Neuroprotective Effects of Macrovipera lebetina Snake Venom in the Model of Alzheimer’s Disease

Pathological features of Alzheimer's disease (AD) include accumulation and deposition of β-amyloid (Aβ) in the brain, activation of astrocytes and microglia, and disruption of cholinergic neurotransmission. In our experiments on rats, a model of AD was created by intracerebroventricular (i.c.v.) injections of Aβ_25–35 amyloid. In another animal group, this was combined with intramuscular (i.m.) injections of small doses of Macrovipera lebetina (ML) snake venom (50 μl of 5% solution of an LD₅₀ dose per animal seven times with one-day-long intervals). In the AD model, the most vulnerable neurons were found in the hippocampal fields CA1 and CA3. The phosphatase activity in the hippocampus of Aβ-injected rats sharply dropped. Systemic administration of small doses of ML venom induced positive changes in the structural characteristics of hippocampal neurons, increased the density of neurons in the above fields, normalized metabolism, and intensified Ca2+-dependent phosphorylation. Under the action of ML venom, the proportion of responses of hippocampal pyramidal neurons after high-frequency tetanic stimulation of the ipsilateral entorhinal cortex in the form of tetanic depression–posttetanic potentiation increased, and an overall increase in the firing rate of hippocampal neurons was observed. The intensity of free radical processes in some tissues of Aβ-affected animals became much lower under the action of ML venom. Thus, small doses of this venom manifest clear neuroprotective effects in the rat AD model.

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