Neuronal Activity and Ion Homeostasis in the Hypoxic Brain

نویسندگان

  • Bas-Jan Zandt
  • Stephan van Gils
  • Richard van Wezel
چکیده

Recent experiments in rats have shown the occurrence of a high amplitude slow brain wavein the EEG approximately 1 minute after decapitation, with a duration of 5-15 s (van Rijn et al, PLoSOne 6, e16514, 2011) that was presumed to signify the death of brain neurons. We present a compu-tational model of a single neuron and its intraand extracellular ion concentrations, which shows thephysiological mechanism for this observation. The wave is caused by membrane potential oscillations,that occur after the cessation of activity of the sodium-potassium pumps has led to an excess of extracel-lular potassium. These oscillations can be described by the Hodgkin-Huxley equations for the sodiumand potassium channels, and result in a sudden change in mean membrane voltage. In combination witha high-pass filter, this sudden depolarization leads to a wave in the EEG. We discuss that this process isnot necessarily irreversible. ∗Published as: BJ Zandt, B ten Haken, JG van Dijk, MJAM van Putten (2011) Neural Dynamicsduring Anoxia and the Wave of Death. PLoS ONE 6(7): e22127. doi:10.1371/journal.pone.0022127

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Neuroprotection of a sesamin derivative, 1, 2-bis [(3-methoxy- phenyl) methyl] ethane-1, 2-dicaroxylic acid (MMEDA) against ischemic and hypoxic neuronal injury

Objective(s): Stroke may cause severe neuronal damage. The sesamin have been demonstrated to possess neuroprotection by its antioxidant and anti-inflammatory properties. One sesamin derivative was artificially composited, 1, 2-bis [(3-methoxyphenyl) methyl] ethane-1, 2-dicaroxylic acid (MMEDA) had been developed to study its antioxidative activity and neuroprotection. Materials and Methods: The...

متن کامل

Heat shock protein 70 protects motor neuronal cells expressing mutant Cu/Zn superoxide dismutase (SOD1) against altered calcium homeostasis

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder characterized by the progressive loss of motor neurons leading to paralysis and death. Mutations of the human Cu/Zn superoxide dismutase (SOD1) are found in some cases of familial ALS (fALS). Recent evidences suggest the accumulation of intracellular calcium is one of the primary mechanisms of motor neuronal degeneration. In th...

متن کامل

Ion channels in the central regulation of energy and glucose homeostasis

Ion channels are critical regulators of neuronal excitability and synaptic function in the brain. Recent evidence suggests that ion channels expressed by neurons within the brain are responsible for regulating energy and glucose homeostasis. In addition, the central effects of neurotransmitters and hormones are at least in part achieved by modifications of ion channel activity. This review focu...

متن کامل

P185: Survey Effect of Histamine on Microglia in Neurodegenerative Diseases

Neurodegenerative diseases contain Multiple Sclerosis (MS), Alzheimer’s disease (AD) and Parkinson’s disease (PD), are characterized by neuronal death and neuronal degeneration in specific regions of the central nervous system (CNS). Microglia are the basic immune brain cells and play a role in homeostasis after inflammation challenge. Microglia involves in Neurodegenerative disease...

متن کامل

Heat shock protein 70 protects motor neuronal cells expressing mutant Cu/Zn superoxide dismutase (SOD1) against altered calcium homeostasis

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder characterized by the progressive loss of motor neurons leading to paralysis and death. Mutations of the human Cu/Zn superoxide dismutase (SOD1) are found in some cases of familial ALS (fALS). Recent evidences suggest the accumulation of intracellular calcium is one of the primary mechanisms of motor neuronal degeneration. In th...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:

دوره   شماره 

صفحات  -

تاریخ انتشار 2014