We measured activity‐dependent changes in [K+]o with K+‐selective microelectrodes in adult rat optic nerve, a CNS white matter tract, to investigate the factors responsible for post‐stimulus recovery of [K+]o. Post‐stimulus recovery of [K+]o followed a double‐exponential time course with an initial, fast time constant, τfast, of 0.9 ± 0.2 s (mean ±s.d.) and a later, slow time constant, τslow, of 4.2 ± 1 s following a 1 s, 100 Hz stimulus. τfast, but not τslow, decreased with increasing activity‐dependent rises in [K+]o. τslow, but not τfast, increased with increasing stimulus duration. Post‐stimulus recovery of [K+]o was temperature sensitive. The apparent temperature coefficients (Q10, 27–37°C) for the fast and slow components following a 1 s, 100 Hz stimulus were 1.7 and 2.6, respectively. Post‐stimulus recovery of [K+]o was sensitive to Na+ pump inhibition with 50 μM strophanthidin. Following a 1 s, 100 Hz stimulus, 50 μM strophanthidin increased τfast and τslow by 81 and 464%, respectively. Strophanthidin reduced the temperature sensitivity of post‐stimulus recovery of [K+]o. Post‐stimulus recovery of [K+]o was minimally affected by the K+ channel blocker Ba2+ (0.2 mm). Following a 10 s, 100 Hz stimulus, 0.2 mm Ba2+ increased τfast and τslow by 24 and 18%, respectively. Stimulated increases in [K+]o were followed by undershoots of [K+]o. Post‐stimulus undershoot amplitude increased with stimulus duration but was independent of the peak preceding [K+]o increase. These observations imply that two distinct processes contribute to post‐stimulus recovery of [K+]o in central white matter. The results are compatible with a model of K+ removal that attributes the fast, initial phase of K+ removal to K+ uptake by glial Na+ pumps and the slower, sustained decline to K+ uptake via axonal Na+ pumps.

Astrocytes contribute to virtually every aspect of brain function, including ionic homeostasis, energy metabolism, and synaptic signaling. The varied and important roles of astrocytes have evolved to allow increasingly complex nervous systems to operate efficiently and with high fidelity. For example, astrocytes figure prominently in glutamatergic synaptic transmission, an elemental event of brain function: high-affinity glutamate uptake into astrocytes improves the temporal and spatial fidelity of glutamatergic signaling and astrocytes subsequently shuttle glutamine back to neurons for the synthesis of more glutamate. The important and dynamic contributions of astrocytes to normal brain function demand that the interactions between neurons and astrocytes be viewed as a "partnership," a harmonious collaboration to produce a desired function. The historical view of astrocytes as simple "support cells" is no longer valid and should be discarded. It is more accurate to view astrocytes as "partner cells." Future investigations of the intimate neuron-astrocyte partnership will require stringent and novel methodologies. This timely book on methodological approaches for studying astrocytes will provide modern neuroscientists with indispensable technical advice to help unravel the mysteries of the beautiful and successful marriage between astrocytes and neurons.

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