Final answer:
The cytoplasmic effects of Huntington's Disease (HD) involve altered calcium signaling due to dysregulated NMDA receptor expression, leading to neuronal cell death. This results from the production of a mutant huntingtin protein and potentially could be mitigated by selective NMDA receptor antagonists.
Step-by-step explanation:
Cytoplasmic Effects of Huntington's Disease (HD):
Huntington's disease (HD) is a genetic condition that affects the cytoplasmic environment of neurons, particularly altering calcium signaling pathways. Evidence suggests that a mutated huntingtin protein is linked to dysregulated NMDA receptor expression, which includes the receptors located at extrasynaptic sites. The aberrant activity of these extrasynaptic NMDA receptors leads to elevated intracellular calcium levels that activate harmful cellular pathways rather than the protective pathways activated by synaptic NMDA receptor activity. These cytoplasmic effects result in disruptions to the mitochondrial membrane potential and ultimately induce neuronal cell death. Agents like memantine are being investigated to selectively block the harmful extrasynaptic NMDA receptors without interfering with normal synaptic function, potentially ameliorating the effects of HD.