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1 ortex (possibly as a consequence of cortical spreading depression).
2 round 30-fold smaller than that of a wave of spreading depression).
3 thermia may be due to a reduced incidence of spreading depression.
4 e feedback in the generation of seizures and spreading depression.
5 time scale of 3 min may have been caused by spreading depression.
6 rea of the brain surface is known to trigger spreading depression.
7 l as during pathological conditions, such as spreading depression.
8 f neurons that showed activation by cortical spreading depression.
9 er loss of function, and higher incidence of spreading depression.
10 h as an increased susceptibility to cortical spreading depression.
11 op severe and prolonged motor deficits after spreading depression.
12 he trigemino-vascular system and in cortical spreading depression.
13 neuronal excitability that leads to cortical spreading depression.
14 ding hearing, vision, epilepsy, and cortical spreading depression.
15 centration of glutamine (2-5 mM) resulted in spreading-depression.
16 Minocycline had no effect on astrogliosis or spreading depression, a wave of ionic transients thought
17 rst time it has been shown that the cortical spreading depression activated the trigeminovascular sys
19 neurovascular dysfunction and evoke cortical spreading depression, an event that is widely thought to
20 cance to migraine of events such as cortical spreading depression and activation of the trigeminovasc
21 ical hypoperfusion responses during cortical spreading depression and alpha-chloralose anaesthesia.
23 e for the occurrence of spontaneous cortical spreading depression and peri-infarct depolarizations in
24 ited increased susceptibility to subcortical spreading depression and reverberating spreading depress
25 flurane anesthesia showed that both cortical spreading depression and terminal anoxic depolarization
26 te MCA occlusion is caused by either or both spreading depression and transient ischemic depolarizati
28 le of glial K buffering against seizures and spreading depression, and provides novel insights into a
29 n other slices, APC was emulated by inducing spreading depression (as determined by a negative DC shi
30 ological ceiling that separates seizure from spreading depression, as well as predicted a second ceil
31 se gain-of-function effects lead to cortical spreading depression, aura, and potentially migraine.
32 ntral) trigeminovascular neurons by cortical spreading depression, but not their activation from the
33 s are the first to demonstrate that cortical spreading depression can be blocked in vivo using single
37 However, the relationship between cortical spreading depression (CSD) and headache has not been ful
38 ow (rCBF) changes that occur during cortical spreading depression (CSD) are considered to be an exper
39 , although, animal models highlight cortical spreading depression (CSD) as a potential candidate.
40 ing has confirmed the importance of cortical spreading depression (CSD) as the pathophysiological mec
41 t and characterize complex waves of cortical spreading depression (CSD) evoked with KCL placed upon t
47 tensive care and were classified as cortical spreading depression (CSD) if they took place in spontan
60 d, if so, the threshold for evoking cortical spreading depression (CSD), a process sharing characteri
61 icient to cause infarcts, triggered cortical spreading depression (CSD), a propagating slow depolariz
62 on exhibit increased propensity for cortical spreading depression (CSD), a propagating wave of neurog
64 mice, we show that a single wave of cortical spreading depression (CSD), an animal model of migraine
65 nnels and are highly susceptible to cortical spreading depression (CSD), the electrophysiologic event
68 ring somatosensory stimulations and cortical spreading depression (CSD), the putative mechanism of th
69 n damage and ischemia often trigger cortical spreading depression (CSD), which aggravates brain damag
70 this study was to determine whether cortical spreading depression (CSD)--an event believed to underli
71 us and evoked activity in naive and cortical spreading depression (CSD)-sensitized trigeminovascular
73 s (with [n=7] or without [n=7] HH), cortical spreading depressions (CSD) were elicited to ascertain t
75 ecovery rate for [K+]o, and interval between spreading depression episodes were measured before and a
78 d the effect of fremanezumab on the cortical spreading depression-evoked activation of mechanosensiti
81 velength optical intrinsic imaging, cortical spreading depression has been shown to have a triphasic
83 The pathological phenomena of seizures and spreading depression have long been considered separate
86 and headache by demonstrating that cortical spreading depression, implicated in migraine visual aura
87 cerebral ischaemia, and blocking of cortical spreading depression improved stroke outcome in these mi
89 ound, global cerebral ischemia, and cortical spreading depression in C57BL6 mice; 1 day after probe d
91 signals evoked by stimulation, seizures and spreading depression in intact brain differ from those o
96 ity in reducing the total number of cortical spreading depressions induced by potassium chloride.
97 mechanism for the susceptibility of cortical spreading depression initiation in migraine disorders.
104 larizations (PIDs) are seemingly spontaneous spreading depression-like waves that negatively impact t
106 Vascular/metabolic uncoupling with cortical spreading depression may have important clinical consequ
107 strated significant activity in the cortical spreading depression model of migraine as we reported pr
108 atine for 3 h failed to prevent hyperthermic spreading depression occurrence; and (2) intracellular A
111 tibility to ischemic depolarizations akin to spreading depression predisposes migraineurs to infarcti
113 ing, and c-fos immunohistochemistry to trace spreading depression propagation into subcortical struct
114 e showed that unlike the wild type, cortical spreading depression readily propagated into subcortical
115 t astrocytes normally extrude calcium during spreading depression, resulting in rapid recovery of the
116 Although intercellular Ca2+ waves resemble spreading depression (SD) and occur in hippocampal organ
117 spontaneous, recurring episodes of cortical spreading depression (SD) as early as 20 min post-inject
127 stigated the role of spontaneous and induced spreading depression (SD) on the evolution of focal isch
130 ant, on fluid shifts, cerebral perfusion and spreading depression (SD) using diffusion- (DWI) and per
138 ous transition between epileptic seizure and spreading depression states as the cell swells and contr
139 ssium or hypoxia induced), mixed seizure and spreading depression states, and the terminal anoxic "wa
140 mone levels in these mice modulated cortical spreading depression susceptibility in much the same way
141 smooth muscle Notch 3 mutations to enhanced spreading depression susceptibility, implicating the neu
142 mutation are highly susceptible to cortical spreading depression, the electrophysiological surrogate
145 We tested the susceptibility of cortical spreading depression, the experimental correlate of migr
147 at cortices, when administered post-cortical spreading depression, transcranial magnetic stimulation
148 unction, one during the propagating cortical spreading depression wave and a second much longer phase
149 t current shift associated with the cortical spreading depression wave was accompanied by marked arte
150 concentration increased during the cortical spreading depression wave, but recovered and remained at
151 After recovery from the initial cortical spreading depression wave, we observed a second phase of
154 h mechanical and chemically-induced cortical spreading depression when administered immediately post-
155 euronal activities, from spikes to seizures, spreading depression (whether high potassium or hypoxia
156 ion and c-fos expression are associated with spreading depression, which is believed to contribute to
157 ity, and enhanced susceptibility to cortical spreading depression, which is the electrophysiological
158 TAC-Red-stained brain cortex in mice during spreading depression, with velocity 4.4 +/- 0.5 mm/min,
159 and transient ischaemia can trigger cortical spreading depression without an enduring tissue signatur
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