The
Human Immunodeficiency Virus (HIV) affects not only the immune system, but also
the Central Nervous System (CNS).
Invasion of the CNS by HIV can cause HIV-associated neurocognitive
disorders (HAND) and damage is usually observed through non-apoptotic pathways.
One prominent
pathway is synaptodendritic
injury,
which
compromises the ability of neurons to communicate with each other. However, the
mechanisms involved in the neuronal damage are still unclear. Previous studies
from our lab show that the HIV-1
envelope
protein, gp120, increases neuronal expression of the protein ferritin heavy
chain (FHC), which is essential in iron homeostasis.
FHC
also plays a critical role in maintenance of dendritic spines and disrupts the
CXCL12/CXCR4 axis, a signaling pathway involved in pro-survival signaling,
neurogenesis, and excitotoxic
pathways in the CNS. In
this study, we specifically focus on the effects of the HIV-1
envelope
protein, gp120, on the dendritic arbor of pyramidal neurons in different areas
of the rat cerebral cortex. We have utilized gp120-treated rats and compared
their dendritic spine density, length, and type with those of untreated rats
using the neurolucida
tracing software in conjunction with a compound microscope. The animals had
also gone through behavioral studies to determine cognitive deficits caused by
the viral protein. The ultimate goal is to be able to correlate the observed
dendritic changes with the ability to learn new tasks.
