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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 ding hearing, vision, epilepsy, and cortical spreading depression.
4 thermia may be due to a reduced incidence of spreading depression.
5 e feedback in the generation of seizures and spreading depression.
6 time scale of 3 min may have been caused by spreading depression.
7 rea of the brain surface is known to trigger spreading depression.
8 l as during pathological conditions, such as spreading depression.
9 f neurons that showed activation by cortical spreading depression.
10 er loss of function, and higher incidence of spreading depression.
11 h as an increased susceptibility to cortical spreading depression.
12 op severe and prolonged motor deficits after spreading depression.
13 he trigemino-vascular system and in cortical spreading depression.
14 neuronal excitability that leads to 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
20 neurovascular dysfunction and evoke cortical spreading depression, an event that is widely thought to
21 cance to migraine of events such as cortical spreading depression and activation of the trigeminovasc
22 ical hypoperfusion responses during cortical spreading depression and alpha-chloralose anaesthesia.
25 e for the occurrence of spontaneous cortical spreading depression and peri-infarct depolarizations in
26 ited increased susceptibility to subcortical spreading depression and reverberating spreading depress
27 flurane anesthesia showed that both cortical spreading depression and terminal anoxic depolarization
28 te MCA occlusion is caused by either or both spreading depression and transient ischemic depolarizati
30 le of glial K buffering against seizures and spreading depression, and provides novel insights into a
31 n other slices, APC was emulated by inducing spreading depression (as determined by a negative DC shi
32 ological ceiling that separates seizure from spreading depression, as well as predicted a second ceil
33 se gain-of-function effects lead to cortical spreading depression, aura, and potentially migraine.
34 ntral) trigeminovascular neurons by cortical spreading depression, but not their activation from the
35 s are the first to demonstrate that cortical spreading depression can be blocked in vivo using single
39 However, the relationship between cortical spreading depression (CSD) and headache has not been ful
40 ow (rCBF) changes that occur during cortical spreading depression (CSD) are considered to be an exper
41 , although, animal models highlight cortical spreading depression (CSD) as a potential candidate.
42 ing has confirmed the importance of cortical spreading depression (CSD) as the pathophysiological mec
44 t and characterize complex waves of cortical spreading depression (CSD) evoked with KCL placed upon t
50 tensive care and were classified as cortical spreading depression (CSD) if they took place in spontan
51 nnelrhodopsin to trigger and record cortical spreading depression (CSD) in freely behaving subjects.
67 to be the key factor for generating cortical spreading depression (CSD), a pathological mechanism of
69 d, if so, the threshold for evoking cortical spreading depression (CSD), a process sharing characteri
70 icient to cause infarcts, triggered cortical spreading depression (CSD), a propagating slow depolariz
71 on exhibit increased propensity for cortical spreading depression (CSD), a propagating wave of neurog
74 mice, we show that a single wave of cortical spreading depression (CSD), an animal model of migraine
75 urological deficits associated with cortical spreading depression (CSD), preceding headache attacks.
76 nnels and are highly susceptible to cortical spreading depression (CSD), the electrophysiologic event
79 ring somatosensory stimulations and cortical spreading depression (CSD), the putative mechanism of th
80 optical triggering and recording of cortical spreading depression (CSD), the slowly propagated wave o
81 n damage and ischemia often trigger cortical spreading depression (CSD), which aggravates brain damag
82 this study was to determine whether cortical spreading depression (CSD)--an event believed to underli
83 ceptors, it significantly reduces a cortical spreading depression (CSD)-induced early response probab
84 us and evoked activity in naive and cortical spreading depression (CSD)-sensitized trigeminovascular
86 s (with [n=7] or without [n=7] HH), cortical spreading depressions (CSD) were elicited to ascertain t
88 ecovery rate for [K+]o, and interval between spreading depression episodes were measured before and a
90 TPase knockout triggers spontaneous cortical spreading depression events that are associated with EEG
92 d the effect of fremanezumab on the cortical spreading depression-evoked activation of mechanosensiti
94 e) that is evident in human (unlike cortical spreading depression) gives rise to specific and selecti
96 ding depolarization, usually termed cortical spreading depression has been proposed as the pathophysi
97 velength optical intrinsic imaging, cortical spreading depression has been shown to have a triphasic
99 The pathological phenomena of seizures and spreading depression have long been considered separate
102 and headache by demonstrating that cortical spreading depression, implicated in migraine visual aura
103 cerebral ischaemia, and blocking of cortical spreading depression improved stroke outcome in these mi
105 ound, global cerebral ischemia, and cortical spreading depression in C57BL6 mice; 1 day after probe d
107 signals evoked by stimulation, seizures and spreading depression in intact brain differ from those o
108 o each headache disorder, including cortical spreading depression in migraine, rhythmicity of attacks
115 ity in reducing the total number of cortical spreading depressions induced by potassium chloride.
116 mechanism for the susceptibility of cortical spreading depression initiation in migraine disorders.
122 ed significantly reduced NVC efficiency upon spreading depression-like (SDL) events, providing a dire
125 larizations (PIDs) are seemingly spontaneous spreading depression-like waves that negatively impact t
127 Vascular/metabolic uncoupling with cortical spreading depression may have important clinical consequ
128 the central autonomic response and cortical spreading depression might drive cerebrovascular reactiv
129 strated significant activity in the cortical spreading depression model of migraine as we reported pr
130 larly, SNC80 was ineffective in the cortical spreading depression model of migraine aura in condition
131 atine for 3 h failed to prevent hyperthermic spreading depression occurrence; and (2) intracellular A
135 tibility to ischemic depolarizations akin to spreading depression predisposes migraineurs to infarcti
137 ing, and c-fos immunohistochemistry to trace spreading depression propagation into subcortical struct
138 e showed that unlike the wild type, cortical spreading depression readily propagated into subcortical
139 t astrocytes normally extrude calcium during spreading depression, resulting in rapid recovery of the
140 Although intercellular Ca2+ waves resemble spreading depression (SD) and occur in hippocampal organ
141 spontaneous, recurring episodes of cortical spreading depression (SD) as early as 20 min post-inject
154 stigated the role of spontaneous and induced spreading depression (SD) on the evolution of focal isch
157 ant, on fluid shifts, cerebral perfusion and spreading depression (SD) using diffusion- (DWI) and per
165 ous transition between epileptic seizure and spreading depression states as the cell swells and contr
166 ssium or hypoxia induced), mixed seizure and spreading depression states, and the terminal anoxic "wa
167 mone levels in these mice modulated cortical spreading depression susceptibility in much the same way
168 smooth muscle Notch 3 mutations to enhanced spreading depression susceptibility, implicating the neu
169 mutation are highly susceptible to cortical spreading depression, the electrophysiological surrogate
172 We tested the susceptibility of cortical spreading depression, the experimental correlate of migr
174 at cortices, when administered post-cortical spreading depression, transcranial magnetic stimulation
175 unction, one during the propagating cortical spreading depression wave and a second much longer phase
176 t current shift associated with the cortical spreading depression wave was accompanied by marked arte
177 concentration increased during the cortical spreading depression wave, but recovered and remained at
178 mum direct current shift associated with the spreading depression wave, then gradually resumed over s
179 After recovery from the initial cortical spreading depression wave, we observed a second phase of
182 h mechanical and chemically-induced cortical spreading depression when administered immediately post-
183 euronal activities, from spikes to seizures, spreading depression (whether high potassium or hypoxia
184 ion and c-fos expression are associated with spreading depression, which is believed to contribute to
185 asses controversies associated with cortical spreading depression, which is less readily observed in
186 ity, and enhanced susceptibility to cortical spreading depression, which is the electrophysiological
187 TAC-Red-stained brain cortex in mice during spreading depression, with velocity 4.4 +/- 0.5 mm/min,
188 and transient ischaemia can trigger cortical spreading depression without an enduring tissue signatur