What kind of stimulus travels from the axon terminal to the sarcoma
Fritzsch, B. Fast axonal diffusion of molecular weight dextran amines. Methods 50, 95— Furth, D. An interactive framework for whole-brain maps at cellular resolution. Furukawa, H. Double innervation occurs in the facial mimetic muscles after facial-hypoglossal end-to-side neural repair: rat model for neural supercharge concept.
Furuta, T. In vivo transduction of central neurons using recombinant Sindbis virus: golgi-like labeling of dendrites and axons with membrane-targeted fluorescent proteins. Gannett, L. Google Scholar. Gao, G. Clades of Adeno-associated viruses are widely disseminated in human tissues.
Garner, J. Differential anterograde transport of HSV type 1 viral strains in the murine optic pathway. Geraghty, R. Entry of alphaherpesviruses mediated by poliovirus receptor-related protein 1 and poliovirus receptor. Gerfen, C. An anterograde neuroanatomical tracing method that shows the detailed morphology of neurons, their axons and terminals: immunohistochemical localization of an axonally transported plant lectin, Phaseolus vulgaris leucoagglutinin PHA-L.
Geue, L. Genetic characterisation of attenuated SAD rabies virus strains used for oral vaccination of wildlife. Vaccine 26, — Gimlich, R. Improved fluorescent compounds for tracing cell lineage. Glees, P. Terminal degeneration within the central nervous system as studied by a new silver method. Glover, J. Retrograde and anterograde axonal tracing with fluorescent dextrans in the embryonic nervous system.
Fluorescent dextran amines used as axonal tracers in the nervous system of chicken embryo. Methods 18, — Gofflot, F. Characterization and validation of cre-driver mouse lines.
Mouse Biol. Goshgarian, H. The pattern and extent of retrograde transsynaptic transport of WGA-Alexa in the phrenic motor system is dependent upon the site of application. Methods , — Grafstein, B. Transport of protein by goldfish optic nerve fibers. Grimm, D. Small but increasingly mighty: latest advances in AAV vector research, design, and evolution. Gross, C. Squire, Oxford: Academic Press , — Guillery, R. Observations of synaptic structures: origins of the neuron doctrine and its current status.
B Biol. Hagmann, P. Henriksen, S. A simple generative model of the mouse mesoscale connectome. Herculano-Houzel, S. The human brain in numbers: a linearly scaled-up primate brain. Hilbert, M. Science , 60— Hirschberg, S. Functional dichotomy in spinal-vs prefrontal-projecting locus coeruleus modules splits descending noradrenergic analgesia from ascending aversion and anxiety in rats.
Hoff, E. Central nerve terminals in the mammalian spinal cord and their examination by experimental degeneration. Howorth, P. Retrograde viral vector-mediated inhibition of pontospinal noradrenergic neurons causes hyperalgesia in rats.
Hwang, D. A high-efficiency synthetic promoter that drives transgene expression selectively in noradrenergic neurons. Jakobsson, J. Targeted transgene expression in rat brain using lentiviral vectors. Jansen, A. Central command neurons of the sympathetic nervous system: basis of the fight-or-flight response. Jia, F. Pseudo-typed semliki forest virus delivers EGFP into neurons. Jonas, E. Could a neuroscientist understand a microprocessor?
PLoS Comput. Junyent, F. Targeting neuronal and glial cell types with synthetic promoter AAVs in mice, non-human primates and humans. Kanaan, N. Nucleic Acids 8, — Kato, S. A lentiviral strategy for highly efficient retrograde gene transfer by pseudotyping with fusion envelope glycoprotein. Katz, L. Fluorescent latex microspheres as a retrograde neuronal marker for in vivo and in vitro studies of visual cortex.
Green fluorescent latex microspheres: a new retrograde tracer. Neuroscience 34, — Kelly, R. Rabies as a transneuronal tracer of circuits in the central nervous system.
Methods , 63— Kim, E. Improved monosynaptic neural circuit tracing using engineered rabies virus glycoproteins. Cell Rep. Kim, J. Methods 9, 96— Circuit-specific co-infection of the neurons in the rat central nervous system with two pseudorabies virus recombinants.
Current concepts in neuroanatomical tracing. Kobiler, O. Herpesviruses carrying a Brainbow cassette reveal replication and expression of limited numbers of incoming genomes. Korim, W. Orexinergic activation of medullary premotor neurons modulates the adrenal sympathoexcitation to hypothalamic glucoprivation.
Diabetes Metab. Kotterman, M. Engineering adeno-associated viruses for clinical gene therapy. Kristensson, K. Retrograde axonal transport of protein. Kshettry, V. The management of cranial injuries in antiquity and beyond. Focus E8. Kuo, H. Retrograde transfer of replication deficient recombinant adenovirus vector in the central nervous system for tracing studies.
Kuypers, H. Double retrograde neuronal labeling through divergent axon collaterals, using two fluorescent tracers with the same excitation wavelength which label different features of the cell. Labetoulle, M. Neuronal pathways for the propagation of herpes simplex virus type 1 from one retina to the other in a murine model. Lanciego, J. A half century of experimental neuroanatomical tracing. Lander, E. Initial impact of the sequencing of the human genome.
Larsen, D. Retrograde tracing with recombinant rabies virus reveals correlations between projection targets and dendritic architecture in layer 5 of mouse barrel cortex. LaVail, J. Retrograde axonal transport in the central nervous system. Lentz, T. Is the acetylcholine receptor a rabies virus receptor? Lerner, T. Intact-Brain analyses reveal distinct information carried by SNc dopamine subcircuits.
Communication in neural circuits: tools. Levy, S. WGA-Alexa conjugates for axonal tracing. Li, L. Visualizing the distribution of synapses from individual neurons in the mouse brain. PLoS One 5:e Li, X. Serotonin receptor 2c-expressing cells in the ventral CA1 control attention via innervation of the Edinger-Westphal nucleus.
Lichtman, J. Liu, Y. Tracing inputs to inhibitory or excitatory neurons of mouse and cat visual cortex with a targeted rabies virus. Llinas, R. The contribution of santiago ramon y cajal to functional neuroscience.
Lo, L. A Cre-dependent, anterograde transsynaptic viral tracer for mapping output pathways of genetically marked neurons. Neuron 72, — Lopez-Munoz, F. Neuron theory, the cornerstone of neuroscience, on the centenary of the Nobel Prize award to Santiago Ramon y Cajal. Lundberg, C. Applications of lentiviral vectors for biology and gene therapy of neurological disorders. Lunde, A.
Molecular profiling defines evolutionarily conserved transcription factor signatures of major vestibulospinal neuron groups. Luo, L. Genetic dissection of neural circuits. Genetic dissection of neural circuits: a decade of progress.
Neuron 98, — Luppi, P. Peptidergic hypothalamic afferents to the cat nucleus raphe pallidus as revealed by a double immunostaining technique using unconjugated cholera toxin as a retrograde tracer. Lykken, E. Recent progress and considerations for AAV gene therapies targeting the central nervous system. Marshel, J. Targeting single neuronal networks for gene expression and cell labeling In Vivo. Neuron 67, — Martin, X.
Neuronal and transneuronal tracing in the trigeminal system of the rat using the herpes virus suis. Matsubayashi, Y. Fluorescent double-labeling with carbocyanine neuronal tracing and immunohistochemistry using a cholesterol-specific detergent digitonin.
Methods , 71— Matsuyama, M. McGovern, A. Transneural tracing of airways-related sensory circuitry using herpes simplex virus 1, strain H Neuroscience , — Anterograde neuronal circuit tracing using a genetically modified herpes simplex virus expressing EGFP. Evidence for multiple sensory circuits in the brain arising from the respiratory system: an anterograde viral tract tracing study in rodents. Distinct brainstem and forebrain circuits receiving tracheal sensory neuron inputs revealed using a novel conditional anterograde transsynaptic viral tracing system.
McPherson, D. Optical imaging of neuronal activity in tissue labeled by retrograde transport of Calcium Green Dextran. Mebatsion, T. Budding of rabies virus particles in the absence of the spike glycoprotein. Cell 84, — Menuet, C. Excessive respiratory modulation of blood pressure triggers hypertension. Cell Metab. Mikula, S. Progress towards mammalian whole-brain cellular connectomics. Mizoguchi, A. Nectin: an adhesion molecule involved in formation of synapses.
Cell Biol. Moghaddam, N. Murlidharan, G. Biology of adeno-associated viral vectors in the central nervous system. A neural signal is the electrical trigger for calcium release from the sarcoplasmic reticulum into the sarcoplasm. Each skeletal muscle fiber is controlled by a motor neuron, which conducts signals from the brain or spinal cord to the muscle. The area of the sarcolemma on the muscle fiber that interacts with the neuron is called the motor-end plate.
A small space called the synaptic cleft separates the synaptic terminal from the motor-end plate. Because neuron axons do not directly contact the motor-end plate, communication occurs between nerves and muscles through neurotransmitters. Neuron action potentials cause the release of neurotransmitters from the synaptic terminal into the synaptic cleft, where they can then diffuse across the synaptic cleft and bind to a receptor molecule on the motor end plate.
And then they're able to bond to the troponin right here, and do everything we talked about in the last video. So what we care about is, just how does it know when to dump its calcium ions into the rest of the cell? This is the inside of the cell. And so this area is what the actin filaments and the myosin heads and all of the rest, and the troponin, and the tropomyosin-- they're all exposed to the environment that is over here.
So you can imagine-- I could just draw it here just to make it clear. I'm drawing it very abstract. We'll see more of the structure in a future video. This is a very abstract drawing, but I think this'll give you a sense of what's going on. So let's say this neuron-- and we'll call this a motor neuron-- it's signaling for a muscle contraction.
So first of all, we know how signals travel across neurons, especially across axons with an action potential. We could have a sodium channel right here.
It's voltage gated so you have a little bit of a positive voltage there. That tells this voltage gated sodium channel to open up. So it opens up and allows even more of the sodium to flow in. That makes it a little bit more positive here. So then that triggers the next voltage gated channel to open up-- and so it keeps traveling down the membrane of the axon-- and eventually, when you get enough of a positive threshold, voltage gated calcium channels open up.
This is all a review of what we learned in the neuron videos. So eventually, when it gets positive enough close to these calcium ion channels, they allow the calcium ions to flow in. And the calcium ions flow in and they bond to those special proteins near the synaptic membrane or the presynaptic membrane right there.
These are calcium ions. They bond to proteins that were docking vesicles. Remember, vesicles were just these membranes around neurotransmitters. When the calcium binds to those proteins, it allows exocytosis to occur. It allows the membrane of the vesicles to merge with the membrane of the actual neuron and the contents get dumped out. This is all review from the neuron videos.
I explained it in much more detail in those videos, but you have-- all of these neurotransmitters get dumped out. And we were talking about the synapse between a neuron and a muscle cell.
The neurotransmitter here is acetylcholine. But just like what would happen at a dendrite, the acetylcholine binds to receptors on the sarcolemma or the membrane of the muscle cell and that opens sodium channels on the muscle cell. So the muscle cell also has a a voltage gradient across its membrane, just like a neuron does.
So when this guy gets some acetylcholene, it allows sodium to flow inside the muscle cell. They do this by controlling the movement of charged particles, called ions, across their membranes to create electrical currents. This is achieved by opening and closing specialized proteins in the membrane called ion channels. Although the currents generated by ions moving through these channel proteins are very small, they form the basis of both neural signaling and muscle contraction.
Both neurons and skeletal muscle cells are electrically excitable, meaning that they are able to generate action potentials. An action potential is a special type of electrical signal that can travel along a cell membrane as a wave. This allows a signal to be transmitted quickly and faithfully over long distances. The myosin then pulls the actin filaments toward the center, shortening the muscle fiber.
In skeletal muscle, this sequence begins with signals from the somatic motor division of the nervous system. The motor neurons that tell the skeletal muscle fibers to contract originate in the spinal cord, with a smaller number located in the brainstem for activation of skeletal muscles of the face, head, and neck. These neurons have long processes, called axons, which are specialized to transmit action potentials long distances— in this case, all the way from the spinal cord to the muscle itself which may be up to three feet away.
The axons of multiple neurons bundle together to form nerves, like wires bundled together in a cable. Signaling begins when a neuronal action potential travels along the axon of a motor neuron, and then along the individual branches to terminate at the NMJ. At the NMJ, the axon terminal releases a chemical messenger, or neurotransmitter , called acetylcholine ACh.
The ACh molecules diffuse across a minute space called the synaptic cleft and bind to ACh receptors located within the motor end-plate of the sarcolemma on the other side of the synapse. Once ACh binds, a channel in the ACh receptor opens and positively charged ions can pass through into the muscle fiber, causing it to depolarize , meaning that the membrane potential of the muscle fiber becomes less negative closer to zero.
As the membrane depolarizes, another set of ion channels called voltage-gated sodium channels are triggered to open. Things happen very quickly in the world of excitable membranes just think about how quickly you can snap your fingers as soon as you decide to do it. Immediately following depolarization of the membrane, it repolarizes, re-establishing the negative membrane potential. Meanwhile, the ACh in the synaptic cleft is degraded by the enzyme acetylcholinesterase AChE so that the ACh cannot rebind to a receptor and reopen its channel, which would cause unwanted extended muscle excitation and contraction.
Propagation of an action potential along the sarcolemma is the excitation portion of excitation-contraction coupling. The arrangement of a T-tubule with the membranes of SR on either side is called a triad Figure. The triad surrounds the cylindrical structure called a myofibril , which contains actin and myosin. Skeletal muscles contain connective tissue, blood vessels, and nerves.
There are three layers of connective tissue: epimysium, perimysium, and endomysium. Skeletal muscle fibers are organized into groups called fascicles.
Blood vessels and nerves enter the connective tissue and branch in the cell. Muscles attach to bones directly or through tendons or aponeuroses.
Skeletal muscles maintain posture, stabilize bones and joints, control internal movement, and generate heat.
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