ABSTRACT
A spreading depression (SD) was elicited in adult rat neocortical slices by microdrop application of high potassium and the SD propagation pattern was analyzed by recording simultaneously the extracellular DC potential and the changes in the intrinsic optical signal. The electrical SD with an average peak amplitude of 13.2+/-3.4 mV showed a good spatial and temporal correlation with the optical signal. In 79% of the slices, the SD was characterized by an initial increase of light reflectance by 2.3+/-1.6%, followed by a reflectance decrease of 0.5+/-2.4% and finally a larger and long-lasting increase by 5+/-2.4%. In the remaining slices, the SD revealed an initial decrease in light reflectance by 5.8+/-1.8% followed by an increase of 1.4+/-1.2%. In all slices, the recovery in the DC recording was faster as in the optical signal. The SD preferentially propagated within layers I-IV and could be blocked in most experiments by a vertical incision through upper layers or by local glutamate receptor blockade following microdrop application of kynurenic acid in layers II-III. The SD could be also blocked by bath application of kynurenic acid, MK-801 and octanol, but not by the more specific gap junction blocker carbenoxolone. Our results indicate that the high density of dendritic processes and glutamate receptors in layers II-IV promote the horizontal spread of the SD in these cortical layers and that gap junctions are not required for the propagation of SD in neocortical slices.
Subject(s)
Cortical Spreading Depression/physiology , Electronic Data Processing/methods , Electrophysiology/methods , Neocortex/physiology , Neurons/drug effects , Animals , Anti-Ulcer Agents/pharmacology , Carbenoxolone/pharmacology , Cortical Spreading Depression/drug effects , Dizocilpine Maleate/pharmacology , Electronic Data Processing/instrumentation , Electrophysiology/instrumentation , Gap Junctions/drug effects , Gap Junctions/metabolism , Kynurenic Acid/pharmacology , Lighting/instrumentation , Lighting/methods , Male , Neocortex/cytology , Neocortex/drug effects , Neurons/cytology , Neurons/physiology , Octanols/pharmacology , Organ Culture Techniques , Potassium Chloride/pharmacology , Rats , Rats, Wistar , Receptors, Glutamate/drug effects , Receptors, Glutamate/metabolismABSTRACT
After CNS trauma a sheet-like, collagen type IV (Coll IV) immunopositive basement membrane (BM) develops in the lesion zone as well as at newly formed blood vessels. The basic scaffold of this BM is composed of Coll IV, laminin and nidogen but numerous other proteins some of which are discussed to be inhibitory for axonal regeneration, i.e. chondroitin- and heparansufate-proteoglycans, are associated with BM. This review will focus on the collagenous wound healing scar, discuss its composition and summarize the experimental results that demonstrate its role in the failure of axonal regeneration in the injured mammalian CNS.
