Formation Of A Full Complement Of Cranial Proprioceptors Requires Multiple Neurotrophins
Anatomy & Morphology; brain-derived neurotrophic factor; central-nervous-system; Developmental Biology; expression; in-vivo; masseter muscle; mesencephalic trigeminal neurons; messenger-rna; mice; muscle spindles; muscle spindles; mutant; neurotrophin-3; neurotrophin-4; nt-3 activation; proprioceptive sensory neurons; sensory neurons; Trk receptors; Trk receptors
Fan G P; Copray S; Huang E J; Jones K; Yan Q; Walro J; Jaenisch R; Kucera J
Developmental Dynamics
2000
2000-06
Journal Article or Conference Abstract Publication
<a href="http://doi.org/10.1002/(sici)1097-0177(200006)218:2%3C359::aid-dvdy9%3E3.0.co;2-l" target="_blank" rel="noreferrer noopener">10.1002/(sici)1097-0177(200006)218:2%3C359::aid-dvdy9%3E3.0.co;2-l</a>
Formation Of A Full Complement Of Cranial Proprioceptors Requires Multiple Neurotrophins (vol 218, Pg 359, 2002)
Anatomy & Morphology; Developmental Biology
Fan G P; Copray S; Huang E J; Jones K; Yan Q; Walro J; Jaenisch R; Kucera J
Developmental Dynamics
2002
2002-12
Journal Article or Conference Abstract Publication
<a href="http://doi.org/10.1002/dvdy.10197" target="_blank" rel="noreferrer noopener">10.1002/dvdy.10197</a>
Formation Of Supernumerary Muscle Spindles At The Expense Of Golgi Tendon Organs In Er81-deficient Mice
Anatomy & Morphology; Developmental Biology; ETS transcription factors; expression; Golgi tendon organs; group; ia afferents; innervation; motor neurons; muscle spindles; mutant mice; myosin heavy-chain; neonatal rats; nerve growth-factor; neurotrophin-3; primary sensory neurons; proprioceptive afferents; transcription factors
ER81, a member of the ETS family of transcription factors, is essential for the formation of connections between sensory and motor neurons in the spinal cord. Mice lacking Er81 genes exhibit reduced monosynaptic sensory-motoneuron connectivity in response to muscle nerve stimulation. Proximal muscle nerve stimulation elicits fewer monosynaptic potentials than stimulation of distal nerves in hind-limbs, a deficit that is paralleled by a paucity of muscle spindles in proximal muscles (Arber et al., 2000). We examined whether a presence of spindles innervated by afferents in distal muscles correlated with the increased preservation of monosynaptic sensory-motor potentials in distal muscle nerves. Not only were spindles and Ia afferents present, but also they were supernumerary in distal muscles such as the soleus, medial gastrocnemius, and extensor hallucis longus. Concomitantly, a deficiency of Golgi tendon organs (GTOs) and Ib afferents was observed in distal muscles, as if supernumerary spindles formed at the expense of tendon organs in the absence of Er81. Thus, ER81 may be involved in mechanisms that regulate acquisition of the Ia and Ib phenotypes by subsets of proprioceptive muscle afferents. Segmental differences in muscle spindle and GTO dependence on ER81 suggest that more than one ETS transcription factor may participate in the regulation of limb proprioceptive system assembly in the mouse. (C) 2002 Wiley-Liss, Inc.
Kucera J; Cooney W; Que A; Szeder V; Stancz-Szeder H; Walro J
Developmental Dynamics
2002
2002-03
Journal Article or Conference Abstract Publication
<a href="http://doi.org/10.1002/dvdy.10066" target="_blank" rel="noreferrer noopener">10.1002/dvdy.10066</a>
Neurotrophin-3 Ameliorates Sensory-motor Deficits In Er81-deficient Mice
afferents; Anatomy & Morphology; connections; Developmental Biology; differentiation; ER81; ETS; innervation; motor neurons; muscle spindles; muscle spindles; mutant mice; neurons; neurotrophins; NT3; rat; regeneration; sensory neurons; specification; spinal-cord; transcription factors
Two factors, the ETS transcription factor ER81 and skeletal muscle-derived neurotrophin-3 (NT3), are essential for the formation of muscle spindles and the function of spindle afferent-motoneuron synapses in the spinal cord. Spindles either degenerate completely or are abnormal, and spindle afferents fail to project to spinal motoneurons in Er81 null mice; however, the interactions between ER81 and NT3 during the processes of afferent neuron and muscle spindle development are poorly understood. To examine if overexpression of NT3 in muscle rescues spindles and afferent-motoneuron connectivity in the absence of ER81, we generated myoNT3;Er81(-/-) double-mutant mice that selectively overexpress NT3 in muscle in the absence of ER81. Spindle reflex arcs in myoNT3;Er81(-/-) mutants differed greatly from Er81 null mice. Muscle spindle densities were greater and more afferents projected into the ventral spinal cord in myoNT3;Er81(-/-) mice. Spindles of myoNT3,Er81(-/-) muscles responded normally to repetitive muscle taps, and the monosynaptic inputs from la afferents to motoneurons, grossly reduced in Er81(-/-) mutants, were restored to wild-type levels in myoNT3,Er81(-/-) mice. Thus, an excess of muscle-derived NT3 reverses deficits in spindle numbers and afferent function induced by the absence of ER81. We conclude that muscle-derived NT3 can modulate spindle density and afferent-motoneuron connectivity independently of ER81.
Li L Y; Wang Z; Sedy J; Quazi R; Walro J M; Frank E; Kucera J
Developmental Dynamics
2006
2006-11
Journal Article or Conference Abstract Publication
<a href="http://doi.org/10.1002/dvdy.20964" target="_blank" rel="noreferrer noopener">10.1002/dvdy.20964</a>