Question

Kainic acid can elicit selective neuronal death in the brain of rodents, of which the pathological changes partially mimic neurodegeneration in the CNS. In neurons and/or microglia, the following occurs:

(1) rapid Ca2+ influx

(2) activation of Ca2+ -dependent enzymes and generation of ROS

(3) excessive Ca2+ & ROS lead to mitochondrial dysfunction

(4) nuclear condensation and DNA fragmentation

How might Kainic acid treatments mimic and elicit similar neurodegeneration pathologies as those seen in Alzheimer’s disease (AD) or Parkinson disease (PD)? That is what pathways are shared between the model and the disease pathologies?

Answer 1

Kanic acid is a potent agonist to -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid it is a class of glutamate receptor. glutamate acts on central nervoussystem by many ways such as excessive ca2+ influx followed by disintegration of endoplasmic reticulum membraneit also leads to neuronal apoptosis and necrosis by generation and detoxification of relative oxygen and causes mitochondrial dysfunction.

   In rodents kanic acid injection resulted in recurrent seizures behavioral changes followed by degeneration of neruronsin brain. there can also be microgial activation and astrocytes proliferation