Immunohistochemical Signs of Apoptosis and Neuroplasticity in the Cerebral Cortex of White Rats after Occlusion of the C
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Immunohistochemical Signs of Apoptosis and Neuroplasticity in the Cerebral Cortex of White Rats after Occlusion of the Common Carotid Arteries D. B. Avdeev, S. S. Stepanov, A. V. Gorbunova, V. A. Akulinin, and A. Yu. Shoronova
UDC 616.831-005.4
Translated from Morfologiya, Vol. 156, No. 6, pp. 19–24, November–December, 2019. Original article submitted July 12, 2019. Revised version received September 25, 2019. Objective. To study the activity of apoptotic proteins (bcl-2, p53, caspase-3) and neuroplasticity proteins (p38, MAP-2) in the sensorimotor cortex (SMC) in the brains of white rats in health and at different times after 20-min occlusion of the common carotid arteries (OCCA). Materials and methods. Light microscopy (hematoxylin and eosin staining), immunohistochemistry, and morphometry methods were used. Study materials: the control group consisted of sham-operated animals (n = 5) and the study group consisted of animals 1, 3, 7, 14, and 30 days after OCCA (n = 25). Results. OCCA was followed, on the background of irreversible destruction of a proportion of SMCC neurons (layer III 25.1%, layer V 19.0%), by reorganization of processes (MAP-2) and synapses (p38) of surviving neurons. The relative contents of labeled anti-p38 and anti-caspase-3 antibodies located in synaptic terminals decreased (on days 1 and 3) and then recovered (on day 7). The most marked changes in caspase-3 during the postischemic period were noted at 7, 14, and 30 days, when its content was greater than that of p38. Conclusions. Postischemic compensatory reorganization of the neuronal communication system (processes, synapses) occurred on the background of a high axon caspase-3 level. No signs of apoptosis (activation of caspase-3 in the perikaryon) were seen. Caspase-3 should be regarded as aspect of pleiotropy, as it is involved in adaptive and restorative processes, i.e., neuroplasticity. Keywords: acute ischemia, neocortex, caspase-3, p53, bcl-2, MAP-2.
Introduction. Acute ischemia is known to trigger mechanisms damaging nervous tissue via necrosis and apoptosis, also adversely affecting neuroplasticity [2, 12, 13]. Irreversible neuron damage in acute ischemia is initiated via activation of c-Jun N-terminal kinase (JNK). This is followed by apoptosis or secondary (delayed) necrosis [10]. Caspase-3 plays an active role here; this has both proand antiapoptotic properties [5, 6]. The neuroprotective and neuroplastic functions of caspase-3 can be activated by a Ca2+-dependent pathway, though the exact mechanisms remain unknown [7–9]. Apoptotic proteinases probably have functions directly linked with neuroplasticity. Caspase-3 is
pleiotropic or multimodal, because of the involvement of this enzyme in a multiplicity of different and directly opposite functions. When cerebral pathology develops, this enzyme mediates both nerve cell death and the compensatory processes required for neuron survival and normal overall brain functioning [7, 8]. There are few morphological studies of nervous tissues in this direction. The key structures linked
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