Neuromuscular junction - Wikipedia
A neuromuscular junction (or myoneural junction) is a chemical synapse formed by the contact between a motor neuron and a muscle fiber. It is at the neuromuscular junction that a motor neuron is able to transmit a signal to the muscle fiber, causing muscle contraction. Muscles require innervation to function-and even just to maintain muscle tone, avoiding atrophy. Synaptic transmission at the neuromuscular junction begins when an action potential reaches the presynaptic terminal of a motor neuron, which activates voltage-dependent calcium channels to allow calcium ions to enter the neuron. Calcium ions bind to sensor proteins (synaptotagmin) on synaptic vesicles, triggering vesicle fusion with the cell membrane and subsequent neurotransmitter release from the motor neuron into the synaptic cleft. In ...https://en.wikipedia.org/wiki/Neuromuscular_junction
Identification and Characterization of Factors Critical in Regulating the Selective Vulnerability of Distinct Motor neuron...
This figure shows neuromuscular junctions with either high or low vulnerability. The red staining represents the part of the neuromuscular junction formed by the muscle. The green represents the part of the neuromuscular junction formed by the neuron. In the examples from the healthy mouse, the green staining very tightly correlates with the red staining implying neuromuscular junctions are intact and functional. In theneck muscles from the SMA mouse, again, neuromuscular junctions appear intact i.e. all the red staining is accompanied by green staining. In the abdominal muscles, there are frequent examples of red staining which has no green staining. This implies that the neuron has been lost and the ...http://curesma.ca/2017/05/11/identification-and-characterization-of-factors-critical-in-regulating-the-selective-vulnerability-of-distinct-motor-neuron-pools-in-spinal-muscular-atrophy-models-of-mice/
"Electron microscopy of Drosophila larval neuromuscular junctions" by Preethi Ramachandran and Vivian Budnik
Over the last two decades, the Drosophila larval neuromuscularjunction has gained immense popularity as a model system forthe study of synaptic development, function, and plasticity.With this model, it is easy to visualize synapses and manipulatethe system genetically with a high degree of temporal and spatialcontrol, which makes it ideal for resolving problems in synapticphysiology and development. This article describes the preparationof Drosophila larval body-wall muscles for imaging by electronmicroscopy. The samples are fixed, stained, and embedded inSpurr's resin before being sectioned for electron microscopy.http://escholarship.umassmed.edu/gsbs_sp/1703/
neuromuscular junction | biochemistry | Britannica.com
neuromuscular junction: Site of chemical communication between a nerve fibre and a muscle cell. The neuromuscular junction is analogous to the synapse between two neurons. A nerve fibre divides into many...https://www.britannica.com/science/neuromuscular-junction
Fak56 functions downstream of integrin alphaPS3betanu and suppresses MAPK activation in neuromuscular junction growth | Neural...
Formation and stabilization of neuronal synapses demands communication between pre- and post-synaptic partners, as well as signals from the extracellular matrix (ECM). These signals can reorganize local cytoskeletal structures or be transduced into the nucleus to regulate transcription, thereby modulating neuronal plasticity [1-3]. One major receptor family for ECM signals comprises the transmembrane protein integrins, which have been shown to play critical roles in sequential steps of neuronal wiring, such as in neurite outgrowth, axon guidance, and synaptic formation and maturation [4-7]. In Drosophila, various integrin subunits have been shown to function in motor axon pathfinding and target recognition, and synaptic morphogenesis at neuromuscular junctions (NMJs) [8-10]. Mutant analyses for the integrin subunits αPS3 and βPS indicate that integrin signaling is involved in synaptic growth and arborization of larval NMJs [8-10]. Although ...https://neuraldevelopment.biomedcentral.com/articles/10.1186/1749-8104-3-26
We show that the increase in mepc amplitude that occurs at the mouse neuromuscular junction following activity blockade is diminished in the Rab3A deletion mouse, and abolished in the Rab3A Earlybird mouse. In wild-type animals, the magnitude of plasticity is inversely related to the mepc amplitude of the untreated neuromuscular junctions, and this relationship is disrupted in both the Rab3A deletion and Earlybird mutant mice. These data suggest that normal Rab3A function is required for activity-dependent modulation of mepc amplitude, and that Rab3A also maintains the inverse relationship between the mepc amplitude on the untreated side and the magnitude of the increase on the TTX-treated side. This is the first demonstration that a presynaptic protein, other than a transmitter transporter, is involved in homeostatic plasticity of quantal amplitude.. The mechanism underlying the homeostatic ...http://www.jneurosci.org/content/31/10/3580
Spred1 Is Required for Synaptic Plasticity and Hippocampus-Dependent Learning | Journal of Neuroscience
Germline mutations in SPRED1, a negative regulator of the Ras/ERK pathway, have recently been reported to cause NFLS (Brems et al., 2007). NFLS belongs to a group of phenotypically overlapping neuro-cardio-facial-cutaneous (NCFC) syndromes, which all present with a variable degree of learning difficulties or mental retardation. In NF1, visuo-spatial problems rank among the most common cognitive deficits (Hyman et al., 2005), and Nf1 heterozygous mice consequently show impairments in visuo-spatial memory and hippocampal LTP (Costa et al., 2001, 2002). Genetic as well as pharmacological compensation for the loss of Ras regulation resulted in rescue of the learning defects in Nf1+/− mice (Costa et al., 2002). Moreover, the role of NF1 in learning and synaptic plasticity appears to be evolutionary conserved, because learning as well as cellular responses at the neuromuscular junction are impaired in Drosophila mutants of Nf1 (Guo et al., 1997, 2000).. Also, in ...http://www.jneurosci.org/content/28/53/14443.long
Toxins | Free Full-Text | Insight into the Mode of Action of Haedoxan A from Phryma leptostachya
Haedoxan A (HA) is a major active ingredient in the herbaceous perennial plant lopseed (Phryma leptostachya L.), which is used as a natural insecticide against insect pests in East Asia. Here, we report that HA delayed the decay rate of evoked excitatory junctional potentials (EJPs) and increased the frequency of miniature EJPs (mEJPs) on the Drosophila neuromuscular junction. HA also caused a significant hyperpolarizing shift of the voltage dependence of fast inactivation of insect sodium channels expressed in Xenopus oocytes. Our results suggest that HA acts on both axonal conduction and synaptic transmission, which can serve as a basis for elucidating the mode of action of HA for further designing and developing new effective insecticides.http://www.mdpi.com/2072-6651/8/2/53
placca neuromuscolare | neuromuscular junction/endplate
(KudoZ) Italian to English translation of placca neuromuscolare e fondamentale: neuromuscular junction/endplate [Neurotransmitters - Medical (general) (Medical)].https://www.proz.com/kudoz/italian_to_english/medical_general/2800510-placca_neuromuscolare_e_fondamentale.html
"Reversible Recruitment of a Homeostatic Reserve Pool of Synaptic Vesic" by Xueyong Wang, Martin J. Pinter et al.
Homeostatic regulation is essential for the maintenance of synaptic strength within the physiological range. The current study is the first to demonstrate that both induction and reversal of homeostatic upregulation of synaptic vesicle release can occur within seconds of blocking or unblocking acetylcholine receptors at the mouse neuromuscular junction. Our data suggest that the homeostatic upregulation of release is due to Ca2+-dependent increase in the size of the readily releasable pool (RRP). Blocking vesicle refilling prevented upregulation of quantal content (QC), while leaving baseline release relatively unaffected. This suggested that the upregulation of QC was due to mobilization of a distinct pool of vesicles that were rapidly recycled and thus were dependent on continued vesicle refilling. We term this pool thehttps://corescholar.libraries.wright.edu/ncbp/1091/
fc10f30: Neuromuscular junction, muscle side (SEM). Micrograph from Desaki, J. and Y. Uehara, 1991. By permission of Don...
fc10f30: Neuromuscular junction, muscle side (SEM). Micrograph from Desaki, J. and Y. Uehara, 1991. By permission of Don Fawcett. ...https://histo.life.illinois.edu/histo/atlas/image.php?sname=fc10f30&iname=15000a1&oid=1349
Gallery • Hiesinger Group • Department of Biology, Chemistry, Pharmacy
Cover Caption: The cover shows the end of a neuronal branch (foreground) at the Drosophila neuromuscular junction (background). Boutons are stained with an antibody against DVAP-33A (yellow to brown), which is excluded from active zones (purple). DVAP-33A is enriched at the neck of budding boutons. The visualization of the surface and underlying triangularized wireframe (top left) are merged with a qualitative volume rendering of a bouton from which the top is removed. Functional characterization of DVAP-33A using these visualization techniques shows that DVAP-33A is a microtubule-interacting protein and tightly regulates bouton budding at neuromuscular junctions in a dosage-dependent manner. For further details, see the article by Pennetta et al. (pp. 291-306 in this issue). ...http://www.bcp.fu-berlin.de/en/biologie/arbeitsgruppen/neurobiologie/ag_hiesinger/galerie/index.html
Neuromuscular Junction Disorders: Diagnosis and Treatment - MERIGGIOLI; | Foyles Bookstore
Promotes early disease detection and screening. This resource covers all aspects of the diagnosis and clinical management of patients with diseases of the neuromuscular junction. Breaks down each disease by pathophysiology, clinical presentation, and natural history and course for improved diagnosis and treatment.http://www.foyles.co.uk/witem/medical-veterinary/neuromuscular-junction-disorders,meriggioli-9780824756956
When a spherical muscle cell (myoball) was manipulated into contact with either the soma or the neurite of an isolated neuron in 2-day-old Xenopus nerve-muscle cultures, depolarizations similar to miniature endplate potentials (MEPPs) were frequently detected in the muscle cell. These depolarizations occurred within minutes after myoball-soma contact and within seconds after myoball-neurite contact. They had time course and amplitude distribution similar to those of the MEPPs recorded from naturally occurring neuromuscular synapses between neurites and muscle cells found in the same cultures, but they occurred at a lower frequency and had smaller average amplitudes. These depolarizations were induced by acetylcholine (ACh) since they were reversibly blocked by addition of d-tubocurarine into the culture, and they were abolished in muscle cells pretreated with alpha-bungarotoxin before contact with the neuron. Greater than 60% of the neuronal population in ...http://www.jneurosci.org/content/5/4/1076
Rabbit polyclonal to SREBP 1. | healthweblognews.info
Ca2+ influx through voltage-activated Ca2+ channels and its feedback regulation by Ca2+-activated K+ (BK) channels is critical in Ca2+-dependent cellular processes including synaptic CB 300919 transmission growth and homeostasis. pre- vs. post-synaptic localization. Antibody staining indicated reduced postsynaptic GluRII receptor subunit density and altered CB 300919 ratio of GluRII A and B subunits in NMJs leading to quantal size reduction. Such larvae correlated with a quantal size reversion to normal in double mutants indicating a role of Ca2+ channels in double mutants the quantal size and quantal content were not drastically different from those of suppressed the and Ca2+ channels differentially contribute to functional and structural aspects of (CaV2) (CaV1) (BK) synaptic homeostasis EJPs mEJPs spontaneous vesicle release larval neuromuscular junction (NMJ) INTRODUCTION Homeostasis CB 300919 of neuronal excitability and synaptic strength has been well ...http://healthweblognews.info/tag/rabbit-polyclonal-to-srebp-1/
last quiz - Questions for Frog Nerve/Muscle Lab 1 The nerve you will dissect(together with the muscle in this week's lab is...
View Notes - last quiz from BIO 206L at University of Texas. Questions for Frog Nerve/Muscle Lab 1. The nerve you will dissect (together with the muscle) in this week's lab is named the _ nerve.https://www.coursehero.com/file/6012548/last-quiz/
M1-M5 mAChR knock-out mice are viable and fertile but display distinct phenotypic changes (for review, see Wess, 2004; Wess et al., 2007). For example, M1−/− mice exhibited a profound increase in locomotor activity, and M2−/− mice displayed impaired regulation of heart rate and deficits in working memory. M3−/− mice were hypophagic and lean, associated with a reduction in food intake. M4−/− mice showed enhanced central dopaminergic transmission, and M5−/− mice displayed reduced cerebral blood flow, associated with deficits in hippocampal long-term potentiation. The present study represents the first systematic analysis of muscarinic signaling at neuromuscular synapses using M1-M5 mAChR knock-out mice. We found that M2 mAChRs are solely expressed in motor neurons and that motor neurons express no other mAChR receptor subtypes. Pharmacological and genetic inhibition of M2 mAChRs caused exclusively presynaptic defects: terminal sprouting and ...http://www.jneurosci.org/content/29/47/14942
Development and pathologies of neuromuscular junctions
Extra-cel-lu-lar matrix pro-teins and adhe-sion pro-teins involved in synapse for-ma-tion, its plas-tic-i-ty and the estab-lish-ment of neu-ronal conec-tiv-i-ty. They also coor-di-nate the pre- and post-sy-nap-tic activ-i-ties and the mat-u-ra-tion of the synapse in the ner-vous sys-tem. To date, how-ev-er their are few datas that high-light mol-e-c-u-lar mecan-isms to which that matri-cials mol-e-cules con-trol the synap-tic devel-op-ment. How Extra-cel-lu-lar matrix pro-teins con-trol the main steps of the synapse's for-ma-tion like the axon-al guid-ance, the for-ma-tion and mat-u-ra-tion of the synap-tic con-tact ? In order to answer this ques-tions, the bio-log-i-cal sys-tem used by our team is the neu-ro-mus-cu-lar junc-tion in ver-te-brates. This synapse is an excel-lent mod-èle for the study of synap-to-ge-n-e-sis and has allowed notable steps for-ward in this domain.. ...https://neurophys.biomedicale.parisdescartes.fr/the-teams/development/
Dr. Jie Liu presents: Functional aging of neuromuscular junction » Institute on Aging » Department of Aging & Geriatric...
UF Health is a collaboration of the University of Florida Health Science Center, Shands hospitals and other health care entities ...http://aging.ufl.edu/seminars/dr-liu-presents-functional-aging-of-neuromuscular-junction/
Neuromuscular transmission and its pharmacological blockade : Part 4: Use of relaxants in paediatric and elderly patients, in...
Neuromuscular transmission and its pharmacological blockade : Part 4: Use of relaxants in paediatric and elderly patients, in obstetrics, and in the intensive care ...http://repository.ubn.ru.nl/handle/2066/24505
The actions of eserine-like compounds upon frog's nerve-muscle preparations, and the blocking of neuromuscular conduction |...
The actions of prostigmine, eserine, and the dimethylcarbamic ester of 8-hydroxymethylquinolinium methylsulphate upon the frog's isolated nervesartorius preparation have been examined by a method developed by Lucas (1911). With Ringer-soaked preparations from frogs kept at 14-18°C for some days before use the minimum interval at which two shocks applied to the nerve could elicit a summated muscular response was about 20% longer than the absolute refractory period of the nerve. Any of the above-mentioned compounds prolonged the minimum interval for a summated response, but caused the time at which an extra interpolated shock began to cut down the response to the final shock to become only a little later. Curarine or atropine reversed the prolongation of minimum interval. By the same method, the actions of the same eserine-like compounds upon preparations which had been treated with Ringer's solution of half the usual calcium content were examined. Either before or after treatment, it was ...http://rspb.royalsocietypublishing.org/content/129/856/392
suga by Marie Altagrace Medastin on Prezi
NMBD molecule (a modified steroid) bound within sugammadex's lipophilic core, is rendered unavailable to bind to the acetylcholine receptor at the neuromuscular junction, bound in a ratio of one sugammadex molecule to one molecule of the ...https://prezi.com/mhkei7g4hiun/suga/
ALZFORUM | NETWORKING FOR A CURE
Simon DJ, Madison JM, Conery AL, Thompson-Peer KL, Soskis M, Ruvkun GB, Kaplan JM, Kim JK. The microRNA miR-1 regulates a MEF-2-dependent retrograde signal at neuromuscular junctions ...http://www.alzforum.org/papers/microrna-mir-1-regulates-mef-2-dependent-retrograde-signal-neuromuscular-junctions
Home Orchard Society Forums - View topic - Grafted Orcas pear
On that sheet I recommend not to instantly remove any leaves below the graft. All leaves help feed the tree, and after a couple 'sets' of leaves you can simply pinch out the terminal growth to keep it from 'taking off.' I've watched some grafts languish as you've described, for some reason (for me) they're usually on a cleft graft of an established tree. Sometimes they just peter out... Other times they'll survive and eventually give you the limb (or tree) you want ...http://www.homeorchardsociety.org/forums/viewtopic.php?f=1&t=717