Moskowitz, M. A. & Macfarlane, R. Neurovascular and molecular mechanisms in migraine headaches. Cerebrovasc. Brain Metab. Rev.5, 159–177 (1993). CASPubMed Google Scholar
May, A. & Goadsby, P. J. The trigeminovascular system in humans: pathophysiologic implications for primary headache syndromes of the neural influences on the cerebral circulation. J. Cereb. Blood Flow Metab.19, 115–127 (1999). ArticleCASPubMed Google Scholar
Goadsby, P. J., Lipton, R. B. & Ferrari, M. D. Migraine — current understanding and treatment. N. Engl. J. Med.346, 257–270 (2002). ArticleCASPubMed Google Scholar
Knight, Y. E. & Goadsby, P. J. The periaqueductal grey matter modulates trigeminovascular input: a role in migraine? Neuroscience106, 793–800 (2001). ArticleCASPubMed Google Scholar
Goadsby, P. J., Edvinsson, L. & Ekman, R. Vasoactive peptide release in the extracerebral circulation of humans during migraine headache. Ann. Neurol.28, 183–187 (1990). ArticleCASPubMed Google Scholar
Sarchielli, P., Alberti, A., Codini, M., Floridi, A. & Gallai, V. Nitric oxide metabolites, prostaglandins and trigeminal vasoactive peptides in internal jugular vein blood during spontaneous migraine attacks. Cephalalgia20, 907–918 (2000). ArticleCASPubMed Google Scholar
Goadsby, P. J. & Edvinsson, L. The trigeminovascular system and migraine: studies characterizing cerebrovascular and neuropeptide changes seen in humans and cats. Ann. Neurol.33, 48–56 (1993). ArticleCASPubMed Google Scholar
Olesen, J., Larsen, B. & Lauritzen, M. Focal hyperemia followed by spreading oligemia and impaired activation of rCBF in classic migraine. Ann. Neurol.9, 344–352 (1981). ArticleCASPubMed Google Scholar
Limmroth, V. et al. Changes in cerebral blood flow velocity after treatment with sumatriptan or placebo and implications for the pathophysiology of migraine. J. Neurol. Sci.138, 60–65 (1996). ArticleCASPubMed Google Scholar
Kruuse, C., Thomsen, L. L., Birk, S. & Olesen, J. Migraine can be induced by sildenafil without changes in middle cerebral artery diameter. Brain126, 241–247 (2003). This observation lent important support to findings from imaging studies and clinical trials with 5-HT1F-selective triptans, indicating that initial vasodilation of extracerebral arteries is not required to trigger migraine attacks. It also indicated that vasodilation might not be as important for the induction of migraine attacks by other vasodilators as previously thought. ArticlePubMed Google Scholar
Leao, A. A. P. Spreading depression of activity in the cerebral cortex. J. Neurophysiol.7, 359–390 (1944). Article Google Scholar
Lauritzen, M. Pathophysiology of the migraine aura. The spreading depression theory. Brain117, 199–210 (1994). ArticlePubMed Google Scholar
Mayevsky, A. et al. Cortical spreading depression recorded from the human brain using a multiparametric monitoring system. Brain Res.740, 268–274 (1996). ArticleCASPubMed Google Scholar
Strong, A. J. et al. Spreading and synchronous depressions of cortical activity in acutely injured human brain. Stroke33, 2738–2743 (2002). ArticlePubMed Google Scholar
Yokota, C. et al. Unique profile of spreading depression in a primate model. J. Cereb. Blood Flow Metab.22, 835–842 (2002). ArticlePubMed Google Scholar
Hadjikhani, N. et al. Mechanisms of migraine aura revealed by functional MRI in human visual cortex. Proc. Natl Acad. Sci. USA98, 4687–4692 (2001). The most thorough investigation of changes in neuronal activity during migraine aura. Signal changes showed a number of characteristics that were consistent with CSD during migriane aura in humans. ArticleCASPubMedPubMed Central Google Scholar
Welch, K. M., Cao, Y., Aurora, S., Wiggins, G. & Vikingstad, E. M. MRI of the occipital cortex, red nucleus, and substantia nigra during visual aura of migraine. Neurology51, 1465–1469 (1998). ArticleCASPubMed Google Scholar
Bowyer, S. M., Aurora, K. S., Moran, J. E., Tepley, N. & Welch, K. M. Magnetoencephalographic fields from patients with spontaneous and induced migraine aura. Ann. Neurol.50, 582–587 (2001). This study provided the important demonstration that CSD-typical changes of direct current neuromagnetic field measurements in animals also occur during spontaneous and visually triggered migraine auras in migraineurs. ArticleCASPubMed Google Scholar
Bowyer, S. M. et al. Analysis of MEG signals of spreading cortical depression with propagation constrained to a rectangular cortical strip. II. Gyrencephalic swine model. Brain Res.843, 79–86 (1999). ArticleCASPubMed Google Scholar
Somjen, G. G. Mechanisms of spreading depression and hypoxic spreading depression- like depolarization. Physiol. Rev.81, 1065–1096 (2001). ArticleCASPubMed Google Scholar
Strassman, A. M., Raymond, S. A. & Burstein, R. Sensitization of meningeal sensory neurons and the origin of headaches. Nature384, 560–564 (1996). ArticleCASPubMed Google Scholar
Wei, E. P., Moskowitz, M. A., Boccalini, P. & Kontos, H. A. Calcitonin gene-related peptide mediates nitroglycerin and sodium nitroprusside-induced vasodilation in feline cerebral arterioles. Circ. Res.70, 1313–1319 (1992). ArticleCASPubMed Google Scholar
Bolay, H. et al. Intrinsic brain activity triggers trigeminal meningeal afferents in a migraine model. Nature Med.8, 136–142 (2002). This study convincingly showed that electrically and pinprick-induced CSD can activate the trigeminovascular afferents and can induce the pathophysiological features of migraine attacks. ArticleCASPubMed Google Scholar
Ebersberger, A., Schaible, H. G., Averbeck, B. & Richter, F. Is there a correlation between spreading depression, neurogenic inflammation, and nociception that might cause migraine headache? Ann. Neurol.49, 7–13 (2001). ArticleCASPubMed Google Scholar
Lambert, G. A., Michalicek, J., Storer, R. J. & Zagami, A. S. Effect of cortical spreading depression on activity of trigeminovascular sensory neurons. Cephalalgia19, 631–638 (1999). ArticleCASPubMed Google Scholar
Woods, R. P., Iacoboni, M. & Mazziotta, J. C. Brief report: bilateral spreading cerebral hypoperfusion during spontaneous migraine headache. N. Engl. J. Med.331, 1689–1692 (1994). ArticleCASPubMed Google Scholar
Bednarczyk, E. M., Remler, B., Weikart, C., Nelson, A. D. & Reed, R. C. Global cerebral blood flow, blood volume, and oxygen metabolism in patients with migraine headache. Neurology50, 1736–1740 (1998). ArticleCASPubMed Google Scholar
Sanchez del Rio, M. et al. Perfusion weighted imaging during migraine: spontaneous visual aura and headache. Cephalalgia19, 701–707 (1999). ArticleCASPubMed Google Scholar
Cao, Y., Aurora, S. K., Nagesh, V., Patel, S. C. & Welch, K. M. Functional MRI-BOLD of brainstem structures during visually triggered migraine. Neurology59, 72–78 (2002). Using BOLD-fMRI, this study showed activation of the red nucleus and substantia nigra during visually triggered migraine and hyperaemia in the occipital cortex, independently of whether the headache was preceded by visual symptoms. ArticleCASPubMed Google Scholar
Goadsby, P. J. Migraine, aura, and cortical spreading depression: why are we still talking about it? Ann. Neurol.49, 4–6 (2001). ArticleCASPubMed Google Scholar
Raskin, N. H., Hosobuchi, Y. & Lamb, S. Headache may arise from perturbation of brain. Headache27, 416–420 (1987). ArticleCASPubMed Google Scholar
Weiller, C. et al. Brain stem activation in spontaneous human migraine attacks. Nature Med.1, 658–660 (1995). First report showing increased blood flow in the brainstem during spontaneous migraine attacks. This finding promoted the hypothesis of a brainstem generator of migraine. ArticleCASPubMed Google Scholar
Bahra, A., Matharu, M. S., Buchel, C., Frackowiak, R. S. & Goadsby, P. J. Brainstem activation specific to migraine headache. Lancet357, 1016–1017 (2001). ArticleCASPubMed Google Scholar
Lima, D. & Almeida, A. The medullary dorsal reticular nucleus as a pronociceptive centre of the pain control system. Prog. Neurobiol.66, 81–108 (2002). ArticlePubMed Google Scholar
May, A., Bahra, A., Buchel, C., Frackowiak, R. S. & Goadsby, P. J. Hypothalamic activation in cluster headache attacks. Lancet352, 275–278 (1998). ArticleCASPubMed Google Scholar
May, A. et al. Experimental cranial pain elicited by capsaicin: a PET study. Pain74, 61–66 (1998). ArticleCASPubMed Google Scholar
Strassman, A., Mason, P., Moskowitz, M. & Maciewicz, R. Response of brainstem trigeminal neurons to electrical stimulation of the dura. Brain Res.379, 242–250 (1986). ArticleCASPubMed Google Scholar
Chronicle, E. P. & Mulleners, W. M. Visual system dysfunction in migraine: a review of clinical and psychophysical findings. Cephalalgia16, 525–535 (1996). ArticleCASPubMed Google Scholar
Brighina, F., Piazza, A., Daniele, O. & Fierro, B. Modulation of visual cortical excitability in migraine with aura: effects of 1 Hz repetitive transcranial magnetic stimulation. Exp. Brain. Res.145, 177–181 (2002). ArticlePubMed Google Scholar
Battelli, L., Black, K. R. & Wray, S. H. Transcranial magnetic stimulation of visual area V5 in migraine. Neurology58, 1066–1069 (2002). ArticlePubMed Google Scholar
Giffin, N. J. & Kaube, H. The electrophysiology of migraine. Curr. Opin. Neurol.15, 303–309 (2002). ArticlePubMed Google Scholar
Afra, J., Mascia, A., Gerard, P., Maertens de Noordhout, A. & Schoenen, J. Interictal cortical excitability in migraine: a study using transcranial magnetic stimulation of motor and visual cortices. Ann. Neuro.44, 209–215 (1998). ArticleCAS Google Scholar
Werhahn, K. J. et al. Motor cortex excitability in patients with migraine with aura and hemiplegic migraine. Cephalalgia20, 45–50 (2000). ArticleCASPubMed Google Scholar
Bocker, K. B., Timsit-Berthier, M., Schoenen, J. & Brunia, C. H. Contingent negative variation in migraine. Headache30, 604–609 (1990). ArticleCASPubMed Google Scholar
Kropp, P., Siniatchkin, M., Stephani, U. & Gerber, W. D. Migraine — evidence for a disturbance of cerebral maturation in man? Neurosci. Lett.276, 181–184 (1999). ArticleCASPubMed Google Scholar
Besken, E., Pothmann, R. & Sartory, G. Contingent negative variation in childhood migraine. Cephalalgia13, 42–43 (1993). ArticleCASPubMed Google Scholar
Bender, S. et al. Lack of age-dependent development of the contingent negative variation (CNV) in migraine children? Cephalalgia22, 132–136 (2002). ArticleCASPubMed Google Scholar
Kropp, P. & Gerber, W. D. Is increased amplitude of contingent negative variation in migraine due to cortical hyperactivity or to reduced habituation? Cephalalgia13, 37–41 (1993). ArticleCASPubMed Google Scholar
Wang, W. & Schoenen, J. Interictal potentiation of passive 'oddball' auditory event-related potentials in migraine. Cephalalgia18, 261–265 (1998). ArticleCASPubMed Google Scholar
Ozkul, Y. & Uckardes, A. Median nerve somatosensory evoked potentials in migraine. Eur. J. Neurol.9, 227–232 (2002). ArticleCASPubMed Google Scholar
Wilson, D. A. Habituation of odor responses in the rat anterior piriform cortex. J. Neurophysiol.79, 1425–1440 (1998). ArticleCASPubMed Google Scholar
Wang, W., Wang, Y. H., Fu, X. M., Sun, Z. M. & Schoenen, J. Auditory evoked potentials and multiple personality measures in migraine and post-traumatic headaches. Pain79, 235–242 (1999). ArticlePubMed Google Scholar
Hegerl, U., Gallinat, J. & Juckel, G. Event-related potentials. Do they reflect central serotonergic neurotransmission and do they predict clinical response to serotonin agonists? J. Affect. Disord.62, 93–100 (2001). ArticleCASPubMed Google Scholar
Evers, S., Quibeldey, F., Grotemeyer, K. H., Suhr, B. & Husstedt, I. W. Dynamic changes of cognitive habituation and serotonin metabolism during the migraine interval. Cephalalgia19, 485–491 (1999). ArticleCASPubMed Google Scholar
Siniatchkin, M., Kropp, P., Gerber, W. D. & Stephani, U. Migraine in childhood — are periodically occurring migraine attacks related to dynamic changes of cortical information processing? Neurosci. Lett.279, 1–4 (2000). ArticleCASPubMed Google Scholar
Siniatchkin, M., Gerber, W. D., Kropp, P. & Vein, A. How the brain anticipates an attack: a study of neurophysiological periodicity in migraine. Funct. Neurol.14, 69–77 (1999). CASPubMed Google Scholar
Bohotin, V. et al. Effects of repetitive transcranial magnetic stimulation on visual evoked potentials in migraine. Brain125, 912–922 (2002). ArticleCASPubMed Google Scholar
Gu, Q. Neuromodulatory transmitter systems in the cortex and their role in cortical plasticity. Neuroscience111, 815–835 (2002). ArticleCASPubMed Google Scholar
Gartside, S. E. et al. Neurochemical and electrophysiological studies on the functional significance of burst firing in serotonergic neurons. Neuroscience98, 295–300 (2000). ArticleCASPubMed Google Scholar
Ferrari, M. D. & Saxena, P. R. On serotonin and migraine: a clinical and pharmacological review. Cephalalgia13, 151–165 (1993). ArticleCASPubMed Google Scholar
Ferrari, M. D., Odink, J., Bos, K. D., Malessy, M. J. & Bruyn, G. W. Neuroexcitatory plasma amino acids are elevated in migraine. Neurology40, 1582–1586 (1990). ArticleCASPubMed Google Scholar
Welch, K. M. & Ramadan, N. M. Mitochondria, magnesium and migraine. J. Neurol. Sci.134, 9–14 (1995). ArticleCASPubMed Google Scholar
Boska, M. D., Welch, K. M., Barker, P. B., Nelson, J. A. & Schultz, L. Contrasts in cortical magnesium, phospholipid and energy metabolism between migraine syndromes. Neurology58, 1227–1233 (2002). ArticleCASPubMed Google Scholar
Parsons, A. A. Recent advances in mechanisms of spreading depression. Curr. Opin. Neurol.11, 227–231 (1998). ArticleCASPubMed Google Scholar
Arakawa, S., Nakamura, S., Kawashima, N., Nishiike, S. & Fujii, Y. Antidromic burst activity of locus coeruleus neurons during cortical spreading depression. Neuroscience78, 1147–1158 (1997). ArticleCASPubMed Google Scholar
Kruger, H., Luhmann, H. J. & Heinemann, U. Repetitive spreading depression causes selective suppression of GABAergic function. Neuroreport7, 2733–2736 (1996). ArticleCASPubMed Google Scholar
May, A. et al. Retinal plasma extravasation in animals but not in humans: implications for the pathophysiology of migraine. Brain121, 1231–1237 (1998). ArticlePubMed Google Scholar
Cumberbatch, M. J., Williamson, D. J., Mason, G. S., Hill, R. G. & Hargreaves, R. J. Dural vasodilation causes a sensitization of rat caudal trigeminal neurones in vivo that is blocked by a 5-HT1B/1D agonist. Br. J. Pharmacol.126, 1478–1486 (1999). ArticleCASPubMedPubMed Central Google Scholar
Lassen, L. H. et al. CGRP may play a causative role in migraine. Cephalalgia22, 54–61 (2002). ArticleCASPubMed Google Scholar
Williamson, D. J., Hill, R. G., Shepheard, S. L. & Hargreaves, R. J. The anti-migraine 5-HT1B/1D agonist rizatriptan inhibits neurogenic dural vasodilation in anaesthetized guinea-pigs. Br. J. Pharmacol.133, 1029–1034 (2001). ArticleCASPubMedPubMed Central Google Scholar
Goldstein, D. J. et al. Selective serotonin 1F (5-HT1F) receptor agonist LY334370 for acute migraine: a randomised controlled trial. Lancet358, 1230–1234 (2001). Although further development of LY334370 was halted, this clinical trial provided good evidence for the efficacy of 5-HT1F-selective antagonists as anti-migraine drugs, and supported the concept that anti-migraine efficacy does not require vasoconstrictory actions. ArticleCASPubMed Google Scholar
Shepheard, S. et al. Possible antimigraine mechanisms of action of the 5HT1F receptor agonist LY334370. Cephalalgia19, 851–858 (1999). ArticleCASPubMed Google Scholar
Kaube, H. et al. Acute migraine headache: possible sensitization of neurons in the spinal trigeminal nucleus? Neurology58, 1234–1238 (2002). ArticleCASPubMed Google Scholar
Burstein, R., Yarnitsky, D., Goor-Aryeh, I., Ransil, B. J. & Bajwa, Z. H. An association between migraine and cutaneous allodynia. Ann. Neurol.47, 614–624 (2000). ArticleCASPubMed Google Scholar
Burstein, R., Yamamura, H., Malick, A. & Strassman, A. M. Chemical stimulation of the intracranial dura induces enhanced responses to facial stimulation in brain stem trigeminal neurons. J. Neurophysiol.79, 964–982 (1998). References 22, 77 and 78 are key papers for our understanding of pain sensitization in migraine. The data provide evidence for sensitization of TNC neurons in humans during migraine attacks and in rats after chemical stimulation of the dura, and are consistent with the idea that initiation, but not maintenance, of central sensitization depends on incoming impulses from nocieptors. ArticleCASPubMed Google Scholar
Burstein, R., Cutrer, M. F. & Yarnitsky, D. The development of cutaneous allodynia during a migraine attack clinical evidence for the sequential recruitment of spinal and supraspinal nociceptive neurons in migraine. Brain123, 1703–1709 (2000). ArticlePubMed Google Scholar
Woolf, C. J. & Salter, M. W. Neuronal plasticity: increasing the gain in pain. Science288, 1765–1769 (2000). ArticleCASPubMed Google Scholar
Sandrini, G. et al. Electrophysiological evidence for trigeminal neuron sensitization in patients with migraine. Neurosci. Lett.317, 135–138 (2002). ArticleCASPubMed Google Scholar
Grosser, K. et al. Olfactory and trigeminal event-related potentials in migraine. Cephalalgia20, 621–631 (2000). ArticleCASPubMed Google Scholar
Thomsen, L. L. & Olesen, J. Nitric oxide in primary headaches. Curr. Opin. Neurol.14, 315–321 (2001). ArticleCASPubMed Google Scholar
Akerman, S., Williamson, D. J., Kaube, H. & Goadsby, P. J. Nitric oxide synthase inhibitors can antagonize neurogenic and calcitonin gene-related peptide induced dilation of dural meningeal vessels. Br. J. Pharmacol.137, 62–68 (2002). ArticleCASPubMedPubMed Central Google Scholar
Pardutz, A., Krizbai, I., Multon, S., Vecsei, L. & Schoenen, J. Systemic nitroglycerin increases nNOS levels in rat trigeminal nucleus caudalis. Neuroreport11, 3071–3075 (2000). ArticleCASPubMed Google Scholar
Hoskin, K. L., Bulmer, D. C. & Goadsby, P. J. Fos expression in the trigeminocervical complex of the cat after stimulation of the superior sagittal sinus is reduced by L-NAME. Neurosci. Lett.266, 173–176 (1999). ArticleCASPubMed Google Scholar
Lambert, G. A., Donaldson, C., Boers, P. M. & Zagami, A. S. Activation of trigeminovascular neurons by glyceryl trinitrate. Brain Res.887, 203–210 (2000). ArticleCASPubMed Google Scholar
Jones, M. G. et al. Nitric oxide potentiates response of trigeminal neurones to dural or facial stimulation in the rat. Cephalalgia21, 643–655 (2001). ArticleCASPubMed Google Scholar
Thomsen, L. L. et al. A population-based study of familial hemiplegic migraine suggests revised diagnostic criteria. Brain125, 1379–1391 (2002). ArticleCASPubMed Google Scholar
Ducros, A. et al. The clinical spectrum of familial hemiplegic migraine associated with mutations in a neuronal calcium channel. N. Engl. J. Med.345, 17–24 (2001). The authors identified several new FHM mutations and correlated the mutations with clinical parameters. The data strongly indicated that pure FHM and FHM with cerebellar signs are associated with distinct mutations inCACNA1A. ArticleCASPubMed Google Scholar
Ophoff, R. A. et al. Familial hemiplegic migraine and episodic ataxia type-2 are caused by mutations in the calcium channel gene CACNL1A4. Cell87, 543–552 (1996). First report showing that missense mutations inCACNA1Acause FHM. Mutations leading to more pronounced structural abnormalities (such as truncations) were identified as the cause of episodic ataxia type 2, an autosomal dominant disease. ArticleCASPubMed Google Scholar
Kors, E. E., van den Maagdenberg, A. M., Plomp, J. J., Frants, R. R. & Ferrari, M. D. Calcium channel mutations and migraine. Curr. Opin. Neurol.15, 311–316 (2002). ArticlePubMed Google Scholar
Pietrobon, D. Calcium channels and channelopathies of the central nervous system. Mol. Neurobiol.25, 31–50 (2002). ArticleCASPubMed Google Scholar
De Fusco, M. et al. Haploinsufficiency of ATP1A2 encoding the Na+/K+ pump α2 subunit gene is responsible for familial hemiplegic migraine type 2. Nature Genet.33, 192–196 (2003). This paper reported the long-awaited identification of the gene in chromosome 1q23 linked to FHM. It was identified asATP1A2, encoding the Na+/K+ ATPase α2-subunit. Functional studies indicate a loss of function of a single allele as the relevant pathophysiological mechanism. ArticleCASPubMed Google Scholar
Terwindt, G. M. et al. Involvement of the CACNA1A gene containing region on 19p13 in migraine with and without aura. Neurology56, 1028–1032 (2001). ArticleCASPubMed Google Scholar
Nyholt, D. R., Lea, R. A., Goadsby, P. J., Brimage, P. J. & Griffiths, L. R. Familial typical migraine: linkage to chromosome 19p13 and evidence for genetic heterogeneity. Neurology50, 1428–1432 (1998). ArticleCASPubMed Google Scholar
Jones, K. W. et al. Migraine with aura susceptibility locus on chromosome 19p13 is distinct from the familial hemiplegic migraine locus. Genomics78, 150–154 (2001). ArticleCASPubMed Google Scholar
Westenbroek, R. E. et al. Immunochemical identification and subcellular distribution of the α1A subunits of brain calcium channels. J. Neurosci.15, 6403–6418 (1995). ArticleCASPubMedPubMed Central Google Scholar
Mintz, I. M., Sabatini, B. L. & Regehr, W. G. Calcium control of transmitter release at a cerebellar synapse. Neuron15, 675–688 (1995). ArticleCASPubMed Google Scholar
Wu, L. G., Westenbroek, R. E., Borst, J. G., Catterall, W. A. & Sakmann, B. Calcium channel types with distinct presynaptic localization couple differentially to transmitter release in single calyx-type synapses. J. Neurosci.19, 726–736 (1999). ArticleCASPubMedPubMed Central Google Scholar
Qian, J. & Noebels, J. L. Presynaptic Ca2+ channels and neurotransmitter release at the terminal of a mouse cortical neuron. J. Neurosci.21, 3721–3728 (2001). ArticleCASPubMedPubMed Central Google Scholar
Bayliss, D. A., Li, Y. -W. & Talley, E. M. Effects of serotonin on caudal raphe neurons: inhibition of N- and P/Q-type calcium channels and the afterhyperpolarization. J. Neurophysiol. 1362–1374 (1997).
Pineda, J. C., Waters, R. S. & Foehring, R. C. Specificity in the interaction of HVA Ca2+ channel types with Ca2+- dependent AHPs and firing behavior in neocortical pyramidal neurons. J. Neurophysiol.79, 2522–2534 (1998). ArticleCASPubMed Google Scholar
Mori, Y. et al. Reduced voltage sensitivity of activation of P/Q-type Ca2+ channels is associated with the ataxic mouse mutation Rolling Nagoya (tgrol). J. Neurosci.20, 5654–5662 (2000). ArticleCASPubMedPubMed Central Google Scholar
Sutton, K. G., McRory, J. E., Guthrie, H., Murphy, T. H. & Snutch, T. P. P/Q-type calcium channels mediate the activity-dependent feedback of syntaxin-1A. Nature401, 800–804 (1999). ArticleCASPubMed Google Scholar
Volsen, S. G. et al. The expression of neuronal voltage-dependent calcium channels in human cerebellum. Brain Res. Mol. Brain Res.34, 271–282 (1995). ArticleCASPubMed Google Scholar
Mintz, I. M., Adams, M. E. & Bean, B. P. P-type calcium channels in rat central and peripheral neurons. Neuron9, 85–95 (1992). ArticleCASPubMed Google Scholar
Randall, A. & Tsien, R. W. Pharmacological dissection of multiple types of calcium channels currents in rat cerebellar granule neurons. J. Neurosci.15, 2995–3012 (1995). ArticleCASPubMedPubMed Central Google Scholar
Tottene, A., Moretti, A. & Pietrobon, D. Functional diversity of P-type and R-type calcium channels in rat cerebellar neurons. J. Neurosci.16, 6353–6363 (1996). ArticleCASPubMedPubMed Central Google Scholar
Iwasaki, S., Momiyama, A., Uchitel, O. D. & Takahashi, T. Developmental changes in calcium channel types mediating central synaptic transmission. J. Neurosci.20, 59–65 (2000). ArticleCASPubMedPubMed Central Google Scholar
Stephens, G. J., Morris, N. P., Fyffe, R. E. & Robertson, B. The Cav2.1/α1A (P/Q-type) voltage-dependent calcium channel mediates inhibitory neurotransmission onto mouse cerebellar Purkinje cells. Eur. J. Neurosci.13, 1902–1912 (2001). ArticleCASPubMed Google Scholar
Matsushita, K. et al. Bidirectional alterations in cerebellar synaptic transmission of tottering and rolling Ca2+ channel mutant mice. J. Neurosci.22, 4388–4398 (2002). ArticleCASPubMedPubMed Central Google Scholar
Eilers, J., Plant, T. & Konnerth, A. Localized calcium signalling and neuronal integration in cerebellar Purkinje neurones. Cell Calcium20, 215–226 (1996). ArticleCASPubMed Google Scholar
Fletcher, C. F. et al. Dystonia and cerebellar atrophy in Cacna1a null mice lacking P/Q calcium channel activity. FASEB J.15, 1288–1290 (2001). ArticleCASPubMed Google Scholar
Jun, K. et al. Ablation of P/Q-type Ca2+ channel currents, altered synaptic transmission, and progressive ataxia in mice lacking the α1A-subunit. Proc. Natl Acad. Sci. USA96, 15245–15250 (1999). ArticleCASPubMedPubMed Central Google Scholar
Zhuchenko, O. et al. Autosomal dominant cerebellar ataxia (SCA6) associated with small polyglutamine expansions in the α1A-voltage-dependent calcium channel. Nature Genet.15, 62–69 (1997). ArticleCASPubMed Google Scholar
Timmermann, D. B., Westenbroek, R. E., Schousboe, A. & Catterall, W. A. Distribution of high-voltage-activated calcium channels in cultured γ-aminobutyric acidergic neurons from mouse cerebral cortex. J. Neurosci. Res.67, 48–61 (2002). ArticleCASPubMed Google Scholar
Lorenzon, N. M. & Foehring, R. C. Characterization of pharmacologically identified voltage-gated calcium channel currents in acutely isolated rat neocortical neurons. I. Adult neurons. J. Neurophysiol.73, 1430–1442 (1995). ArticleCASPubMed Google Scholar
Koester, H. J. & Sakmann, B. Calcium dynamics associated with action potentials in single nerve terminals of pyramidal cells in layer 2/3 of the young rat neocortex. J. Physiol. (Lond.)529, 625–646 (2000). ArticleCAS Google Scholar
Turner, T. J., Adams, M. E. & Dunlap, K. Calcium channels coupled to glutamate release identified by ω-Aga-IVA. Science258, 310–313 (1992). ArticleCASPubMed Google Scholar
Wakamori, M. et al. Single tottering mutations responsible for the neuropathic phenotype of the P-type calcium channel. J. Biol. Chem.273, 34857–34867 (1998). ArticleCASPubMed Google Scholar
Dove, L. S., Abbott, L. C. & Griffith, W. H. Whole-cell and single-channel analysis of P-type calcium currents in cerebellar Purkinje cells of leaner mutant mice. J. Neurosci.18, 7687–7699 (1998). ArticleCASPubMedPubMed Central Google Scholar
Ayata, C., Shimizu-Sasamata, M., Lo, E. H., Noebels, J. L. & Moskowitz, M. A. Impaired neurotransmitter release and elevated threshold for cortical spreading depression in mice with mutations in the α1A subunit of P/Q type calcium channels. Neuroscience95, 639–645 (2000). This study exploited naturally occuring Cav2.1α1mutations inleanermouse mutants to show that P/Q-type channels contribute to the initiation and propagation of CSD in the neocortex. A defect in KCl-induced transmitter release and a striking elevation of CSD threshold in both types of mice were identified. ArticleCASPubMed Google Scholar
Richter, F., Ebersberger, A. & Schaible, H. G. Blockade of voltage-gated calcium channels in rat inhibits repetitive cortical spreading depression. Neurosci. Lett.334, 123–126 (2002). ArticleCASPubMed Google Scholar
Hillmann, D. et al. Localization of P-type calcium channels in the central nervous system. Proc. Natl Acad. Sci. USA88, 7076–7080 (1991). Article Google Scholar
Craig, P. J. et al. Distribution of the voltage-dependent calcium channel α1A subunit throughout the mature rat brain and its relationship to neurotransmitter pathways. J. Comp. Neurol.397, 251–267 (1998). ArticleCASPubMed Google Scholar
Kim, C. J., Rhee, J. S. & Akaike, N. Modulation of high-voltage activated Ca2+ channels in the rat periaqueductal gray neurons by μ-type opioid agonist. J. Neurophysiol.77, 1418–1424 (1997). ArticleCASPubMed Google Scholar
Connor, M. & Christie, M. J. Modulation of Ca2+ channel currents of acutely dissociated rat periaqueductal grey neurons. J. Physiol. (Lond.)509, 47–58 (1998). ArticleCAS Google Scholar
Chieng, B. & Bekkers, J. M. GABAB, opioid and α2 receptor inhibition of calcium channels in acutely-dissociated locus coeruleus neurones. Br. J. Pharmacol.127, 1533–1538 (1999). ArticleCASPubMedPubMed Central Google Scholar
Ishibashi, H., Rhee, J. S. & Akaike, N. Regional difference of high voltage-activated Ca2+ channels in rat CNS neurones. Neuroreport6, 1621–1624 (1995). ArticleCASPubMed Google Scholar
Knight, Y. E., Bartsch, T., Kaube, H. & Goadsby, P. J. P/Q-type calcium-channel blockade in the periaqueductal gray facilitates trigeminal nociception: a functional genetic link for migraine? J. Neurosci.22, RC213 (2002). The first study to investigate P/Q-type channel function on descending antinociceptive activity. By recording electrical responses of TNC neurons to electrical, dural stimulation, it was shown that the agatoxin IVA-induced P/Q-channel block in the ventrolateral PAG facilitated responses of second-order neurons. This indicated a role of P/Q-type channels in the PAG for trigeminal antinociception. ArticlePubMedPubMed Central Google Scholar
Borgland, S. L., Connor, M. & Christie, M. J. Nociceptin inhibits calcium channel currents in a subpopulation of small nociceptive trigeminal ganglion neurons in mouse. J. Physiol. (Lond.)536, 35–47 (2001). ArticleCAS Google Scholar
Hong, K. W., Kim, C. D., Rhim, B. Y. & Lee, W. S. Effect of ω-conotoxin GVIA and ω-agatoxin IVA on the capsaicin-sensitive calcitonin gene-related peptide release and autoregulatory vasodilation in rat pial arteries. J. Cereb. Blood Flow Metab.19, 53–60 (1999). ArticleCASPubMed Google Scholar
Asakura, K. et al. α-Eudesmol, a P/Q-type Ca2+ channel blocker, inhibits neurogenic vasodilation and extravasation following electrical stimulation of trigeminal ganglion. Brain Res.873, 94–101 (2000). ArticleCASPubMed Google Scholar
Westenbroek, R. E., Hoskins, L. & Catterall, W. A. Localization of Ca2+ channel subtypes on rat spinal motor neurons, interneurons, and nerve terminals. J. Neurosci.18, 6319–6330 (1998). ArticleCASPubMedPubMed Central Google Scholar
Vanegas, H. & Schaible, H. Effects of antagonists to high-threshold calcium channels upon spinal mechanisms of pain, hyperalgesia and allodynia. Pain85, 9–18 (2000). ArticleCASPubMed Google Scholar
Takahashi, T. & Momiyama, A. Different types of calcium channels mediate central synaptic transmission. Nature366, 156–158 (1993). ArticleCASPubMed Google Scholar
Ogasawara, M., Kurihara, T., Hu, Q. & Tanabe, T. Characterization of acute somatosensory pain transmission in P/Q-type Ca2+ channel mutant mice, leaner. FEBS Lett.508, 181–6 (2001). ArticleCASPubMed Google Scholar
Kors, E. E. et al. Delayed cerebral edema and fatal coma after minor head trauma: role of the CACNA1A calcium channel subunit gene and relationship with familial hemiplegic migraine. Ann. Neurol.49, 753–760 (2001). ArticleCASPubMed Google Scholar
Kraus, R. L., Sinnegger, M. J., Glossmann, H., Hering, S. & Striessnig, J. Familial hemiplegic migraine mutations change α1A calcium channel kinetics. J. Biol. Chem.273, 5586–5590 (1998). ArticleCASPubMed Google Scholar
Hans, M. et al. Functional consequences of mutations in the human α1A calcium channel subunit linked to familial hemiplegic migraine. J. Neurosci.19, 1610–1619 (1999). ArticleCASPubMedPubMed Central Google Scholar
Kraus, R. L. et al. Three new familial hemiplegic migraine mutants affect P/Q-type Ca2+ channel kinetics. J. Biol. Chem.275, 9239–9243 (2000). ArticleCASPubMed Google Scholar
Tottene, A. et al. Familial hemiplegic migraine mutations increase Ca2+ influx through single human Cav2.1 channels and decrease maximal Cav2.1 current density in neurons. Proc. Natl Acad. Sci. USA99, 13284–13289 (2002). This paper reported the expression of FHM mutant Cav2.1α1constructs in Cav2.1α1deficient neurons, and disclosed two functional effects that are common to all analysed FHM mutations: increase of single-channel Ca2+influx over a broad range of negative voltages and decrease of channel density. These findings provide a unifying hypothesis for the pathophysiology of FHM. ArticleCASPubMedPubMed Central Google Scholar
Meinrenken, C. J., Borst, J. G. & Sakmann, B. Calcium secretion coupling at calyx of Held governed by nonuniform channel-vesicle topography. J. Neurosci.22, 1648–1667 (2002). ArticleCASPubMedPubMed Central Google Scholar
Borst, J. G. & Sakmann, B. Calcium current during a single action potential in a large presynaptic terminal of the rat brainstem. J. Physiol. (Lond.)506, 143–157 (1998). ArticleCAS Google Scholar
Juhaszova, M. & Blaustein, M. P. Na+ pump low and high ouabain affinity α subunit isoforms are differently distributed in cells. Proc. Natl Acad. Sci. USA94, 1800–1805 (1997). ArticleCASPubMedPubMed Central Google Scholar
Snow, V., Weiss, K., Wall, E. M. & Mottur-Pilson, C. Pharmacologic management of acute attacks of migraine and prevention of migraine headache. Ann. Intern. Med.137, 840–849 (2002). ArticleCASPubMed Google Scholar
Goadsby, P. J., Hoskin, K. L., Storer, R. J., Edvinsson, L. & Connor, H. E. Adenosine A1 receptor agonists inhibit trigeminovascular nociceptive transmission. Brain125, 1392–1401 (2002). ArticleCASPubMed Google Scholar
Penn, R. D. & Paice, J. A. Adverse effects associated with the intrathecal administration of ziconotide. Pain85, 291–296 (2000). ArticleCASPubMed Google Scholar
Sang, C. N. et al. AMPA/kainate antagonist LY293558 reduces capsaicin-evoked hyperalgesia but not pain in normal skin in humans. Anesthesiology89, 1060–1067 (1998). ArticleCASPubMed Google Scholar
Gilron, I. et al. Effects of the 2-amino-3-hydroxy-5-methyl-4-isoxazole-proprionic acid/kainate antagonist LY293558 on spontaneous and evoked postoperative pain. Clin. Pharmacol. Ther.68, 320–327 (2000). ArticleCASPubMed Google Scholar
Ramadan, N. M. Acute treatments: future developments. Curr. Med. Res. Opin.17, Suppl. S81–86 (2001). ArticlePubMed Google Scholar
Le Grand, B., Panissie, A., Perez, M., Pauwels, P. J. & John, G. W. Zolmitriptan stimulates a Ca2+-dependent K+ current in C6 glioma cells stably expressing recombinant human 5-HT1B receptors. Eur. J. Pharmacol.397, 297–302 (2000). ArticleCASPubMed Google Scholar
John, G. W. et al. F-11356, a novel 5-hydroxytryptamine (5-HT) derivative with potent, selective, and unique high intrinsic activity at 5-HT1B/1D receptors in models relevant to migraine. J. Pharmacol. Exp. Ther.290, 83–95 (1999). CASPubMed Google Scholar
Diamond, S., Freitag, F., Phillips, S. B., Bernstein, J. E. & Saper, J. R. Intranasal civamide for the acute treatment of migraine headache. Cephalalgia20, 597–602 (2000). ArticleCASPubMed Google Scholar
Mulleners, W. M., Chronicle, E. P., Vredeveld, J. W. & Koehler, P. J. Visual cortex excitability in migraine before and after valproate prophylaxis: a pilot study using TMS. Eur. J. Neurol.9, 35–40 (2002). ArticleCASPubMed Google Scholar
Kaube, H., Herzog, J., Kaufer, T., Dichgans, M. & Diener, H. C. Aura in some patients with familial hemiplegic migraine can be stopped by intranasal ketamine. Neurology55, 139–141 (2000). ArticleCASPubMed Google Scholar
Bradley, D. P. et al. Diffusion-weighted MRI used to detect in vivo modulation of cortical spreading depression: comparison of sumatriptan and tonabersat. Exp. Neurol.172, 342–353 (2001). ArticleCASPubMed Google Scholar