Katayun Cohen-Kashi Malina

Learn More
Numerous in-vitro models of the blood-brain barrier (BBB) have been developed in the hope to mimic as closely as possible the in-vivo BBB characteristics. Most models however display BBB tightness properties still very remote from those found in-vivo. We describe here the properties of an in-vitro BBB model in three configurations: primary porcine brain(More)
Adaptation is typically associated with attenuation of the neuronal response during sustained or repetitive sensory stimulation, followed by a gradual recovery of the response to its baseline level thereafter. Here, we examined the process of recovery from sensory adaptation in layer IV cells of the rat barrel cortex using in vivo intracellular recordings.(More)
Autoantibodies to the GluR3-subtype of AMPA/glutamate receptors are found in the sera and cerebrospinal fluid of some individuals with epilepsy. They could possibly play a role in the pathophysiology of epilepsy since anti-GluR3 sera display glutamatergic agonist activity. We have investigated here the ability of affinity-purified antibodies (Abs) directed(More)
BACKGROUND/AIM The sporadic form of the disease affects the majority of amyotrophic lateral sclerosis (ALS) patients. The role of glutamate (Glu) excitotoxicity in ALS has been extensively documented and remains one of the prominent hypotheses of ALS pathogenesis. In light of this evidence, the availability of a method to remove excess Glu from brain and(More)
Thalamic inputs of cells in sensory cortices are outnumbered by local connections. Thus, it was suggested that robust sensory response in layer 4 emerges due to synchronized thalamic activity. To investigate the role of both inputs in the generation of correlated cortical activities, we isolated the thalamic excitatory inputs of cortical cells by(More)
We studied here the interactions of PrP 106-126, a peptide corresponding to the prion protein (PrP) amyloidogenic region, with a blood-brain barrier in vitro model consisting of confluent porcine brain endothelial cells (PBEC). PrP 106-126 interacted selectively with PBEC via their luminal side, and caused cumulative cell death, as shown by lactate(More)
  • 1