Quantitative analysis of locomotor defects in neonatal mice lacking proprioceptive feedback

被引:8
|
作者
Dallman, Marisela A. [1 ]
Ladle, David R. [1 ]
机构
[1] Wright State Univ, Dept Neurosci Cell Biol & Physiol, Dayton, OH 45435 USA
关键词
Proprioception; Locomotion; Development; Behavior; RAT NERVOUS-SYSTEM; VESTIBULAR DYSFUNCTION; MOTOR-NEURONS; PARVALBUMIN; CALBINDIN-D-28K; SECRETION; MUNC18-1; BEHAVIOR; ABSENCE; BRAIN;
D O I
10.1016/j.physbeh.2013.07.005
中图分类号
B84 [心理学];
学科分类号
04 ; 0402 ;
摘要
Proprioceptive feedback derived from specialized receptors in skeletal muscle is critical in forming an accurate map of limb position in space, and is used by the central nervous system to plan future movements and to determine accuracy of executed movements. Knockout mouse strains for genes expressed by proprioceptive sensory neurons have been generated that result in generalized motor deficits, but these deficits have not been quantitatively characterized. Here we characterize a conditional knockout mouse model wherein proprioceptive sensory neuron synaptic transmission has been blocked by selective ablation of munc18-1, a synaptic vesicle associated protein required for fusion of synaptic vesicles with the plasma membrane. Proprioceptive munc18-1 conditional mutants are impaired in surface righting - a dynamic postural adjustment task - and display several specific deficits in pivoting, an early locomotor behavior. Before the emergence of forward locomotion during postnatal development, animals explore their surroundings through pivoting, or rotating the upper torso around the relatively immobile base of the hind limbs. 3-D kinematic analysis was used to quantitatively describe this pivoting behavior at postnatal days 5 and 8 in control and munc18-1 conditional mutants. Mutant animals also pivot, but demonstrate alterations in movement strategy and in postural placement of the forelimbs during pivoting when compared to controls. In addition, brief forelimb stepping movements associated with pivoting are altered in mutant animals. Step duration and step height are increased in mutant animals. These results underscore the importance of proprioceptive feedback even at early stages in postnatal development. (C) 2013 Elsevier Inc. All rights reserved.
引用
收藏
页码:97 / 105
页数:9
相关论文
共 50 条
  • [1] The role of proprioceptive feedback in the regulation and adaptation of locomotor activity
    Lam, T
    Pearson, KG
    [J]. SENSORIMOTOR CONTROL OF MOVEMENT AND POSTURE, 2002, 508 : 343 - 355
  • [2] Degradation of mouse locomotor pattern in the absence of proprioceptive sensory feedback
    Akay, Turgay
    Tourtellotte, Warren G.
    Arber, Silvia
    Jessell, Thomas M.
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2014, 111 (47) : 16877 - 16882
  • [3] A quantitative genetic analysis of locomotor activity in CXB recombinant inbred mice
    Toth, LA
    Williams, RW
    [J]. BEHAVIOR GENETICS, 1999, 29 (05) : 319 - 328
  • [4] A Quantitative Genetic Analysis of Locomotor Activity in CXB Recombinant Inbred Mice
    L. A. Toth
    R. W. Williams
    [J]. Behavior Genetics, 1999, 29 : 319 - 328
  • [5] A proprioceptive feedback circuit drives Caenorhabditis elegans locomotor adaptation through dopamine signaling
    Ji, Hongfei
    Fouad, Anthony D.
    Li, Zihao
    Ruba, Andrew
    Fang-Yen, Christopher
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2023, 120 (20)
  • [6] Motor hypertonia and lack of locomotor coordination in mutant mice lacking DSCAM
    Lemieux, Maxime
    Laflamme, Olivier D.
    Thiry, Louise
    Boulanger-Piette, Antoine
    Frenette, Jerome
    Bretzner, Frederic
    [J]. JOURNAL OF NEUROPHYSIOLOGY, 2016, 115 (03) : 1355 - 1371
  • [7] Circadian locomotor analysis of male mice lacking the gene for neuronal nitric oxide synthase (nNOS-/-)
    Kriegsfeld, LJ
    Demas, GE
    Lee, SE
    Dawson, TM
    Dawson, VL
    Nelson, RJ
    [J]. JOURNAL OF BIOLOGICAL RHYTHMS, 1999, 14 (01) : 20 - 27
  • [8] Embryonic heart and skin defects in mice lacking plakoglobin
    Bierkamp, C
    McLaughlin, KJ
    Schwarz, H
    Huber, O
    Kemler, R
    [J]. DEVELOPMENTAL BIOLOGY, 1996, 180 (02) : 780 - 785
  • [9] Fertilization defects in sperm from mice lacking fertilinβ
    Cho, CH
    Bunch, DO
    Faure, JE
    Goulding, EH
    Eddy, EM
    Primakoff, P
    Myles, DG
    [J]. SCIENCE, 1998, 281 (5384) : 1857 - 1859
  • [10] Embryonic heart and skin defects in mice lacking plakoglobin
    Bierkamp, C
    Schwarz, H
    McLaughlin, J
    Huber, O
    Kemler, R
    [J]. EUROPEAN JOURNAL OF CELL BIOLOGY, 1997, 72 : 176 - 176