Death, survival, and morphological development of hippocampal granule cells born in an inflammatory environment

The brain continues to form new neurons throughout life. This process of adult neurogenesis has been thoroughly documented in several species including birds, rodents and humans. Adult neurogenesis is not a global process, but is confined to two subcompartments of the brain; the subventricular zone lining the lateral ventricles, and the subgranular zone (SGZ) in the hippocampal formation. A variety of stimuli such as voluntary exercise, epileptic seizure activity and inflammation can affect the basal level of neurogenesis. In the course of pathological conditions such as Alzheimer’s disease, multiple sclerosis, epilepsy and stroke, an inflammatory response is initiated in the brain. Prolonged epileptic seizure activity, status epilepticus (SE), strongly imposes on the integrity of the delicate brain structure and cell communication. SE not only induces inflammation, but also neuronal death and a transient increase of basal adult neurogenesis in the hippocampal formation. What role inflammation plays in a disease such as epilepsy, and how it affects the neurons born in the aftermath of seizure activity, is largely unknown. The specific aim of the four studies included in this thesis was to investigate the effect inflammation has on the amount of basal and seizure-induced neurogenesis, and if the morphological development or functional characteristics of new neurons is affected when the neuron is born into an inflammatory environment. In brief, the purpose was to investigate the quantity and quality of the neurogenic outcome in inflammation. To comprehend the interplay between neurogenesis and inflammation would provide a valuable insight into disease progression, and could ultimately be part of the treatment or even a cure for pathological conditions involving seizure activity and inflammation.