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Neuronal Proteins

The intracytoplasmic proteins of neurons give information on neuronal function. Tomimoto and Yana-gihara (2000; see also Tomimoto et al. 1996) could demonstrate that microtubule-associated proteins (MAPs) are more vulnerable than tubulin to ische-mic insults. Using immunohistochemistry for MAPs, the earliest ischemic lesion in gerbils occurred in the CA1 and CA2 sector of the hippocampus after transient global ischemia for 3 min (see also Fig. 14.14).

Fig. 14.10a-d. Astrocytic reactivity in brain ischemia. a final stage of reactivity d partly replaced by astrocytic fi-Astrocytic hyperplasia in white matter; b increase of as- bers (a, b, d GFAP immunoreactivity; c H&E; magnification trocytic fibers; c loss of Purkinje cells which are during the a, b X200, c, d X300)

Fig. 14.10a-d. Astrocytic reactivity in brain ischemia. a final stage of reactivity d partly replaced by astrocytic fi-Astrocytic hyperplasia in white matter; b increase of as- bers (a, b, d GFAP immunoreactivity; c H&E; magnification trocytic fibers; c loss of Purkinje cells which are during the a, b X200, c, d X300)

These lesions were reversible but became irreversible when the duration of ischemia was extended to 4 min.

The immunoreactivity of so-called motor proteins, such as cytoplasmic dynein (CD) and kinesin, begins to decrease at 1 h in CA1 neurons (Abe et al. 1995); the decrease becomes more evident at 3 h after ischemia, whereas the immunoreactivity of other neurons remains at a normal level. The motor proteins are linear motors that convert the energy of ATP hydrolysis into mechanical work and move cellular organelles such as mitochondria along microtubu-les. CD, also referred to as MAP-1C (Paschal et al. 1987), translocates organelles to the proximal end of microtubules. Kinesin is thought to mediate axo-nal transport to the peripheral end of microtubules. Moreover, we also know that one consequence of ischemia will be a non-disruptive axonal injury (AI), i.e., axonal swellings, and axonal bulbs as described by Maxwell et al. (1997 - see also: Oehmichen et al. 1998, 1999; Kaur et al. 1999) will be demonstrable 1.5-3.0 h after the incidence of the ischemic insult by application of an antibody to P-amyloid precursor protein (fi-APP).

Martí et al. (2001) described the temporal pattern of expression of proteins of the chromogranin/ secretogranin family by immunohistochemistry. In gerbils, these authors could demonstrate a strong increase in reactivity of chromogranin A and sec-retoneurin in the CA3 sector, starting at 12 h with a peak at 24 h and a decrease at 48 h after transient ischemia.

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