Changes of Cognition Related Neurotransmitters after Traumatic Brain Injury (review)

  • ZHANG Yue ,
  • ZHANG Xiao-nian ,
  • ZHANG Hao
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  • 1. Department of Neural Rehabilitation, Beijing Bo'ai Hospital, China Rehabilitation Research Centre, Beijing 100068, China
    2. Capital Medical University School of Rehabilitation Medicine, Beijing 100068, China

Received date: 2017-07-23

  Revised date: 2017-12-04

  Online published: 2018-01-31

Supported by

Special Fund Project for Basic Scientific Research Business of Central Public Scientific Research Institute (No. 2015CZ-27)

Abstract

Many cognition related neurotransmitters varied after traumatic brain injury, such as dopamine, acetylcholine, norepinephrine, and excitatory amino acids, etc. This paper summarized the changes of these neurotransmitters and their receptors in different stages after traumatic brain injury.

Cite this article

ZHANG Yue , ZHANG Xiao-nian , ZHANG Hao . Changes of Cognition Related Neurotransmitters after Traumatic Brain Injury (review)[J]. Chinese Journal of Rehabilitation Theory and Practice, 2018 , 24(1) : 71 -75 . DOI: 10.3969/j.issn.1006-9771.2018.01.013

References

[1] Walder B, Haller G, Rebetez MM, et al. Severe traumatic brain injury in a high-income country: an epidemiological study [J]. J Neurotrauma, 2013, 30(23): 1934-1942.
[2] Ponsford JL, Spitz G, Cromarty F, et al. Costs of care after traumatic brain injury [J]. J Neurotrauma, 2013, 30(17): 1498-1505.
[3] Graham DP, Cardon AL. An update on substance and treatment following traumatic brain injury [J]. Ann N Y Acad Sci, 2008, 1141: 148-162.
[4] Rotaru DC, Lewis DA, Gonzalez-Burgos G. Dopamine D1 receptor activation regulates sodium channel-dependent EPSP amplification in rat prefrontal cortex pyramidal neurons [J]. J Physiol, 2007, 581(Pt 3): 981-1000.
[5] Huger F, Patrick G. Effect of concussive head injury on central catecholamine levels and synthesis rates in rat brain regions [J]. J Neurochem, 1979, 33(1): 89-95.
[6] Dunn-Meynerll A, Pan S, Levin BE. Forcoal traumatic brain injury cause widespread reductions in rat brain norepinephrine turnover from 6 to 24 h [J]. Brain Res, 1994, 660(1): 88-95.
[7] McIntosh TK, Yu T, Gennarelli TA. Alterations in regional brain catecholamine concentrations after experimental brain injury in the rat [J]. J Neurochem, 1994, 63(4): 1426-1433.
[8] Massucci JL, Kline AE, Ma X, et al. Time dependent alterations in dopamine tissue levels and metabolism after experimental traumatic brain injury in rats [J]. J Neurosci Lett, 2004, 372(1-2): 127-131.
[9] Kobori N, Clifton GL, Dash PK. Enhanced catecholamine synthesis in the prefrontal cortex after traumatic brain injury: implications for prefrontal dysfunction [J]. J Neurotrauma, 2006, 23(7): 1094-1102.
[10] Globus MY, Busto R, Dietrich WD, et al. Effect of ischemia on the in vivo release of striatal dopamine, glutamate, and γ-aminobutyric acid studied by intracerebral microdialysis [J]. J Neurochem, 1988, 51(5): 1455-1464.
[11] Dietrich WD, Alonso O, Halley M. Early microvascular and neuronal consequences of traumaticbrain injury: a light and electron microscopic study in rats [J]. J Neurotrauma, 1994, 11(3): 289-301.
[12] Wagner AK, Sokoloski JE, Ren D, et al. Controlled cortical impact injury affects dopaminergic transmission in the rat striatum [J]. J Neurochem, 2005, 95(2): 457-465.
[13] van Bregt DR, Thomas TC, Hinzman JM, et al. Substantia nigra vulnerability after a single moderate diffuse brain injury in the rat [J]. Exp Neurol, 2012, 234(1): 8-19.
[14] Hutson CB, Lazo CR, Mortazavi F, et al. Traumatic brain injury in adult rats causes progressive nigrostriatal dopaminergic cell loss and enhanced vulnerability to the pesticide paraquat [J]. J Neurotrauma, 2011,28(9): 1783-1801.
[15] Chen YH, Huang EY, Kuo TT, et al. Dopamine relaease in the nucleus accumbens is altered following traumatic brain injury [J]. Neuroscience, 2017, 348: 180-190.
[16] Blanchard V, Chritin M, Vyas S, et al. Long-term induction of tyrosine hydroxylase expression: compensatory response to partial degeneration of the dopaminergic nigrostriatal system in the rat brain [J]. J Neurochem, 1995, 64(4): 1669-1679.
[17] Mura A, Feldon J. Spatial learning in rats is impaired after degeneration of the nigrostriatal dopaminergic system [J]. Mov Disord, 2003, 18(8): 860-871.
[18] Onn SP, Berger TW, Stricker EM, et al. Effects of intraventricular 6-hydroxydopamine on the dopaminergic innervation of striatum: histochemical and neurochemical analysis [J]. Brain Res, 1986, 376(1): 8-19.
[19] Redell JB, Dash PK. Traumatic brain injury stimulates hippocampal catechol-O-methyl transferase expression in microglia [J]. Neurosci Lett, 2007, 413(1): 36-41.
[20] Yan HQ, Ma X, Chen X, et al. Delayed increase of tyrosine hydroxylase expression in rat nigrostriatal system after traumatic brain injury [J]. Brain Res, 2007, 1134(1): 171-179.
[21] Yan HQ, Kline AE, Ma X, et al. Traumatic brain injury reduces dopamine transporter protein expression in the rat frontal cortex [J]. Neuroreport, 2002, 13(15): 1899-1901.
[22] Henry JM, Talukder NK, Lee AB, et al. Cerebral trauma-induced changes in corpusstriatal dopamine receptor subtypes [J]. Invest Surg, 1997, 10(5): 281-286.
[23] Wagner AK, Sokoloski JE, Chen X, et al. Controlled cortical impact injury influences methylphenidate-induced changes in striatal dopamine neurotransmission [J]. J Neurochem, 2009, 110(3): 801-810.
[24] Wagner AK, Scanlon JM, Becker CR, et al. The influence of genetic variants on striatal dopaminetransporter and D2 receptor binding after TBI [J]. Cereb Blood Flow Metab, 2014, 34(8): 1328-1339.
[25] Donnemiller E, Brenneis C, Wissel J, et al. Impaired dopaminergic neurotransmission in patients with traumatic brain injury: a SPECT study using 123 I-beta-CIT and 123 I-IBZM [J]. Eur J Nucl Med, 2000, 27(9): 1410-1414.
[26] Phillis JW. Acetylcholine release from the central nervous system: A 50-year retrospective [J]. Crit Rev Neurobiol, 2005, 17(3-4): 161-217.
[27] Winkler J, Suhr ST, Gage FH, et al. Essential role of neocortical acetylcholine in spatial memeoty [J]. Nature, 1995, 375(6531): 484-487.
[28] Gorman LK, Fu K, Hovad DA, et al. Analysis of acetylcholine release following concussive brain injury in the rat [J]. J Neurotrauma, 1988, 6: 203.
[29] Sajia A, Hayes RL, Lyeth BG, et al. The effect of concussive head injury on central cholinergic neurons [J]. Brain Res, 1988, 452(1-2): 303-311.
[30] Sachs E Jr. Acetylcholine and serotonin in the spinal fluid [J]. J Neurosurg, 1957, 14(1): 22-27.
[31] Dixon CE, Ma X, Marion DW. Reduced evokes release of acetylcholine in the rodent neocortex following traumatic brain injury [J]. Brain Res, 1997, 749(1): 127-130.
[32] Scremin OU, Li MG, Roch M, et al. Acetylcholine and choline dynamics provide early and late markers of traumatic brain injury [J]. Brain Res, 2006, 1124(1): 155-166.
[33] 李坪,于建云,赵小林,等. 脑震荡对大鼠脑内乙酰胆碱M1受体亚型的影响[J]. 解剖学杂志, 2007, 30(2): 235-237.
[34] Shao L, Ciallella JR, Yan HQ, et al. Differential effects of traumatic brain injury on vesicular acetylcholine transporter and M2 muscarinic receptor mRNA and protein in rat [J]. J Neurotrauma, 1999, 16(7): 555-566.
[35] Shin SS, Dixon CE. Targeting α7 nicotinic acetylcholine receptors: a future potential for neuroprotection from traumatic brain injury [J]. Neural Regan Res, 2015, 10(10): 1552-1554.
[36] Pullman SL, Watts RL, Juncos JL, et al. Dopaminergic effects on simple and choice reaction time performance in Parkinson's disease [J]. Neurology, 1988, 38(2): 249-254.
[37] Halliday R, Callaway E, Lannon R. The effects of clonidine and yohimbineon human information processing [J]. Psychopharmacology (Berl), 1989, 99(4): 563-566.
[38] Carli M, Robbins TW, Evenden JL, et al. Effects of lesions to ascending noradrenergic neurones on performance of a 5-choice serial reaction task in rats; implications for theories of dorsal noradrenergic bundle function based on selective attention and arousal [J]. Behav Brain Res, 1983, 9(3): 361-380.
[39] Cole BJ, Robbins TW. Forebrain norepinephrine: role in controlled information processing in the rat [J]. Neuropsychopharmacology, 1992, 7(2): 129-142.
[40] Aston-Jones G, Rajkowski J, Cohen J. Role of locus coeruleus in attention and behavioral flexibility [J]. Biol Psychiatry, 1999, 46(6): 1309-1320.
[41] Roozendaal B, McEwen BS, Chattarji S. Stress, memory and the amygdala [J]. Nat Rev Neurosci, 2009, 10(6): 423-433.
[42] Levin BE, Brown KL, Pawar G, et al. Widespread and lateralization effects of acute traumatic brain injury on norepinephrine turnover in the rat brain [J]. Brain Res, 1995, 674(2): 307-313.
[43] Dunn-Meynell AA, Hassanain M, Levin BE. Norepinephrine and traumatic brain injury: a possible role in post-traumatic edema [J]. Brain Res, 1998, 800(2): 245-252.
[44] McIntosh TK, Yu T, Gennarelli TA. Alterations in regionalbrain catecholamine concentrations after experimentalbrain injury in the rat [J]. J Neurochem, 1994, 63(4): 1426-1433.
[45] Fujinaka T, Kohmura E, Yuguchi T, et al. The morphological and neurochemical effects of diffuse brain injury on rat central noradrenergic system [J]. Neurol Res, 2003, 25(1): 35-41.
[46] Boyeson MG, Feeney DM. Intraventricular norepinephrine facilitates motor recovery following sensorimotor cortex injury [J]. Pharmacol Biochem Behav, 1990, 35(3): 497-501.
[47] Sutton RL, Feeney DM. alpha-Noradrenergic agonists and antagonists affect recovery and maintenance of beam-walking ability after sensorimotorcortex ablation in the rat [J]. Restor Neurol Neurosci, 1992, 4(1): 1-11.
[48] Prasad MR, Tzigaret CM, Smith D, et al. Decreased alpha 1-adrenergic receptors after experimental brain injury [J]. J Neurotrauma, 1992, 9(3): 269-279.
[49] Clifton GL, Robertson CS, Kyper K, et al. Cardiovascular response to severe headinjury [J]. J Neurosurg, 1983, 59(3): 447-454.
[50] Mautoes AE, Muller M, Cortbus F, et al. Alterations of norepinephrine levels in plasma and CSF of patients after traumatic brain injury in relation to disruption of the blood-brain barrier [J]. Acta Neurochir, 2001, 143(1): 51-55.
[51] Levin BE, Pan S, Dunn-Meynell A. Chronic alterations in rat brain alpha-adrenoceptors following traumatic brain injury [J]. Restor Neurol Neurosci, 1994, 7(1): 5-12.
[52] Faden AI, Demediuk P, Panter SS, et al. The role of excitatory amino acids and NMDA receptors in traumatic brain injury [J]. Science, 1989, 44(4906): 798-800.
[53] Baker AJ, Moulton RJ, MacMillan VH, et al. Excitatory amino acids in cerebrospinal fluid following traumatic brain injury in humans [J]. J Neurosurg, 1993, 79(3): 369-372.
[54] Zhang H, Zhang X, Zhang T, et al. Excitatory amino acids in cerebrospinal fluid of patients with acute head injuries [J]. Clin Chem, 2001, 47(8): 1458-1462.
[55] Hayes RL, Jenkins LW, Lyeth BG. Neurotransmitter-mediated mechanisms of traumatic brain injury: acetylcholine and excitatory amino acids [J]. J Neurotrauma, 1992, 9(Suppl 1): 173-187.
[56] Kline AE, Yu J, Horvath E, et al. The selective 5-HT(1A) receptor agonist repinotan HCl attenuates histopathology and spatial learning deficits following traumatic brain injury in rats [J]. Neuroscience, 2001, 106(3): 547-555.
[57] Christofides J, Bridel M, Egerton M, et al. Blood 5-hydroxytryptamine, 5-hydroxyindoleacetic acid and melatonin levels in patients with either Huntington's disease or chronic brain injury [J]. Eur J Neurol, 2006, 13(1): 30-42.
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