Abstract
BACKGROUND: Mauthner goldfish (Carassius auratus (L)) cells serve as model objects for studying brain pathologies at the level of identified neurons and their individual dendrites. L-dopa may be an agent that decelerates the destruction of neurons caused by the toxic effects of beta-amyloid.
AIMS: To study the three-dimensional structure of Mauthner neurons in goldfish and the ultrastructure of their afferent synapses under the influence of L-dopa and the toxic 2535 fragment of beta-amyloid.
MATERIAL AND METHODS: This study was performed on the Mauthner neurons of goldfish fry (n=12) by using light and electron microscopy. Serial sections 3 m thick were used to identify and integrally reconstruct the structure of Mauthner neurons; determine the volume of the soma and ventral and lateral dendrites; and study the structure of afferent synapses.
RESULTS: The use of L-dopa stabilized the size of the soma and ventral dendrites. The reduction in the volume of lateral dendrites was accompanied either by an increase in the volume of their branches under the action of beta-amyloid followed by that of L-dopa or by an increase in the volume of medial dendrites under the action of L-dopa followed by that of beta-amyloid. Although pathological changes in the ultrastructure of neurons and afferent synapses were not found, signs of early amyloidosis were detected.
CONCLUSION: The use of L-dopa decelerates the degeneration of Mauthner neurons. The resistance of whole neurons to the neurotoxic action of beta-amyloid has been suggested to be due to the mechanism of structural homeostasis aiming at the compensatory restoration of the morphological organization of neurons.