Background and purpose: Astrocytes support neuronal functions by regulating the extracellular ion-homeostasis and levels of neurotransmitters, and by providing fuel such as lactate to the neurons via their astrocytic processes (APs). Whether injured APs are associated with neuronal survival/death is still an unanswered question. We investigated APs in the neuropil, especially those around astrocytes and normal-appearing, degenerating, and dead neurons in cerebral cortical regions peripheral to the cortical infarction (RPI).
Methods: Stroke-positive gerbils were euthanized at various times after the ischemic insult. Ultrathin sections were obtained from the RPI sectioned coronally at the infundibular level. We counted the number of normal-appearing, degenerated, and dead neurons and astrocytes in paraffin sections, the number of cut-ends and mitochondria in APs in the neuropil on electron-microscopic photographs, and determined the percent-volume of APs by Weibel point-counting method. We compared the number of cut-ends and mitochondria and percent-volume of APs around astrocytes at 5 hours and 48 hours, and around normal-appearing, degenerated, and dead neurons at 12 hours.
Results: Although the number of astrocytes did not change (average of 12.3+/-0.20%) during 0 to 48 hours, that of the dead neurons increased from 9.71+/-1.34 to 44.39+/-1.40% during 5 to 48 hours postischemia. The number of normal-appearing APs and mitochondria in APs decreased respectively from 13.49+/-0.65 to 1.61+/-0.14/28.20 microm(2) and from 1.86+/-0.18 to 0.61+/-0.07/28.20 microm(2) in the neuropil during 0 to 48 hours. The number of normal-appearing APs around astrocytes decreased from 12.3+/-0.19 to 1.7+/-0.05/38.33 microm(2) with an increase in percent-volume of degenerated APs from 1.17+/-0.04 to 11.45+/-0.23%, from 5 to 48 hours postischemia. The number of normal-appearing APs decreased from 4.36+/-0.52 to 1.56+/-0.17/38.33 microm(2) with an increase in percent-volume of degenerated APs, from 2.41+/-0.52 to 12.55+/-1.0%, from around the normal-appearing to dead neurons, at 12 hours.
Conclusions: In the RPI, heterogeneous degeneration of APs was closely associated with disseminated selective neuronal necrosis and the maturation phenomenon seen in ischemic neuronal injury.