Your browser does not support JavaScript!

Home    Search  

Results - Details

Search command : Author="Πανεπιστήμιο"  And Author="Κρήτης."

Current Record: 43 of 88

Back to Results Previous page
Next page
Add to Basket
[Add to Basket]
Identifier 000381234
Title Μελέτη της νευροπροστατευτικής δράσης των νευροστεροειδών σε in vivo μοντέλο ampa διέγερσι-τοξικότητας στον αμφιβληστροειδή αρουραίου
Alternative Title Study of the neuroprotective properties of neurosteroids in an in vivo model of ampa excitoxicity in rat retina
Author Κοκονά, Δέσποινα
Thesis advisor Θερμού, Κυριακή
Reviewer Γραβάνης, Αχιλλέας
Select a value Πανεπιστήμιο Κρήτης.
Abstract Degenerative retinal diseases involve retinal ischemia and excitotoxicity which lead to visual impairment and blindness. Neurosteroids such as DHEA have recently been shown to have antiapoptotic actions via a mechanism involving the NGF receptor, TrkA [Charalampopoulos et al., FEBS Journal, 275, Suppl. 1, 2008]. The aim of the present study was to investigate whether DHEA and NGF could protect retinal cells from cell death in an in vivo model of AMPA excitotoxicity. Sprague-Dawley rats were administered intravitreally: AMPA (42 nmol per eye) or AMPA and DHEA (10-6,10-7,10-8M) or NGF (60pg/eye), or a TrkA receptor inhibitor (10-6, 10-5M) and AMPA and DHEA (10-6M) or AMPA and NGF (60pg/eye), or one of the DHEA synthetic analogs TC50 and TC93 (10-6,10-7,10-8M) with AMPA, or vehicle. Twenty four hours after treatment, eye cups were removed and prepared for immunohistochemistry. Antibodies raised against retinal markers such as ChAT and calbindin were employed to label cholinergic amacrine cells, and horizontal, cone bipolar and calbindin amacrine cells, respectively. To determine retinal cell death, immunohistochemistry using a rabbit polyclonal antibody against cleaved caspase-3 was performed. AMPA injections led to retinal cell loss, as previously reported [Kiagiadaki & Thermos, IOVS, 49:3080-3089, 2008], 24 hours after administration. Co- administration of AMPA and DHEA or DHEA analogs protected the retina in a dose dependent manner. In addition, NGF mimicked the DHEA neuroprotective effects. The TrkA inhibitor reversed the neuroprotection afforded to the retina by DHEA. TUNEL studies confirmed the above results. These results support that the endogenous neurosteroid DHEA protects the retina from AMPA excitotoxicity via a mechanism involving the TrkA receptor..
Language Greek
Subject Excitotoxicity
Neuroprotection
Neurosteroids
Rat
Αμφιβληστροειδής
Αρουραίος
Διέγερσι-τοξικότητα
Νευρικός αυξητικός παράγοντας
Νευροπροστασία
Νευροστεροειδή
Issue date 2010-12-14
Collection   School/Department--School of Medicine--Department of Medicine--Post-graduate theses
  Type of Work--Post-graduate theses
Permanent Link https://elocus.lib.uoc.gr//dlib/f/8/5/metadata-dlib-1386071715-763502-14481.tkl Bookmark and Share
Views 215

Digital Documents
No preview available

Download document
View document
Views : 18