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The Pathophysiology of Traumatic Brain Injury
Published in Mark R. Lovell, Ruben J. Echemendia, Jeffrey T. Barth, Michael W. Collins, Traumatic Brain Injury in Sports, 2020
Christopher C. Giza, David A. Hovda
In the normal brain, excess extracellular K+ is subject to reuptake by surrounding glial cells (Ballanyi, Grafe, & Bruggencate, 1987; Kuffler, 1967; Paulson & Newman, 1987). This compensatory mechanism can maintain physiologic extracellular K+ levels even after mild concussion or ongoing seizure activity (Moody, Futamachi, & Prince, 1974; Sypert & Ward, 1974) but is overcome by more severe brain trauma (D’Ambrosio, Maris, Grady, Winn, & Janigro, 1999) or ischemia (Astrup, Rehncrona, & Siesjo, 1980; Hansen, 1977; Hanson, 1988). Initially there is a slow rise in extracellular K+, followed by an abrupt increase as the physiologic ceiling for K+ balance is overcome. This triggers neuronal depolarization, release of EAAs, and further massive K+ flux through EAA/ligand-gated ion channels. In the wake of this wave of excitation is a subsequent wave of hyperpolarization and relative suppression of neuronal activity (Nicholson & Kraig, 1981; Prince, Lux, & Neher, 1973; Sugaya, Takato, & Noda, 1975; Van Harreveld, 1978; Somjen & Giacchino, 1985), a phenomenon termed “spreading depression”. One important difference between classic “spreading depression” and post-concussive K+ release is that TBI affects wide areas of the brain simultaneously. Thus, loss of consciousness, amnesia and cognitive impairment may be clinical correlations to post-TBI K+ release and a “spreading depression-like” state.
Studies on Anoxic Depolarization
Published in Avital Schurr, Benjamin M. Rigor, BRAIN SLICES in BASIC and CLINICAL RESEARCH, 2020
Thus, AD is very likely not the result of the simple opening of voltage-gated Na+ channels; more complex events must take place. In our laboratory, a possible role of cell swelling has been investigated. It is well known that cells swell at the time of SD and during anoxia or ischemia.8,49 Swelling during anoxia has been explained54 as being due to Cl- and Na+ influx into the cells. In fact, neuronal depolarization disrupts the electrochemical balance of Cl- ions, which then flow into the cells. Cl- ions entering the cells attract more Na+ ions, and this in turn causes a net increase in intracellular osmolarity, entry of water, and neuronal swelling. In fact, it should be remembered that the entry of Cl- ions cannot be counterbalanced by the exit of intracellular anions, as these are too large to cross the plasma membrane.27
Brain Stimulation Therapies
Published in Bahman Zohuri, Patrick J. McDaniel, Electrical Brain Stimulation for the Treatment of Neurological Disorders, 2019
Bahman Zohuri, Patrick J. McDaniel
With these laws, changing magnetic field easily penetrates the skin, skull, brain meninges and induces secondary electric current in the neurons that are beneath the coil. This leads to the neuronal depolarization and generation of action potentials as demonstrated in Figure 7.3.
Alpha adrenergic receptors have role in the inhibitory effect of electrical low frequency stimulation on epileptiform activity in rats
Published in International Journal of Neuroscience, 2023
Mahmoud Rezaei, Nooshin Ahmadirad, Zahra Ghasemi, Amir Shojaei, Mohammad Reza Raoufy, Victoria Barkley, Yaghoub Fathollahi, Javad Mirnajafi-Zadeh
There are several in vitro and in vivo models for studying LFS’ anticonvulsant mechanisms. In vitro models are useful for determining different agents’ effects on EAs under controlled conditions. Elevating extracellular K+ concentration is a widely-used model in epilepsy research. By increasing extracellular K+ concentration, long lasting neuronal depolarization and large ionic changes in hippocampal sub-regions occur. High levels of extracellular K+ concentration promote EA generation through neuronal depolarization, cell swelling, and decreasing several factors, including potassium currents, action potential threshold, and inhibitory synaptic potentials [9]. The high-K+ model of EA in brain slices is somewhat similar to in vivo studies, in which an elevated level of K+, up to 12 mM, is detectable in the hippocampus during a seizure state. In addition, glial cells’ functional impairment can lead to an increase in K+ concentration and EA’s occurrence [10].
Glutamatergic dysregulation in mood disorders: opportunities for the discovery of novel drug targets
Published in Expert Opinion on Therapeutic Targets, 2020
Panek Małgorzata, Kawalec Paweł, Malinowska Lipień Iwona, Tomasz Brzostek, Pilc Andrzej
Glutamate is the main stimulatory neurotransmitter in the central nervous system. Glu is the anion of glutamic acid and is the predominant form in physiological conditions. It plays an important role in the maturation of neurons, regulating their proliferation and migration processes during nervous system development. Additionally, it has a significant impact on cognition (e.g. learning and memory) as well as many other processes (e.g. it regulates the conduction of pain sensation in the spinal cord and brain). Glu is synthesized from glutamine in glutamatergic neurons by the mitochondrial enzyme glutaminase. With the aid of the vesicular glutamate transporter, Glu enters synaptic vesicles. During neuronal depolarization, the released Glu enters the synaptic space, stimulating numerous receptors. After its release, glutamate does not undergo enzymatic decomposition but is intercepted into the neighboring glial cells through the EAAT. Then, under the influence of the glutamine synthetase enzyme, it is converted into glutamine [13,25] Centelles et al. [25] depicted graphically the exact metabolism of glutamate)
L-Carnitine and Potential Protective Effects Against Ischemia-Reperfusion Injury in Noncardiac Organs: From Experimental Data to Potential Clinical Applications
Published in Journal of Dietary Supplements, 2018
Azadeh Moghaddas, Simin Dashti-Khavidaki
Some reports have declared that I/R injury plays an important role in retinal diseases such as glaucoma, diabetic retinopathy, and age-related macular degeneration. The mechanism of the cell death induced by retinal ischemia is not completely understood. It is suggested that cellular energy failure and glutamatergic stimulation initiate a destructive cascade involving neuronal depolarization, calcium influx, and oxidative stress, resulting in ischemic retinal injury. However, compared to many organs, such as the brain, the retina exhibits a remarkable natural resistance to ischemic injury, which reflects its peculiar metabolism and unique environment. LC's esters enhance optic nerve growth and increase visual function. In addition, LC and its esters are capable of protecting the chaperone activity of α-lens crystalline, which is a water-soluble protein found in the lens and cornea of the eyes, helping in transparency of objects. They can also decrease posttranslational modifications induced by oxidative stress and prevent cataract formation (Osborne et al., 2004; Szabadfi et al., 2010). Despite significant concentrations of LC in various ocular tissues, there is a paucity of literature regarding the role of LC in this organ. In the literature review, only three animal studies and one in vivo study evaluated the protective effects of LC against I/R-induced retinal injury (Alagoz, 2002; Derin, Aydin, et al., 2006; Kocer et al., 2002; Shamsi et al., 2007).