Effect of hypoxia on spontaneous neural activity in the cortex of neonate mouse pups

Hypoxia caused by inadequate oxygenation has profound effects on the normal functioning of the brain in mammals. Acute or chronic hypoxic insults occur in the brain depending on the duration of hypoxic exposure. Hypoxia is known to occur in the human womb and exerts adverse effects on the developing fetus. Most of the ongoing research on hypoxia is performed on rodent brain slice taken from various brain regions using intracellular recording. Extensive work has been carried out to understand the effects of chronic hypoxia on the developing nervous system, specifically during intrauterine development. However, effects of acute hypoxia occurring perinatally, on neuronal activity remain less studied. Spontaneous neural activity occurring during the first weeks of development is important for priming the nervous system to function efficiently when encountering sensory-evoked inputs. This calls for the need to understand the effects of acute hypoxia on spontaneously arising neural activity in-vivo in awake and unanesthetized animals at an age corresponding to the perinatal period in human fetus (36 – 40 weeks). This study utilized wide-field epifluorescence imaging to indirectly record neural activity in the form of fluorescence signals arising from a large volume of brain (from lambda suture to bregma) under normal air and hypoxic air in SNAP-25-2A-GCaMP-6s transgenic mice at postnatal day 7. Results of this study demonstrated a statistically significant reduction in frequency and increase in amplitude of neuronal activity in the entire cortex under hypoxic air when compared to normal air. Bilateral synchrony in neuronal activity was observed during normal and hypoxic conditions