Pattern of Glial Fibrillary Acidic Protein Expression Following Kainate-Induced Cerebellar Lesion in Rats

Abstract

In the present study glial fibrillary acidic protein (GFAP) expression was assessed following intravermian injection of kainic acid (KA) or physiological saline to adult rat cerebellum. After 2- to 30-day recovery period, free-floating sections cut with a microtome were obtained and were proccessed for immunocytochemistry against GFAP. Injection of both kainate and physiological saline elicited significant astrogliotic reaction, i.e. in the area around the lesion thick GFAP-positive Bergmann fibers with typical orientation appeared in the molecular and hypertrophied astrocytes abundantly appeared in the granular layer. However, following kainate intoxication lesion was not surrounded by typical demarcation glial scar during 30-day recovery period in contrast to the appearance of usual glial scar in the group injected with physiological saline, as early as 7-day postlesion. Preserved spatial organization of Bergmann fibers and the absence of typical demarcating glial scar after kainate-induced cerebellar lesion suggest distinct pattern of astrogliosis that presents an interesting model system to study the importance of glial scar in the recovery after ischemic brain insults.

Uteroplacental Inflammation Results in Blood Brain Barrier Breakdown, Increased Activated Caspase 3 and Lipid Peroxidation in the Late Gestation Ovine Fetal Cerebellum

“…It is possible that damage to Purkinje cells and cells of the molecular layer, as shown by the increased expression of activated caspase 3 protein, resulted in a reactive response in astrocytes and Bergmann fibers. Increased neuronal death produced by kainic acid or methylazoxymethanol significantly increased the GFAP immunoreactivity of Bergmann glia in the cerebellum of 5-day-old rats [32,36] .…”

Bridging the divide between neuroprosthetic design, tissue engineering and neurobiology

“…The cellular mechanism behind the effectiveness of EGFR inhibition relates to intracellular signaling cascades involving known players in cancer biology, including the MAPK, Akt and JNK pathways that impact DNA synthesis and cell proliferation (Oda et al, 2005). Interestingly, EGFR is not the only mediator of these pathways that has been linked to CNS injury (Di Giovanni et al, 2005; Milenkovic et al, 2005; Neary and Kang, 2005; Nicole et al, 2005; Kaneko et al, 2007; Lim et al, 2007) and several molecules that inhibit these pathways are already approved as potential drugs for cancer treatment. Thus, a promising and immediately feasible line of research is to test these drugs in conjunction with neuroprosthetic devices to promote neuronal survival and inhibit scar formation and inflammation.…”

PKCε induces astrocyte stellation by modulating multiple cytoskeletal proteins and interacting with Rho A signalling pathways: implications for neuroinflammation

“…Stellation is a hallmark of the astrogliosis caused by neural insults (Milenkovic et al, 2005), and it can also be triggered by proinflammatory mediators, hormones, neurotransmitters and cell-cell interactions. Such a notorious plasticity is crucial for the complex functionality of astrocytes.…”