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TSG101 is a new member of the G(2)-G(0)/M-specific class of WD-repeat proteins. This protein contains a carboxy-terminal WD-repeat domain which has been proposed to mediate interactions with beta-COP or ubiquitin. In the present report we demonstrate that a gene encoding a functional murine homolog of human TSG101 is confined to the X chromosome and is expressed in late stages of oocyte growth and maturation. Specifically, expression was confined to GV oocytes and was absent from

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The pathophysiological mechanisms of migraine are related to cortical spreading depression (CSD), an excitatory wave spreading slowly in a focal area of the cerebral cortex. Given that vagal afferent fibers are distributed close to the trigeminal nucleus caudalis and that intracranial electrical stimulation activates C fibers, a possible relationship between migraine and vagus nerve paralysis has been hypothesized. However, there is no evidence to date that either vagus nerve paralysis or vagotomy affects the pathophysiology of migraine. The present work was undertaken to test this hypothesis in the context of CSD. In the first experiment we measured C fiber activity in the trigeminal nucleus caudalis of anaesthetized rats during CSD elicited by electrical stimulation of the parietal cortex. In the second experiment we used the same experimental model to test for the influence of saphenous branch vagotomy and posttraumatic vagus nerve paralysis on the pain behavior induced by electrical stimulation of the parietal cortex. Both the C fiber responses of trigeminal nucleus caudalis and the pain behaviors induced by cortical stimulation were significantly reduced in vagotomized rats. Vagotomy alone did not affect the C fiber responses or the pain behavior of non-vagotomized rats, indicating that the effects observed in the vagotomized rats were not mediated by a general reduction of afferent input to the trigeminal nucleus caudalis. Vagotomy did not affect the responses to intracranial activation of the inferior colliculus, a potential source of bulbar afferents to the trigeminal nucleus caudalis. In vagotomized rats posttraumatic vagus nerve paralysis did not affect the C fiber responses or the pain behavior induced by cortical stimulation. This result confirms and extends previous findings demonstrating the involvement of vagal afferents in the pathophysiology of migraine. We propose that vagus nerve paralysis and posttraumatic vagus nerve paralysis lead to reduced afferent input to
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