Apamin is a neurotoxin extracted from honey bee venom and is a selective blocker of small-conductance Ca²⁺-activated K⁺ channels (SK). Several behavioral and electrophysiological studies indicate that SK-blockade by apamin may enhance neuron excitability, synaptic plasticity, and long-term potentiation in the CA1 hippocampal region, and, for that reason, apamin has been proposed as a therapeutic agent in Alzheimer's disease treatment. However, the dendritic morphological mechanisms implied in such enhancement are unknown. In the present work, Golgi-Cox stain protocol and Sholl analysis were used to study the effect of apamin on the dendritic morphology of pyramidal neurons from hippocampus and the prefrontal cortex as well as on the medium spiny neurons from the nucleus accumbens and granule cells from the dentate gyrus (DG) of the hippocampus. We found that only granule cells from the DG and pyramidal neurons from dorsal and ventral hippocampus were altered in senile rats injected with apamin. Our research suggests that apamin may increase the dendritic morphology in the hippocampus, which could be related to the neuronal excitability and synaptic plasticity enhancement induced by apamin.
The dendritic length and dendritic-spine density of the pyramidal neurons of the prefrontal cortex and the CA1 hippocampus of rats using the nonselective nitric oxide synthase inhibitor N-omega-nitro-L-arginine (L-NNA) at different postnatal day (P) periods of the brain development (P1-P3, P4-P6, and P7-P9) were assessed using Golgi-Cox staining after puberty (P60). At P4-P6, the L-NNA treatment produced a significant decrease of the dendritic length and dendritic-spine density of the pyramidal cells of the CA1 hippocampus. In addition, the dendritic length of the pyramidal neurons of the CA1 hippocampus decreased because of the L-NNA treatment at P1-P3. These data suggest that during a specific step in the development of the brain, the nitric oxide levels may play a critical role in the morphological modifications of the pyramidal neurons of the CA1 hippocampus at postpubertal age.
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