Traumatic brain injury receptors

Traumatic brain injury is the most common cause of death in subjects under the age of 40, and an important risk factor for AD. Loss of hippocampal cells and depletion of ACh and of muscarinic receptors can be attenuated in injured experimental animals, improve blood perfusion in ischemic areas and increase cholinergic transmission in cortex and hippocampus the same mechanism invoked for treatment of VD. 

Dempsey RJ, BaskayaMK, Dogan A (2000) Attenuation of brain edema, blood-brain barrier breakdown, and injury volume by ifenprodil, a polyamine-site N-methyl-d-aspartate receptor antagonist, after experimental traumatic brain injury in rats. Neurosurgery 47 399-404... 

Indicative of serotonergic dysfunction, abused children with depression were shown to exhibit increased prolactin, but normal cortisol responses to the injection of E-5-hydroxytryptophan, a precursor of 5-HT, as compared to nonabused depressed children and controls (Kaufman et ah, 1998). Likewise, increased prolactin responses to fenfluramine were observed in boys with adverse rearing environment (Pine et ah, 1997). Since prolactin, but not cortisol release, is mediated via 5-HTia receptors, these findings suggest sensitization of these receptors due to early-life stress. Another study recently reported that children with traumatic brain injury (TBl) who had experienced abuse have dramatic increases in CSE concentrations of glutamate, compared to nonabused TBI children (Ruppel et ah, 2001). 

Boockvar, J.A., Schouten, J., Royo, N., Millard, M., Spangler, Z., Castelbuono, D., Snyder, E., O Rourke, D., McIntosh, T. (2005). Experimental traumatic brain injury modulates the survival, migration, and terminal phenotype of transplanted epidermal growth factor receptor-activated neural stem cells. Neurosurgery, 56,163-71. 

Sullivan P. G., Bruce-Keller A. J., Rabchevsky A. G., Christakos S., Clair D. K., Mattson M. P., and Schelf S. W. (1999). Exacerbation of damage and altered NF-rcB activation in mice lacking tumor necrosis factor receptors after traumatic brain injury. J. Neurosci. 19 6248-6256. 

Ikonomidou C. and Turski L. (2002). Why did NMDA receptor antagonists fail clinical trials for stroke and traumatic brain injury Lancet Neurol. 1 383-386. 

Lea P. M. and Faden A. I. (2001). Traumatic brain injury developmental differences in glutamate receptor response and the impact on treatment. Ment. Retard. Dev. Disabil. Res. Rev. 7 235-248. 

PCP inhibits brain nitric oxide synthase irreversibly (Osawa and Davila, 1993 Jewett et al., 1996 Klamer et al., 2005). Depending upon its levels, nitric oxide acts as a neuroprotective or neurodestructive molecule (Lipton, 1993 Lipton et al., 1998). NMDA receptor antagonists that have treated ischemic injury of the brain in animal models with some benefit are presented in Tables 10.1 and 10.2. All studies on their use in humans have been unsuccessful because they not only block normal neuronal function, but also produce serious side effects such as headache, anxiety, agitation, nausea, vomiting, hallucinations, dizziness, and coma (Schehr, 1996 Koroshetz and Moskowitz, 1996 Ratan et al., 1994). Clinical trials of NMDA antagonists for stroke and traumatic brain injury have been abandoned (Kemp and McKeman, 2002 Lees et al., 2000 Sacco et al., 2001). 

Faden A. I., DemediukP., PanterS. S., andVinkR. (1989) The role of excitatory amino acids and NMD A receptors in traumatic brain injury. Science 244, 798-800. 

Pappius HM, Dayes LA (1965) Hypertonic urea. Its effect on the distribution of water and electrolytes in normal and edematous brain tissues. Arch Neurol 13 395-402 Pascale CL, Szmydynger-Chodobska J, Sarri JE, Chodobski A (2006) Traumatic brain injury results in a concomitant increase in neocortical expression of vasopressin and its Via receptor. J Physiol Pharmacol 57(Suppl 11) 161-167... 

Szmydynger-Chodobska J, Chung I, Kozniewska E, Tran B, Harrington FJ, Duncan JA, Chodobski A (2004) Increased expression of vasopressin via receptors after traumatic brain injury. J Neurotrauma 21 1090-1102... 

Trabold R, Krieg S, SchoUer K, Plesnila N (2008) Role of vasopressin V(la) and V(2) receptors for the development of secondary brain damage after traumatic brain injury in mice. J Neurotrauma 25 1459-1465... 

Jones NC, Prior MJW, Burden-The E, Marsden CA, Morris P, Murphy S (2005) Antagonism of the interleukin-1 receptor following traumatic brain injury in the mouse reduces the number of nitric oxide synthase-2-positive cells and improves anatomical and functional outcomes. Eur J Neurosci 22 72-78... 

O Dell, D.M., Gibson, C.J., Wilson, M.S., DeFord, S.M., Hamm, R.J. (2000). Positive and negative modulation of GABA(A) receptor and outcome after traumatic brain injury in rats. Brain Res. 861 325-32. 

Namjoshi DR, Martin G, Donkin J, Wilkinson A, Stukas S, Fan J et al (2013) The liver X receptor agonist GW3965 improves recovery from mild repetitive traumatic brain injury in mice partly through apolipoprotein E. PLoS One 8 e53529. doi 10.1371/journal. pone.0053529... 

Mauler F, Horvath E, de Vry J, Jaeger R, Schwarz T, Sandmann S, Weinz C, Heinig R, Boettcher M (2003) BAY 38-7271 a novel highly selective and highly potent cannabinoid receptor agonist for the treatment of traumatic brain injury. CNS Drug Rev 9 343-358... 

Qiu J, Whalen MJ, Lowenstein P, Fiskum G, Fahy B, Darwish R, Aarabi B, Yuan J, Moskowitz MA. Upregulation of the fas receptor death-inducing signaling complex after traumatic brain injury in mice and humans. J Neurosci. 2002 22 3504-3511... 

Bajetto A, Bonavia R, Barbero S, Florio T, Schettini G (2001) Chemokines and their receptors in the central nervous system. Front Neuroendocrinol 22 147-184 Bales JW, Ma X, Yan HQ, Jenkins LW, Dixon CE (2010) Expression of protein phosphatase 2B (calcineurin) subunit A isoforms in rat hippocampus after traumatic brain injury. J Neurotrauma 27 109-120... 

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