Consequence of parvalbumin deficiency in the mdx mouse: histological, biochemical and mechanical phenotype of a new double mutant

Raymackers, Jean-Marc; Debaix, Huguette; Schoor, M Colson-Van; Backer, Fabienne De; Tajeddine, Nicolas; Schwaller, Beat; Gailly, Philippe; Gillis, Jean-Marie

doi:10.1016/s0960-8966(03)00031-2

Cited by 41 publications

(34 citation statements)

References 45 publications

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“…Parvalbumin is a Ca 2ϩ -binding protein present in the cytosol, and in fast-twitch muscles such as the TA, the expression of parvalbumin is reduced starting at disease onset in mdx mice (39). Mdx:parvalbumin doubleknockout mice display greater decrements in force-generating capacity of EDL muscles compared with mdx mice, demonstrating further that reductions in Ca 2ϩ -handling proteins can negatively affect muscle function (36). Therefore, the increased parvalbumin that was measured after repeated bouts may be an adaptation that is beneficial for dystrophic muscle in terms of both strength and relaxation (Fig.…”

Section: Improved Contractility As a Results Of Repeated Bouts Of Eccementioning

confidence: 99%

Adaptive strength gains in dystrophic muscle exposed to repeated bouts of eccentric contraction

Call¹,

Eckhoff²,

Baltgalvis

et al. 2011

Journal of Applied Physiology

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Section: Improved Contractility As a Results Of Repeated Bouts Of Eccementioning

confidence: 99%

Adaptive strength gains in dystrophic muscle exposed to repeated bouts of eccentric contraction

Call¹,

Eckhoff²,

Baltgalvis

et al. 2011

Journal of Applied Physiology

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“…To compensate for these shortcomings of the mdx mouse, other mouse models of muscular dystrophy have been generated [17][18][19]. Nevertheless, we should take into consideration that double mutant mice like mdx mice deficient for MyoD [20], utrophin [18], parvalbumin [21], α7 integrin [22], or mTR (telomerase) [23] do not resemble the genetic background of DMD patients and are therefore less appropriate to predict therapeutic effects.…”

Section: Animal Models Of Muscular Dystrophymentioning

confidence: 99%

Insights into the Pathogenic Secondary Symptoms Caused by the Primary Loss of Dystrophin

Forcina

Pelosi

Miano

et al. 2017

JFMK

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Duchenne muscular dystrophy (DMD) is an X-linked genetic disease in which the dystrophin gene is mutated, resulting in dysfunctional dystrophin protein. Without dystrophin, the dystrophin-glycoprotein complex (DGC) is unstable, leading to an increase in muscle damage. Moreover, the imbalance between muscle damage and repair leads to a chronic inflammatory response and an increase in the amount of fibrosis over time. The absence of dystrophin at the sarcolemma also delocalizes and downregulates nitric oxide synthase (nNOS) and alters enzymatic antioxidant responses, leading to an increase in oxidative stress. In this review, we analyze the pathogenic role of both inflammation and oxidative stress in muscular dystrophy.

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“…235,Swant) was produced by hybridization of mouse myeloma cells with spleen cells from mice immunized with PV purified from carp muscles (Celio et al, 1988). It recognized a single 12 kD protein (pI 4.9) on a 2-dimensional immunoblot of rat cerebellar tissue; values identical to those expected for purified PV (Celio et al, 1988); and labeled a subpopulation of neurons in normal brain, but did not stain the brain of PV knockout mice (Raymackers et al, 2003).…”

Section: Antibody Characterizationmentioning

confidence: 99%

Distribution and targets of the relaxin‐3 innervation of the septal area in the rat

Olucha-Bordonau¹,

Otero-García²,

Sánchez-Pérez³

et al. 2012

J of Comparative Neurology

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Neural tracing studies have revealed that the rat medial and lateral septum are targeted by ascending projections from the nucleus incertus, a population of tegmental GABA neurons. These neurons express the relaxin‐family peptide, relaxin‐3, and pharmacological modulation of relaxin‐3 receptors in medial septum alters hippocampal theta rhythm and spatial memory. In an effort to better understand the basis of these interactions, we have characterized the distribution of relaxin‐3 fibers/terminals in relation to different septal neuron populations identified using established protein markers. Dense relaxin‐3 fiber plexuses were observed in regions of medial septum containing hippocampal‐projecting choline acetyltransferase (ChAT)‐, neuronal nitric oxide synthase (nNOS)‐, and parvalbumin (PV)‐positive neurons. In lateral septum (LS), relaxin‐3 fibers were concentrated in the ventrolateral nucleus of rostral LS and the ventral nucleus of caudal LS, with sparse labeling in the dorsolateral and medial nuclei of rostral LS, dorsal nucleus of caudal LS, and ventral portion nuclei. Relaxin‐3 fibers were also observed in the septofimbrial and triangular septal nuclei. In the medial septum, we observed relaxin‐3‐immunoreactive contacts with ChAT‐, PV‐, and glutamate decarboxylase‐67‐positive neurons that projected to hippocampus, and contacts between relaxin‐3 terminals and calbindin‐ and calretinin‐positive neurons. Relaxin‐3 colocalized with synaptophysin in nerve terminals in all septal areas, and ultrastructural analysis revealed these terminals were symmetrical and contacted spines, somata, dendritic shafts, and occasionally other axonal terminals. These data predict that this GABA/peptidergic projection modulates septohippocampal activity and hippocampal theta rhythm related to exploratory navigation, defensive and ingestive behaviors, and responses to neurogenic stressors. J. Comp. Neurol. 520:1903–1939, 2012. © 2011 Wiley Periodicals, Inc.

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Consequence of parvalbumin deficiency in the mdx mouse: histological, biochemical and mechanical phenotype of a new double mutant

Cited by 41 publications

References 45 publications

Adaptive strength gains in dystrophic muscle exposed to repeated bouts of eccentric contraction

Adaptive strength gains in dystrophic muscle exposed to repeated bouts of eccentric contraction

Insights into the Pathogenic Secondary Symptoms Caused by the Primary Loss of Dystrophin

Distribution and targets of the relaxin‐3 innervation of the septal area in the rat

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