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Fig. 5 | The Journal of Headache and Pain

Fig. 5

From: Mechanisms of initiation of cortical spreading depression

Fig. 5

Effect of blocking the voltage-gated Ca2+ channels on the neuronal depolarization elicited near the site of CSD induction by CSD threshold and just subthreshold KCl stimuli. A Representative membrane potential traces recorded in response to a CSD threshold KCl stimulus in a L2/3 pyramidal cell located near the KCl puffer (as in Figure 1) in the absence (ctrl, red trace) and presence (Ni2+, green trace) of a saturating concentration of Ni2+ (5 mM) (upper panel). The corresponding, simultaneously recorded, IOS changes are shown in the lower panel. Ni2+ completely inhibited the CSD peak depolarization (3rd peak) as well as the steep CSD IOS rise. Ni2+ also eliminated the 2nd peak of the early depolarization as well as the slow IOS rise preceding CSD initiation, and it inhibited 45 % of the amplitude (relative to the resting potential) of the 1st peak of the depolarization elicited by the CSD threshold stimulus. B Representative membrane potential traces recorded in response to a CSD just subthreshold KCl stimulus in the same L2/3 pyramidal cell of panel A in the absence (ctrl, black trace) and presence (Ni2+, green trace) of Ni2+. Ni2+ inhibited 57 % of the amplitude (relative to the resting potential) of the 1st peak of the depolarization elicited by the just subthreshold stimulus, and eliminated both the 2nd peak and its shoulder, thus decreasing the duration (at half amplitude) of the just subthreshold depolarization from 11.7 to 2.1 s. C Average peak voltage of the depolarizations produced by KCl stimuli of increasing intensity in the presence of Ni2+ (5 mM) as a function of stimulus intensity (KCl puff duration) (n= 4; N =4). Inset: representative membrane potential traces recorded in response to subthreshold KCl stimuli of increasing intensity up to the threshold stimulus in the presence of Ni2+ (5 mM) in the same L2/3 pyramidal cell of panels A, B

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