorylated tau protein levels, but it increased the expressions of the BDNF/CREB proteins in the mPFC.

Journal of Cellular Neuroscience and Oxidative Stress is an online journal that publishes original research articles, reviews and short reviews on the molecular basis of biophysical, physiological and pharmacological processes that regulate cellular function, and the control or alteration of these processes by the action of receptors, neurotransmitters, second messengers, cation, anions, drugs or disease.Areas of particular interest are four topics. They are;A-Ion Channels (Na + -K + Channels, Clchannels, Ca 2+ channels, ADP-Ribose and metabolism of NAD + , Patch-Clamp applications) B-Oxidative Stress (Antioxidant vitamins, antioxidant enzymes, metabolism of nitric oxide, oxidative stress, biophysics, biochemistry and physiology of free oxygen radicals) C-Interaction Between Oxidative Stress and Ion Channels in Neuroscience (Effects of the oxidative stress on the activation of the voltage sensitive cation channels, effect of ADP-Ribose and NAD + on activation of the cation channels which are sensitive to voltage, effect of the oxidative stress on activation of the TRP channels in neurodegenerative diseases such Parkinson's and Alzheimer's diseases) D-Gene and Oxidative Stress (Gene abnormalities. Interaction between gene and free radicals. Gene anomalies and iron. Role of radiation and cancer on gene polymorphism)

INTRODUCTION: Many studies support the notion that neuroinflammation involving glial cells may be the fundamental pathogenic event that lead to brain damage and degeneration in Alzheimer’s disease (AD). The effects of minocycline on glial cells activation in the lipopolysaccharide (LPS) rat model is studied here. MATERIALS AND METHODS: Fifty adult male Sprague Dawley rats were split into five groups: control, LPS, LPS-treated with minocycline 25 mg/kg, LPS-treated with minocycline 50 mg/kg, and LPS treated with memantine 10 mg/kg. For two weeks, rats were treated with minocycline and memantine intraperitoneally daily, while were injected with LPS intraperitoneally once on day 5. Morris water maze (MWM) test was performed to evaluate the learning and working memory behaviour. Immunohistochemistry and Western blot were performed to measure ionized calcium-binding adaptor molecule 1 (Iba-1) and glial fibrillary acidic protein (GFAP) expressions in the hippocampal tissue. RESULTS: LPS injection caused significant learning and working memory deficits (p<0.05) as well as increased expressions of Iba-1 and GFAP (p<0.05), indicating microglia and astrocytes activation, respectively. Minocycline treatment significantly improved learning and working memory performance (p<0.05) and reduced microglia/astrocytes activation (p<0.05) in a dose-dependent manner, similar to the effect of memantine. CONCLUSIONS: Our results suggest that minocycline modulates LPS-induced microglia and astrocytes activation as well as improves learning and working memory comparable to memantine. Thus, minocycline may have  preventive-therapeutic effect in diseases involving neuroinflammation such as AD.