How glia power
and protect
the brain.

After an experimental stroke, injury volumes were about forty percent smaller when astrocytes lacked their main glucose transporter.

In the zone surrounding the infarct, astrocytes lacking the transporter were less ramified, hinting at a dampened reactive response.

When axons fire fast, oligodendrocytes burn glucose about nine times faster than at rest.

Oligodendrocytes sense fast axonal firing chiefly through the potassium active axons release; glutamate contributes only modestly.

During fast firing, lactate rises inside axons; blocking the potassium channel through which oligodendrocytes sense firing cuts that rise by forty percent.

Without the oligodendrocyte potassium channel, axons take up and burn about forty percent less glucose, at rest and during activity.

By seven to eight months, axons whose oligodendrocytes lack the potassium channel show degeneration and giant swellings, without noticeable myelin changes.

Across cortex, hippocampus, midbrain, thalamus and hypothalamus, all but three of more than eighteen hundred astrocytes touched a blood vessel directly.

Most cortical astrocytes contact three blood vessels, and a single astrocyte can reach as many as nine.

Only in the hippocampus, the least vascularised region examined, did a few astrocytes lack apparent vascular contact: about three in a hundred.

Breaking the astrocyte network in the adult brain weakens hippocampal synaptic plasticity and abolishes spatial learning and memory.

Within seconds of arousal, lactate drops inside cortical astrocytes while extracellular lactate rises, pointing to release from astrocytes.

When the brain is depleted of glycogen, the arousal-evoked lactate surges shrink, pointing to glycogen as a source of that lactate.

Networks of coupled astrocytes connect certain brain regions and leave others out, rather than spreading indiscriminately through the brain.

Prolonged sensory deprivation shrinks the corresponding cortical astrocyte network and largely removes its long-range connection to prefrontal cortex.

Astrocyte networks directly link brain regions that neurons do not connect, suggesting a channel of communication outside the neuronal connectome.

After one capillary endothelial cell is lost, its neighbours extend toward each other and restore blood flow within one to two days.

Capillary endothelial cells close the gap themselves, without help from glia or the cells wrapped around the vessel wall.

Hippocampal capillaries repair more slowly and less efficiently than cortical ones, a regional difference that could shape resilience to injury and disease.

In isolated optic nerves deprived of glucose for a day, nearly all oligodendrocytes survived while more than seventy percent of astrocytes died.

When glucose runs low, fatty acid breakdown keeps axons conducting and their ATP up, though not during rapid firing.

Oligodendrocytes support starving axons partly through peroxisomes, fat-burning organelles, many of which sit inside the myelin sheath.

Raised kynurenic acid quietened one class of inhibitory interneurons and released pyramidal cells from their inhibition, sparing a second class.

Blocking the enzyme that makes kynurenic acid fully restored memory and filtering, with no effect on unaffected animals.

A rise in extracellular potassium, the ion neurons release when they fire, sharply quiets calcium activity in capillary pericytes.

Brief oxygen deprivation silences capillary pericyte calcium completely while neighbouring astrocytes surge, and capillaries widen by about a tenth.

Regional differences in glutamate clearance may explain why hyperexcitability disorders like epilepsy and migraine strike some brain areas harder than others.

A brief burst of activity floods neurons with sodium at once; the pump that clears it speeds up only afterwards.

The sodium pump has a permissive role: mitochondrial ATP production and glycolysis both depend on its activity.