Presynaptic excitability as a potential target for the treatment of the traumatic cerebellum.
Using an extracellular recording method, we have previously shown a hyperexcitability of the presynaptic response in fluid percussion injury (FPI) in rats. In this study, we demonstrated that treatment with cis-ACBD, a glutamate reuptake inhibitor, depressed the presynaptic potential (PSP) in naive/sham controls, while it potentiated the PSP in FPI rats. On the contrary, (RS)-APICA, a selective group II metabotropic glutamate receptor antagonist, potentiated PSP in controls, but depressed PSP in FPI rats. These results indicate that an alteration of the normal function of metabotropic glutamate receptors and glutamate reuptake system or an altered reactivity of presynaptic fibers was induced by FPI. This alteration may contribute to the reported loss of Purkinje cells after FPI. PSP may be used as a potential tool for evaluating treatments of FPI or as a potential target for the prevention of Purkinje cell death.
Ai
Jinglu
J
Traumatic Brain Injury Laboratory, Cara Phelan Centre for Trauma Research, St. Michael's Hospital, University of Toronto, Toronto, Ont., Canada. aij@smh.toronto.on.ca
Baker
Andrew
A
D000818:Animals; D001930:Brain Injuries / Q000378:metabolism* / Q000503:physiopathology; D002531:Cerebellum / Q000293:injuries / Q000378:metabolism* / Q000503:physiopathology; D004558:Electric Stimulation; D005971:Glutamates / Q000494:pharmacology; D018698:Glutamic Acid / Q000378:metabolism; D066298:In Vitro Techniques; D008297:Male; D014179:Neurotransmitter Uptake Inhibitors / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D018094:Receptors, Metabotropic Glutamate / Q000037:antagonists & inhibitors; D017661:Receptors, Presynaptic / Q000502:physiology*; D009435:Synaptic Transmission / Q000502:physiology
D005971:Glutamates; D014179:Neurotransmitter Uptake Inhibitors; D018094:Receptors, Metabotropic Glutamate; D017661:Receptors, Presynaptic; C066302:2,4-methanoglutamate; D018698:Glutamic Acid