from the axon

18 examples (0.04 sec)
  • The neurotransmitters that are released from the axon continue on to stimulate other cells such as other neurons or muscle cells.
  • Axonal transport is also responsible for moving molecules destined for degradation from the axon back to the cell body, where they are broken down by lysosomes.
  • Hypothetically, a synapse strong enough to produce an action potential will trigger the myonuclei directly across from the axon to release synaptotrophins that will strengthen and maintain well-established synapses.
  • The longer distal apical dendrites project from the pyramidal cell body (soma) opposite from the axon.
  • If the sum of the stimuli reaches a certain voltage, known as the threshold potential, depolarization will continue from the axon hillock down the axon.
  • The surge of depolarization traveling from the axon hillock to the axon terminal is known as an action potential.
  • Groups of sodium channels opened by the change in membrane potential strengthen the signal as it travels away from the axon hillock, allowing it to move the length of the axon.
  • Retrograde transport is mediated by dynein, and is used for example to send chemical messages and endocytosis products headed to endolysosomes from the axon back to the cell.
  • Neurotransmitter vesicles containing acetylcholine collide spontaneously with the nerve terminal and release acetylcholine into the neuromuscular junction even without a signal from the axon.
  • Neurotransmitters are released in discrete packets known as quanta from the axon terminal of one neuron to the dendrites of another across a synapse.
  • Also both seem to be mechanically related to a disruption of the delivery of neurofilament to the axon due to a decreased transport of a trophic factor from the axon to the cell body.
  • If a specific input signal is initiated in the dendrites of a neuron, then a hypervariability exists in the number of vesicles released from the axon terminal fiber into the synapse.
  • Liquid shear detaches the nerve terminals from the axon and the plasma membrane surrounding the nerve terminal particle reseals.
  • Presynaptic neurotoxins disrupt neurotransmitter release from the axon terminal.
  • From the axon hillock, an action potential can be generated and propagated down the neuron's axon, causing sodium ion channels in the axon to open as the impulse travels.
  • These vesicles are released from the axon swellings and nerve terminals by exocytosis in response to calcium entry through voltage-gated channels, which occurs when action potentials are propagated down the axons.
  • The signals that initiate post-synaptic differentiation may be neurotransmitters released directly from the axon to the myotube, or they may arise from changes activated in the extracellular matrix of the synaptic cleft.
  • It is hypothesized that anterograde transneuronal degeneration causes the hyperphosphorylation of the tau protein and redistributing those proteins from the axon to the dendrites, which begins the breakdown of routing and sorting mechanisms.