Spinal and cortical spreading depression enhance spinal cord activity

Gorji, Ali; Zahn, Peter; Pogatzki, Esther M.; Speckmann, E.‐J.

doi:10.1016/j.nbd.2003.09.014

Cited by 33 publications

(20 citation statements)

References 40 publications

(47 reference statements)

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“…The incidence of CSD events as well as their amplitude and propagation speed was not significantly different among treatments. As reported previously (37), a significant difference was found in duration of events, in which pinprick plus KCl evoked CSD events of longer duration than those elicited by cortical pinprick alone or pinprick plus water. Although similarly effective in eliciting CSD events, chemical stimuli such as KCl have an extended duration of action when compared to electrical and mechanical stimulation (38).…”

Section: Discussionsupporting

confidence: 86%

Evaluation of cutaneous allodynia following induction of cortical spreading depression in freely moving rats

et al. 2011

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Background Cortical spreading depression (CSD) is a wave of depolarization followed by depression of bioelectrical activity that slowly propagates through the cortex. CSD is believed to be the underlying mechanism of aura in migraine; however, whether CSD can elicit pain associated with migraine headache is unclear. Methods Awake, freely moving rats were monitored for both CSD events and behavioral responses resulting from dural-cortical pinprick and/or KCl injection to the occipital cortex. Results We observed tactile allodynia of the face and hindpaws, as well as enhanced Fos expression within the trigeminal nucleus caudalis (TNC) following CSD induced by KCl injection into the cortex, but not by pinprick. Application of KCl onto the dura elicited cutaneous allodynia and increased Fos staining in the TNC but did not elicit CSD events. Conclusions These data suggest that sustained activation of trigeminal afferents that may be required to establish cutaneous allodynia may not occur following CSD events in normal animals.

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Section: Discussionsupporting

confidence: 86%

Evaluation of cutaneous allodynia following induction of cortical spreading depression in freely moving rats

et al. 2011

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“…For example, SD enhances excitatory postsynaptic field potentials as well as the repetition rate and amplitude of spontaneous rhythmic potentials 20-90 minutes after its induction; it augments long-term potentiation in human neocortical slices (67,68). SD is followed by hyperexcitability in rat neocortex and spinal cord after transient depression of neuronal activity (69,70). Last but not least, SD can directly precipitate seizure-like electrocorticogram activity, as first demonstrated by Leão (2).…”

Section: Figurementioning

confidence: 87%

Genetic and hormonal factors modulate spreading depression and transient hemiparesis in mouse models of familial hemiplegic migraine type 1

Eikermann-Haerter¹,

Dileköz²,

Kudo³

et al. 2008

J. Clin. Invest.

187

290

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Familial hemiplegic migraine type 1 (FHM1) is an autosomal dominant subtype of migraine with aura that is associated with hemiparesis. As with other types of migraine, it affects women more frequently than men. FHM1 is caused by mutations in the CACNA1A gene, which encodes the α 1A subunit of Ca v 2.1 channels; the R192Q mutation in CACNA1A causes a mild form of FHM1, whereas the S218L mutation causes a severe, often lethal phenotype. Spreading depression (SD), a slowly propagating neuronal and glial cell depolarization that leads to depression of neuronal activity, is the most likely cause of migraine aura. Here, we have shown that transgenic mice expressing R192Q or S218L FHM1 mutations have increased SD frequency and propagation speed; enhanced corticostriatal propagation; and, similar to the human FHM1 phenotype, more severe and prolonged post-SD neurological deficits. The susceptibility to SD and neurological deficits is affected by allele dosage and is higher in S218L than R192Q mutants. Further, female S218L and R192Q mutant mice were more susceptible to SD and neurological deficits than males. This sex difference was abrogated by ovariectomy and senescence and was partially restored by estrogen replacement, implicating ovarian hormones in the observed sex differences in humans with FHM1. These findings demonstrate that genetic and hormonal factors modulate susceptibility to SD and neurological deficits in FHM1 mutant mice, providing a potential mechanism for the phenotypic diversity of human migraine and aura.

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“…This led to the idea that perhaps SD and epilepsy mechanisms would share some common features (Leao, 1944;1972;Guedes and Do Carmo, 1980). Recently, an LTPenhancement after induction of SD has been demonstrated in the rat spinal cord, suggesting a facilitation of synaptic transmission, resulting in increased excitability (Gorji et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Malnutrition and REM-sleep Deprivation Modulate in Rats the Impairment of Spreading Depression by a Single Sub-convulsing Dose of Pilocarpine

Vasconcelos¹,

Oliveira²,

Costa³

et al. 2004

Nutritional Neuroscience

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This study aimed to investigate the effect of a single injection of pilocarpine upon the phenomenon of cortical spreading depression (SD), in adult rats submitted to early malnutrition and/or to REM-sleep deprivation for 72h prior to the SD-recordings. The SD was recorded continuously for 3-4h in 13 well-nourished (W) and 15 early-malnourished (M) adult rats. One to two hours after the beginning of the recording session, a sub-convulsing intraperitoneal (i.p.) injection of pilocarpine (190mg/kg) was applied and its effects on SD were studied during the rest of the recording session. Pilocarpine reduced markedly the ECoG amplitudes in all animals and decreased the SD velocity of propagation in the M-, but not in the W-rats, as compared with the pre-drug values for the same animals. In additional 9W- and 10 M-animals, REM-sleep deprivation was induced during the 72 h preceding the SD-recording session. This condition enhanced the pilocarpine effects on SD in the W-, but not in the M-rats, as compared to the respective non-deprived (ND) groups. The results indicate an important acute cholinergic influence on SD, acting by means of pilocarpine-activated muscarinic receptors. This effect seems to be differentially modulated by sleep deprivation and malnutrition.

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Spinal and cortical spreading depression enhance spinal cord activity

Cited by 33 publications

References 40 publications

Evaluation of cutaneous allodynia following induction of cortical spreading depression in freely moving rats

Evaluation of cutaneous allodynia following induction of cortical spreading depression in freely moving rats

Genetic and hormonal factors modulate spreading depression and transient hemiparesis in mouse models of familial hemiplegic migraine type 1

Malnutrition and REM-sleep Deprivation Modulate in Rats the Impairment of Spreading Depression by a Single Sub-convulsing Dose of Pilocarpine

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