Affiliations: Biological Research Institute: "Drs. Orlando
Castejón and Haydée Viloria de Castejón", Faculty of Medicine,
University of Zulia, Maracaibo, Venezuela
Note: [] Correspondence: Orlando J. Castejón, Instituto de
Investigaciones Biológicas, Facultad de Medicina, Universidad del Zulia,
Apartado 526, Maracaibo, Venezuela. Tel./Fax: +58 261 7414370; E-mail:
ocastejo@cantv.net
Abstract: Cortical biopsies of 13 infant patients with clinical diagnosis of
congenital hydrocephalus, Arnold-Chiari malformation, and postmeningitis
hydrocephalus were examined with transmission electron microscopy to study the
synaptic plasticity and synaptic degenerative changes in hydrocephalic edema.
The immature cortical neuropil of different cortical regions showed swollen
nerve cell processes separated by enlarged extracellular space. Isolated and
swollen presynaptic endings with few or numerous synaptic vesicles, disruption
of limiting plasma membrane, and absent postsynaptic partners were also
observed. Activated flat and invaginated axodendritic and axospinodendritic
asymmetric synaptic contacts showed synaptic vesicles anchored to the
presynaptic membrane, and short or large synaptic active zones. The swollen and
degenerated synaptic contacts, including axosomatic synapses exhibited
enlargement of few synaptic vesicles and lack of pre- and postsynaptic
densities. Synaptic disassembly was observed in elevated intracranial pressure-
hydrocephalus. Megaspines making multiple asymmetric synaptic junctions were
also distinguished. Phagocytic astrocytes engulfed the degenerated synapses.
The potential role of hydrocephalic edema and ischemia, oxidative stress,
increased calcium concentration, activation of N-methyl D-aspartate receptors,
and disturbance of ion homeostasis are discussed in relation with the observed
synaptic plasticity and synaptic degenerative changes.
