Differential consequences of lateral and central fluid percussion brain injury on receptor coupling in rat hippocampus

被引:33
作者
Delahunty, TM
Jiang, JY
Gong, QZ
Black, RT
Lyeth, BG
机构
[1] Division of Neurosurgery, Medical College of Virginia/Virginia Commonwealth University, Richmond, Virginia 23298-0693, Box 980693, MCV Station
关键词
brain trauma; fluid percussion; hippocampus; muscarinic receptor; metabotropic;
D O I
10.1089/neu.1995.12.1045
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
We have identified alterations in the responses of muscarinic and metabotropic receptors in rat hippocampus that persist for at least 15 days after central fluid percussion injury, This study compares the effect of lateral fluid percussion and central fluid percussion on these responses, Moderate injury was obtained by displacement and deformation of the brain within the closed cranial cavity using a fluid percussion device positioned either centrally or laterally, Carbachol and (+/-)-1-aminocyclopentane-trans-1,3-dicarboxylic acid (trans-ACPD)-stimulated polyphosphoinositide (PPI) hydrolysis was assayed in hippocampus from injured and sham-injured controls at 15 days following injury, At 15 days after central fluid percussion traumatic brain injury (TBI), the response to carbachol was enhanced by 30% and the response to trans-ACPD was enhanced by 75% compared to sham-injured animals, At 15 days after lateral fluid percussion TBI the response to trans-ACPD was enhanced by 40% both ipsilateral and contralateral to the side of injury, In contrast, the response to carbachol was enhanced by 29% contralateral to the side of injury but was diminished by 12% ipsilateral to the side of injury, Cresyl violet staining shows no hippocampal cell death after central fluid percussion injury or on the side contralateral to lateral fluid percussion injury but on the ipsilateral side cell death was identified in hippocampal area CA3, Thus, abnormal hippocampal cell signaling through the phosphoinositide pathway occurs in the absence of cell death and may contribute to cognitive impairment.
引用
收藏
页码:1045 / 1057
页数:13
相关论文
共 82 条
  • [21] THE ROLE OF EXCITATORY AMINO-ACIDS AND NMDA RECEPTORS IN TRAUMATIC BRAIN INJURY
    FADEN, AI
    DEMEDIUK, P
    PANTER, SS
    VINK, R
    [J]. SCIENCE, 1989, 244 (4906) : 798 - 800
  • [22] EXCITATORY AMINO-ACID RECEPTORS, NEURAL MEMBRANE PHOSPHOLIPID-METABOLISM AND NEUROLOGICAL DISORDERS
    FAROOQUI, AA
    HORROCKS, LA
    [J]. BRAIN RESEARCH REVIEWS, 1991, 16 (02) : 171 - 191
  • [23] INOSITOL LIPIDS AND SIGNAL TRANSDUCTION IN THE NERVOUS-SYSTEM - AN UPDATE
    FISHER, SK
    HEACOCK, AM
    AGRANOFF, BW
    [J]. JOURNAL OF NEUROCHEMISTRY, 1992, 58 (01) : 18 - 38
  • [24] FOTUHI M, 1993, J NEUROSCI, V13, P2001
  • [25] GENARELLI TA, 1994, J NEUROTRAUM, V11, P357
  • [26] GORMAN LK, 1989, J NEUROTRAUM, V6, P203
  • [27] GORMAN LK, 1994, SOC NEUR ABSTR, P195
  • [28] THE EFFECT OF AGE ON MOTOR AND COGNITIVE DEFICITS AFTER TRAUMATIC BRAIN INJURY IN RATS
    HAMM, RJ
    WHITEGBADEBO, DM
    LYETH, BG
    JENKINS, LW
    HAYES, RL
    [J]. NEUROSURGERY, 1992, 31 (06) : 1072 - 1078
  • [29] Pretreatment with Phencyclidine, an N-Methyl-D-Aspartate Antagonist, Attenuates Long-Term Behavioral Deficits in the Rat Produced by Traumatic Brain Injury
    Hayes, R. L.
    Jenkins, L. W.
    Lyeth, B. G.
    Balster, R. L.
    Robinson, S. E.
    Clifton, G. L.
    Stubbins, J. F.
    Young, H. F.
    [J]. JOURNAL OF NEUROTRAUMA, 1988, 5 (04) : 259 - U24
  • [30] MILD EXPERIMENTAL BRAIN INJURY IN THE RAT INDUCES COGNITIVE DEFICITS ASSOCIATED WITH REGIONAL NEURONAL LOSS IN THE HIPPOCAMPUS
    HICKS, RR
    SMITH, DH
    LOWENSTEIN, DH
    MARIE, RS
    MCINTOSH, TK
    [J]. JOURNAL OF NEUROTRAUMA, 1993, 10 (04) : 405 - 414