Photothrombotic brain infarction results in seizure activity in aging Fischer 344 and Sprague Dawley rats.

This study was designed to determine whether photothrombotic brain infarction could result in epileptic seizures in adult animals. Male Fischer 344 (F344) rats at 2, 6, 12, 24, and 30 months of age and male Sprague Dawley (SD) rats at 2 and 6 months of age underwent photothrombotic brain infarction with the photosensitive dye rose bengal by focusing a wide (6 mm) or narrow (3 mm) diameter white light beam on the skull overlying left hemisphere anterior frontal, midfrontal, frontoparietal, or parietal areas. Animals were monitored with video and EEG recordings. Morphological analysis of infarct size was performed with a computer-assisted image analysis system. The primary finding of this study was that epileptic seizures were recorded in post-mature rats 2 months after lesioning the frontoparietal cortex with large photothrombotic infarcts that extended to the cortical-subcortical interface. These seizures were characterized behaviorally by motor arrest, appeared to originate in the periinfarct area, and could be distinguished from inherited spontaneous bilateral cortical discharges by the morphology, frequency, duration, and laterality of the ictal discharges. Small cortical lesions were ineffective in producing seizures except for one animal that demonstrated recurrent prolonged focal discharges unaccompanied by behavioral change. Stage 3 seizures were observed in a small number of mid-aged and aged animals lesioned with large infarcts in anterior frontal and frontoparietal areas. These results suggest that the technique of photothrombosis can be used to produce neocortical infarction as a means to study mechanisms of secondary epileptogenesis.

Ultraprofound cerebral hypothermia and blood substitution with an acellular synthetic solution maintains neuronal viability in rat hippocampus.

The acute effects of ultraprofound hypothermia and blood substitution (UHBS) on neuronal cell viability were examined in adult rat hippocampus, a brain region particularly vulnerable to ischemic cell death. UHBS was performed using either artificial cerebrospinal fluid (ACSF) or Hypothermosol, an "intracellular-type" hypothermic preservation solution. After the procedure, the hippocampus was sliced and tested for cellular viability using a combination of cellular fluorochromes that are markers for live cells (acridine orange) and dead cells (propidium iodide). UHBS with ACSF resulted in a variable degree of neuronal death within the hippocampal subfields CA1/CA3, and dentate granular layer and hilus (CA4). In contrast, UHBS with Hypothermosol consistently resulted in hippocampal slices with only mild neuronal death. Our results of preserved hippocampal neuronal viability with use of UHBS and Hypothermosol support the demonstrated central nervous system (CNS) protective effects of UHBS and Hypothermosol when used during prolonged cardiac arrest. The results of this study also suggest that UHBS and Hypothermosol may be useful in the preparation and maintenance of viable hippocampal tissue for physiological studies, especially those involving aged animals, which are particularly vulnerable to hypoxic-ischemic cellular injury