Muller, C. Quantitative proteomics of the Cav2 channel nano-environments in the mammalian brain. USA , — Neef, J. Dolphin, A. Jay, S. De Jongh, K. Subunits of purified calcium channels. Davies, A. Qin, N. Dahimene, S. Cell Rep. Canti, C. Cassidy, J. Wang, Y. Neuron 93 , — e Fell, B. Geisler, S. Kadurin, I. Letts, V. Tomita, S. Functional studies and distribution define a family of transmembrane AMPA receptor regulatory proteins.
Cell Biol. Meyer, J. Cell Reports 29 , 22—33 Waithe, D. Altier, C. Page, K. Nieto-Rostro, M. USA , E—E Ferron, L. Macabuag, N. Alternative splicing in CaV2. Bauer, C. Doughty, J. Bonifacino, J. Adaptor proteins involved in polarized sorting. Koike, S. SNAREs define targeting specificity of trafficking vesicles by combinatorial interaction with tethering factors.
Binotti, B. Functions of Rab proteins at presynaptic sites. Cells 5 , E7 Britt, D. Mechanisms of polarized organelle distribution in neurons. Cell Neurosci. Jacobson, C. A change in the selective translocation of the kinesin-1 motor domain marks the initial specification of the axon.
Neuron 49 , — Jenkins, B. A novel split kinesin assay identifies motor proteins that interact with distinct vesicle populations. Zhai, R. Assembling the presynaptic active zone: a characterization of an active zone precursor vesicle. Neuron 29 , — Bell, M. Dynamics of nascent and active zone ultrastructure as synapses enlarge during long-term potentiation in mature hippocampus. Schneider, R. Mobility of calcium channels in the presynaptic membrane. Neuron 86 , — Regus-Leidig, H.
Early steps in the assembly of photoreceptor ribbon synapses in the mouse retina: the involvement of precursor spheres. Dittman, J. The control of release probability at nerve terminals. Kaeser, P.
Molecular mechanisms for synchronous, asynchronous, and spontaneous neurotransmitter release. Wheeler, D. Takahashi, T. Different types of calcium channels mediate central synaptic transmission. Iwasaki, S. Developmental changes in calcium channel types mediating central synaptic transmission.
Stephens, G. The Ca v 2. Hefft, S. Asynchronous GABA release generates long-lasting inhibition at a hippocampal interneuron-principal neuron synapse. Li, L. Dietrich, D. Functional specialization of presynaptic Cav2. Neuron 39 , — Breustedt, J. Ermolyuk, Y. T-type channel-mediated neurotransmitter release. Huang, Z. Kopp-Scheinpflug, C. Modulation and control of synaptic transmission across the MNTB. Nakamura, Y. Neuron 85 , — Fedchyshyn, M. Developmental transformation of the release modality at the calyx of Held synapse.
Bornschein, G. Ishikawa, T. Developmental changes in calcium channel types mediating synaptic transmission in rat auditory brainstem. Eggermann, E. Kusch, V. Yang, Y.
Neuron 67 , — Fekete, A. Underpinning heterogeneity in synaptic transmission by presynaptic ensembles of distinct morphological modules. Ricoy, U. Distinct roles for Cav2.
Matthews, G. The diverse roles of ribbon synapses in sensory neurotransmission. Snellman, J. Acute destruction of the synaptic ribbon reveals a role for the ribbon in vesicle priming. Platzer, J. Cell , 89—97 Mansergh, F. Mutation of the calcium channel gene Cacna1f disrupts calcium signaling, synaptic transmission and cellular organization in mouse retina.
Liu, X. Dysregulation of Ca v 1. Channels 7 , — Google Scholar. Katiyar, R. Ball, S. Ben-Johny, M. Calmodulin regulation calmodulation of voltage-gated calcium channels. Yang, P. Haeseleer, F. Yang, T. PLoS One 11 , e Cui, G. Schrauwen, I. A mutation in CABP2, expressed in cochlear hair cells, causes autosomal-recessive hearing impairment.
Picher, M. Shen, Y. Alternative splicing of the Ca v 1. Gebhart, M. Modulation of Cav1. Singh, A. Wahl-Schott, C. Switching off calcium-dependent inactivation in L-type calcium channels by an autoinhibitory domain. Williams, B. Splicing of an automodulatory domain in Cav1.
Tan, G. Alternative splicing at C terminus of Ca V 1. Characterization of C-terminal splice variants of Cav1. Han, Y. Neuron 69 , — Biederer, T. Transcellular nanoalignment of synaptic function. Neuron 96 , — Cell , — Kiyonaka, S. Hirano, M. Hibino, H. Neuron 34 , — Acuna, C. Neuron 91 , — Jung, S. Krinner, S. RIM-binding protein 2 promotes a large number of CaV1. Lubbert, M. A novel region in the CaV2. Lu, J. Liu, C. Practice: Neuronal synapses questions.
Signal propagation: The movement of signals between neurons. Neurotransmitter release. Types of neurotransmitters. Types of neurotransmitter receptors. Neurotransmitter removal. Next lesson. Current timeTotal duration Google Classroom Facebook Twitter.
Otto Loewi's Experiment Neurotransmitter Criteria Neuroscientists have set up a few guidelines or criteria to prove that a chemical is really a neurotransmitter.
The chemical must be produced within a neuron. The chemical must be found within a neuron. When a neuron is stimulated depolarized , a neuron must release the chemical. When a chemical is released, it must act on a post-synaptic receptor and cause a biological effect. After a chemical is released, it must be inactivated. Inactivation can be through a reuptake mechanism or by an enzyme that stops the action of the chemical.
If the chemical is applied on the post-synaptic membrane, it should have the same effect as when it is released by a neuron. Neurotransmitter Types There are many types of chemicals that act as neurotransmitter substances. Transport and Release of Neurotransmitters Neurotransmitters are made in the cell body of the neuron and then transported down the axon to the axon terminal.
Inactivation of Neurotransmitters The action of neurotransmitters can be stopped by four different mechanisms: 1. Diffusion: the neurotransmitter drifts away, out of the synaptic cleft where it can no longer act on a receptor. Diffusion 2. Enzymatic degradation deactivation : a specific enzyme changes the structure of the neurotransmitter so it is not recognized by the receptor. For example, acetylcholinesterase is the enzyme that breaks acetylcholine into choline and acetate.
Enzymatic degradation 3. Glial cells: astrocytes remove neurotransmitters from the synaptic cleft. Glial Cells Astrocyte Image courtesy of Biodidac 4. Reuptake: the whole neurotransmitter molecule is taken back into the axon terminal that released it.
This is a common way the action of norepinephrine, dopamine and serotonin is stopped Reuptake Try it! Do you like interactive word search puzzles?
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