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In the neonate forebrain, network formation is driven by the spontaneous synchronized activity of pyramidal cells and interneurons, consisting of bursts of electrical activity and intracellular Ca²⁺ oscillations. By employing ratiometric Na⁺ imaging in tissue slices obtained from animals at postnatal day 2−4 (P2−4), we found that 20% of pyramidal neurons and 44% of astrocytes in neonatal mouse hippocampus also exhibit transient fluctuations in intracellular Na⁺. These occurred at very low frequencies (~2/h), were exceptionally long (~8 min), and strongly declined after the first postnatal week. Similar Na⁺ fluctuations were also observed in the neonate neocortex. In the hippocampus, Na⁺ elevations in both cell types were diminished when blocking action potential generation with tetrodotoxin. Neuronal Na⁺ fluctuations were significantly reduced by bicuculline, suggesting the involvement of GABA_A-receptors in their generation. Astrocytic signals, by contrast, were neither blocked by inhibition of receptors and/or transporters for different transmitters including GABA and glutamate, nor of various Na⁺-dependent transporters or Na⁺-permeable channels. In summary, our results demonstrate for the first time that neonatal astrocytes and neurons display spontaneous ultraslow Na⁺ fluctuations. While neuronal Na⁺ signals apparently largely rely on suprathreshold GABAergic excitation, astrocytic Na⁺ signals, albeit being dependent on neuronal action potentials, appear to have a separate trigger and mechanism, the source of which remains unclear at present.