Gain of function in FHM-1 CaV2.1 knock-in mice is related to the shape of the action potential
Familial hemiplegic migraine type-1 FHM-1 is caused by missense mutations in the CACNA1A gene that encodes the α1A pore-forming subunit of CaV2.1 Ca2+ channels. We used knock-in (KI) transgenic mice harboring the pathogenic FHM-1 mutation R192Q to study neurotransmission at the calyx of Held synapse...
Guardado en:
| Autor principal: | |
|---|---|
| Otros Autores: | , , , , , |
| Formato: | Capítulo de libro |
| Lenguaje: | Inglés |
| Publicado: |
2010
|
| Acceso en línea: | Registro en Scopus DOI Handle Registro en la Biblioteca Digital |
| Aporte de: | Registro referencial: Solicitar el recurso aquí |
| LEADER | 12485caa a22012617a 4500 | ||
|---|---|---|---|
| 001 | PAPER-22873 | ||
| 003 | AR-BaUEN | ||
| 005 | 20230518205429.0 | ||
| 008 | 190411s2010 xx ||||fo|||| 00| 0 eng|d | ||
| 024 | 7 | |2 scopus |a 2-s2.0-77954434991 | |
| 024 | 7 | |2 cas |a calcium ion, 14127-61-8; CACNA1A protein, human; Calcium Channels; Neurotransmitter Agents | |
| 040 | |a Scopus |b spa |c AR-BaUEN |d AR-BaUEN | ||
| 030 | |a JONEA | ||
| 100 | 1 | |a Inchauspe, C.G. | |
| 245 | 1 | 0 | |a Gain of function in FHM-1 CaV2.1 knock-in mice is related to the shape of the action potential |
| 260 | |c 2010 | ||
| 270 | 1 | 0 | |m Uchitel, O. D.; Inst. de Fisiología, Biología Molecular Y Neurociencias (LFBM-IFIBYNE), UBA, CONICET, Intendente Guiraldes 2670, C1428BGA Buenos Aires, Argentina; email: odu@fbmc.fcen.uba.ar |
| 506 | |2 openaire |e Política editorial | ||
| 504 | |a Ali, A.B., Bannister, A.P., Thomson, A.M., Robust correlations between action potential duration and the properties of synaptic connections in layer 4 interneurones in neocortical slices from juvenile rats and adult rat and cat (2007) J Physiol, 580, pp. 149-169 | ||
| 504 | |a Aurora, S.K., Wilkinson, F., The brain is hyperexcitable in migraine (2007) Cephalalgia, 27, pp. 1442-1453 | ||
| 504 | |a Barrett, C.F., Cao, Y.Q., Tsien, R.W., Gating deficiency in a familial hemiplegic migraine type 1 mutant P/Q-type calcium channel (2005) J Biol Chem, 280, pp. 24064-24071 | ||
| 504 | |a Bischofberger, J., Geiger, J.R., Jonas, P., Timing and efficacy of Ca2+ channel activation in hippocampal mossy fiber boutons (2002) J Neurosci, 22, pp. 10593-10602 | ||
| 504 | |a Borst, J.G., Sakmann, B., Effect of changes in action potential shape on calcium currents and transmitter release in a calyx-type synapse of the rat auditory brainstem (1999) Philos Trans R Soc Lond B Biol Sci, 354, pp. 347-355 | ||
| 504 | |a Bucurenciu, I., Bischofberger, J., Jonas, P., A small number of open Ca2+ channels trigger transmitter release at a central GABAergic synapse (2010) Nat Neurosci, 13, pp. 19-21 | ||
| 504 | |a Cao, Y.Q., Tsien, R.W., Effects of familial hemiplegic migraine type 1 mutations on neuronal P/Q-type Ca2+ channel activity and inhibitory synaptic transmission (2005) Proc Natl Acad Sci USA, 102, pp. 2590-2595 | ||
| 504 | |a Fedchyshyn, M.J., Wang, L.-Y., Developmental transformation of the release modality at the calyx of held synapse (2005) Journal of Neuroscience, 25 (16), pp. 4131-4140. , DOI 10.1523/JNEUROSCI.0350-05.2005 | ||
| 504 | |a Felmy, F., Neher, E., Schneggenburger, R., Probing the intracellular calcium sensitivity of transmitter release during synaptic facilitation (2003) Neuron, 37 (5), pp. 801-811. , DOI 10.1016/S0896-6273(03)00085-0 | ||
| 504 | |a Ferrari, M.D., Van Amjm, D.M., Frants, R.R., Goadsby, P.J., Migraine as a cerebral ionopathy with impaired central sensory processing (2008) Molecular Neurology, pp. 439-461. , edited by Waxman SG. Oxford, UK: Elsevier | ||
| 504 | |a Forsythe, I.D., Direct patch recording from identified presynaptic terminals mediating glutamatergic EPSCs in the rat CNS, in vitro (1994) J Physiol, 479, pp. 381-387 | ||
| 504 | |a González Inchauspe, C., Forsythe, I.D., Uchitel, O.D., Changes in synaptic transmission properties due to the expression of N-type calcium channels at the calyx of Held synapse of mice lacking P/Q-type calcium channels (2007) J Physiol, 584, pp. 835-851 | ||
| 504 | |a Hans, M., Luvisetto, S., Williams, M.E., Spagnolo, M., Urrutia, A., Tottene, A., Brust, P.F., Pietrobon, D., Functional consequences of mutations in the human α1A calcium channel subunit linked to familial hemiplegic migraine (1999) J Neurosci, 19, pp. 1610-1619 | ||
| 504 | |a Gonzalez Inchauspe, C., Martini, F.J., Forsythe, I.D., Uchitel, O.D., Functional compensation of P/Q by N-type channels blocks short-term plasticity at the calyx of Held presynaptic terminal (2004) Journal of Neuroscience, 24 (46), pp. 10379-10383. , DOI 10.1523/JNEUROSCI.2104-04.2004 | ||
| 504 | |a Iwasaki, S., Momiyama, A., Uchitel, O.D., Takahashi, T., Developmental changes in calcium channel types mediating central synaptic transmission (2000) J Neurosci, 20, pp. 59-65 | ||
| 504 | |a Iwasaki, S., Takahashi, T., Developmental changes in calcium channel types mediating synaptic transmission in rat auditory brainstem (1998) J Physiol, 509, pp. 419-423 | ||
| 504 | |a Kaja, S., Van De Ven, R.C., Broos, L.A., Veldman, H., Van Dijk, J.G., Verschuuren, J.J., Frants, R.R., Plomp, J.J., Gene dosage-dependent transmitter release changes at neuromuscular synapses of CACNA1A R192Q knockin mice are non-progressive and do not lead to morphological changes or muscle weakness (2005) Neuroscience, 135, pp. 81-95 | ||
| 504 | |a Kraus, R.L., Sinnegger, M.J., Glossmann, H., Hering, S., Striessnig, J., Familial hemiplegic migraine mutations change α1A Ca2+ channel kinetics (1998) J Biol Chem, 273, pp. 5586-5590 | ||
| 504 | |a Kraus, R.L., Sinnegger, M.J., Koschak, A., Glossmann, H., Stenirri, S., Carrera, P., Striessnig, J., Three new familial hemiplegic migraine mutants affect P/Q-type Ca(2+) channel kinetics (2000) J Biol Chem, 275, pp. 9239-9243 | ||
| 504 | |a Lauritzen, M., Pathophysiology of the migraine aura: The spreading depression theory (1994) Brain, 117, pp. 199-210 | ||
| 504 | |a Li, L., Bischofberger, J., Jonas, P., Differential gating and recruitment of P/Q-,N-, and R-type Ca 2+ channels in hippocampal mossy fiber boutons (2007) J Neurosci, 27, pp. 13420-13429 | ||
| 504 | |a Muller, M., Felmy, F., Schneggenburger, R., A limited contribution of Ca2+ current facilitation to paired-pulse facilitation of transmitter release at the rat calyx of Held (2008) J Physiol, 586, pp. 5503-5520 | ||
| 504 | |a Shu, Y., Duque, A., Yu, Y., Haider, B., McCormick, D.A., Properties of action-potential initiation in neocortical pyramidal cells: Evidence from whole cell axon recordings (2007) J Neurophysiol, 97, pp. 746-760 | ||
| 504 | |a Takahashi, T., Dynamic aspects of presynaptic calcium currents mediating synaptic transmisión (2005) Cell Calcium, 37, pp. 507-511 | ||
| 504 | |a Tottene, A., Conti, R., Fabbro, A., Vecchia, D., Shapovalova, M., Santello, M., Van Den Maagdenberg, A.M., Pietrobon, D., Enhanced excitatory transmission at cortical synapses as the basis for facilitated spreading depression in Ca(v)2.1 knockin migraine mice (2009) Neuron, 61, pp. 762-773 | ||
| 504 | |a Tottene, A., Fellin, T., Pagnutti, S., Luvisetto, S., Striessnig, J., Fletcher, C., Pietrobon, D., Familial hemiplegic migraine mutations increase Ca2+ influx through single human CaV2.1 channels and decrease maximal Ca V2.1 current density in neurons (2002) Proc Natl Acad Sci USA, 99, pp. 13284-13289 | ||
| 504 | |a Tottene, A., Pivotto, F., Fellin, T., Cesetti, T., Van Den Maagdenberg, A.M.J.M., Pietrobon, D., Specific kinetic alterations of human CaV2.1 calcium channels produced by mutation S218L causing familial hemiplegic migraine and delayed cerebral edema and coma after minor head trauma (2005) J Biol Chem, 280, pp. 17678-17686 | ||
| 504 | |a Van Den Maagdenberg, A.M., Pietrobon, D., Pizzorusso, T., Kaja, S., Broos, L.A., Cesetti, T., Van De Ven, R.C., Ferrari, M.D., A Cacna1a knockin migraine mouse model with increased susceptibility to cortical spreading depression (2004) Neuron, 41, pp. 701-710 | ||
| 504 | |a Weiss, N., Sandoval, A., Felix, R., Van Den Maagdenberg, A.M., De Waard, M., The S218L familial hemiplegic migraine mutation promotes deinhibition of Cav2.1 calcium channels during direct G-protein regulation (2008) Pfluegers, 457, pp. 315-326 | ||
| 504 | |a Yang, Y.M., Wang, L.Y., Amplitude and kinetics of action potential-evoked Ca2+ current and its efficacy in triggering transmitter release at the developing calyx of Held synapse (2006) J Neurosci, 23, pp. 5698-5708 | ||
| 520 | 3 | |a Familial hemiplegic migraine type-1 FHM-1 is caused by missense mutations in the CACNA1A gene that encodes the α1A pore-forming subunit of CaV2.1 Ca2+ channels. We used knock-in (KI) transgenic mice harboring the pathogenic FHM-1 mutation R192Q to study neurotransmission at the calyx of Held synapse and cortical layer 2/3 pyramidal cells (PCs). Using whole cell patch-clamp recordings in brain stem slices, we confirmed that KI CaV2.1 Ca2+ channels activated at more hyperpolarizing potentials. However, calyceal presynaptic calcium currents (IpCa) evoked by presynaptic action potentials (APs) were similar in amplitude, kinetic parameters, and neurotransmitter release. CaV2.1 Ca2+ channels in cortical layer 2/3 PCs from KI mice also showed a negative shift in their activation voltage. PCs had APs with longer durations and smaller amplitudes than the calyx of Held. AP-evoked Ca2+ currents (I Ca) from PCs were larger in KI compared with wild-type (WT) mice. In contrast, when ICa was evoked in PCs by calyx of Held AP waveforms, we observed no amplitude differences between WT and KI mice. In the same way, Ca2+ currents evoked at the presynaptic terminals (IpCa)of the calyx of Held by the AP waveforms of the PCs had larger amplitudes in R192Q KI mice that in WT. These results suggest that longer time courses of pyramidal APs were a key factor for the expression of a synaptic gain of function in the KI mice. In addition, our results indicate that consequences of FHM-1 mutations might vary according to the shape of APs in charge of triggering synaptic transmission (neurons in the calyx of Held vs. excitatory/inhibitory neurons in the cortex), adding to the complexity of the pathophysiology of migraine. Copyright © 2010 The American Physiological Society. |l eng | |
| 593 | |a Inst. de Fisiología, Biología Molecular Y Neurociencias (LFBM-IFIBYNE), UBA, CONICET, Intendente Guiraldes 2670, C1428BGA Buenos Aires, Argentina | ||
| 593 | |a Neurotoxicity at the Synaptic Interface, Medical Research Council Toxicology Unit, University of Leicester, Leicester, United Kingdom | ||
| 593 | |a Department of Neurology, Leiden University Medical Centre, Leiden, Netherlands | ||
| 593 | |a Department of Human Genetics, Leiden University Medical Centre, Leiden, Netherlands | ||
| 690 | 1 | 0 | |a CALCIUM CHANNEL |
| 690 | 1 | 0 | |a CALCIUM ION |
| 690 | 1 | 0 | |a ACTION POTENTIAL |
| 690 | 1 | 0 | |a ARTICLE |
| 690 | 1 | 0 | |a CALCIUM CURRENT |
| 690 | 1 | 0 | |a CONTROLLED STUDY |
| 690 | 1 | 0 | |a EXCITATORY POSTSYNAPTIC POTENTIAL |
| 690 | 1 | 0 | |a FAMILIAL HEMIPLEGIC MIGRAINE |
| 690 | 1 | 0 | |a GENE MUTATION |
| 690 | 1 | 0 | |a MISSENSE MUTATION |
| 690 | 1 | 0 | |a MOUSE |
| 690 | 1 | 0 | |a NEUROTRANSMISSION |
| 690 | 1 | 0 | |a NEUROTRANSMITTER RELEASE |
| 690 | 1 | 0 | |a NONHUMAN |
| 690 | 1 | 0 | |a PATCH CLAMP |
| 690 | 1 | 0 | |a PRIORITY JOURNAL |
| 690 | 1 | 0 | |a PYRAMIDAL NERVE CELL |
| 690 | 1 | 0 | |a SYNAPSE |
| 690 | 1 | 0 | |a SYNAPTIC TRANSMISSION |
| 690 | 1 | 0 | |a SYNAPTOSOME |
| 690 | 1 | 0 | |a TRANSGENIC MOUSE |
| 690 | 1 | 0 | |a WHOLE CELL |
| 690 | 1 | 0 | |a ACTION POTENTIALS |
| 690 | 1 | 0 | |a ANIMALS |
| 690 | 1 | 0 | |a CALCIUM CHANNELS |
| 690 | 1 | 0 | |a CEREBRAL CORTEX |
| 690 | 1 | 0 | |a ELECTRIC STIMULATION |
| 690 | 1 | 0 | |a ELECTROPHYSIOLOGICAL PHENOMENA |
| 690 | 1 | 0 | |a EXCITATORY POSTSYNAPTIC POTENTIALS |
| 690 | 1 | 0 | |a HUMANS |
| 690 | 1 | 0 | |a MICE |
| 690 | 1 | 0 | |a MICE, INBRED C57BL |
| 690 | 1 | 0 | |a MICE, TRANSGENIC |
| 690 | 1 | 0 | |a MIGRAINE DISORDERS |
| 690 | 1 | 0 | |a MIGRAINE WITH AURA |
| 690 | 1 | 0 | |a NEURONS, AFFERENT |
| 690 | 1 | 0 | |a NEUROTRANSMITTER AGENTS |
| 690 | 1 | 0 | |a PATCH-CLAMP TECHNIQUES |
| 690 | 1 | 0 | |a PYRAMIDAL CELLS |
| 690 | 1 | 0 | |a SYNAPSES |
| 690 | 1 | 0 | |a SYNAPTIC TRANSMISSION |
| 700 | 1 | |a Urbano, F.J. | |
| 700 | 1 | |a Di Guilmi, M.N. | |
| 700 | 1 | |a Forsythe, I.D. | |
| 700 | 1 | |a Ferrari, M.D. | |
| 700 | 1 | |a Van Den Maagdenberg, A.M.J.M. | |
| 700 | 1 | |a Uchitel, O.D. | |
| 773 | 0 | |d 2010 |g v. 104 |h pp. 291-299 |k n. 1 |p J. Neurophysiol. |x 00223077 |w (AR-BaUEN)CENRE-5710 |t Journal of Neurophysiology | |
| 856 | 4 | 1 | |u https://www.scopus.com/inward/record.uri?eid=2-s2.0-77954434991&doi=10.1152%2fjn.00034.2010&partnerID=40&md5=2320cca45ab849f07bad0ee81cc95502 |y Registro en Scopus |
| 856 | 4 | 0 | |u https://doi.org/10.1152/jn.00034.2010 |y DOI |
| 856 | 4 | 0 | |u https://hdl.handle.net/20.500.12110/paper_00223077_v104_n1_p291_Inchauspe |y Handle |
| 856 | 4 | 0 | |u https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00223077_v104_n1_p291_Inchauspe |y Registro en la Biblioteca Digital |
| 961 | |a paper_00223077_v104_n1_p291_Inchauspe |b paper |c PE | ||
| 962 | |a info:eu-repo/semantics/article |a info:ar-repo/semantics/artículo |b info:eu-repo/semantics/publishedVersion | ||
| 999 | |c 83826 | ||