Glial signalling in response to neuronal activity in the leech central nervous system

Deitmer, Joachim W.; Lohr, Christian; Britz, Frank C.; Schmidt, Joachim

doi:10.1016/s0079-6123(01)32078-2

Cited by 1 publication

(1 citation statement)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In astrocytes, this event can trigger the production of interleukin (IL)-6 and IL-1 via nuclear factor-κB (NF-κB) activation (Deli et al, 1995; Schwaninger et al, 1999; Didier et al, 2003; Perry et al, 2003). The role of the microglia in pathological NVU activity has been proposed to induce damage to the endothelium and the basal lamina via receptors for nucleotides, such as ATP, and opening new routes of communication between ECs, pericytes, astrocytes and microglia is important for BBB repair (Deitmer et al, 2001; Andersson et al, 2005). However, recent studies have demonstrated that enhancing the activation of microglia promotes tissue repair and remodeling after stroke by decreasing the levels of the inflammatory markers IL-1β and TNF-α and increasing IL-1ra, IL-10, and arginase 1 expression (Gelosa et al, 2014; Shin et al, 2014).…”

Section: Bbb Dysfunction In Cerebral Ischemiamentioning

confidence: 99%

Protection after stroke: cellular effectors of neurovascular unit integrity

Posada‐Duque

Barreto

Cardona‐Gómez

2014

Front. Cell. Neurosci.

106

View full text Add to dashboard Cite

Neurological disorders are prevalent worldwide. Cerebrovascular diseases (CVDs), which account for 55% of all neurological diseases, are the leading cause of permanent disability, cognitive and motor disorders and dementia. Stroke affects the function and structure of blood-brain barrier, the loss of cerebral blood flow regulation, oxidative stress, inflammation and the loss of neural connections. Currently, no gold standard treatments are available outside the acute therapeutic window to improve outcome in stroke patients. Some promising candidate targets have been identified for the improvement of long-term recovery after stroke, such as Rho GTPases, cell adhesion proteins, kinases, and phosphatases. Previous studies by our lab indicated that Rho GTPases (Rac and RhoA) are involved in both tissue damage and survival, as these proteins are essential for the morphology and movement of neurons, astrocytes and endothelial cells, thus playing a critical role in the balance between cell survival and death. Treatment with a pharmacological inhibitor of RhoA/ROCK blocks the activation of the neurodegeneration cascade. In addition, Rac and synaptic adhesion proteins (p120 catenin and N-catenin) play critical roles in protection against cerebral infarction and in recovery by supporting the neurovascular unit and cytoskeletal remodeling activity to maintain the integrity of the brain parenchyma. Interestingly, neuroprotective agents, such as atorvastatin, and CDK5 silencing after cerebral ischemia and in a glutamate-induced excitotoxicity model may act on the same cellular effectors to recover neurovascular unit integrity. Therefore, future efforts must focus on individually targeting the structural and functional roles of each effector of neurovascular unit and the interactions in neural and non-neural cells in the post-ischemic brain and address how to promote the recovery or prevent the loss of homeostasis in the short, medium and long term.

show abstract