Geon Wireless Communication in the Brain
III. Evidence from Traumatic Brain Injury

 

Abstract

Traumatic brain injury (TBI) is caused by an external mechanical force which may excite neurons in a manner similar to ultrasound stimulation discussed in Paper 12. Briefly, the mechanical force may cause neuronal deformation, resulting in microtubule bending at the axon initial segment (AIS) which, according to the Microtubule Model for Excitability (Paper 2), would excite neurons. The excessive neural activity elicited by the mechanical force may lead to calcium overload and subsequent pathological events such as AIS shortening, post-traumatic epilepsy and increased risk for Parkinson's disease and Alzheimer's disease. The shortened AIS could arise from Ca2+-induced microtubule depolymerization and Ca2+-activated calcineurin which dephosphorylates sodium and potassium channels in the AIS membrane. The post-traumatic epilepsy and neurodegeneration risk could result from BDNF reduction by inflammation and the upregulation of amyloid precursor protein for repairing axonal damages. Within 1-4 hr post-trauma, the neuronal excitability is attenuated, which could be due to the depolymerized free tubulin. Further evidence for the inhibitory action of free tubulin comes from the studies of seizure termination, memory consolidation and memory retrieval, which will be discussed in the next several papers.

 

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