Final answer:
Increased blockade of dopamine in the basal ganglia leads to the development of Extrapyramidal Symptoms (EPS), movements disorders caused by antipsychotic medications. In Parkinson's disease, dopamine neuron degeneration affects neurotransmitter balance, leading to excitotoxicity and movement symptoms. In schizophrenia, excessive glutamate release contributes to excitotoxicity and cognitive dysfunction.
Step-by-step explanation:
Increased blockade of dopamine leads to Extrapyramidal Symptoms (EPS), which are drug-induced movement disorders that may arise from antipsychotic treatment. This occurs because antipsychotic medications function as dopamine antagonists, blocking dopamine's effects and preventing it from signaling information to adjacent neurons. When dopamine signaling is excessively blocked, particularly in the basal ganglia, it can lead to EPS, manifesting as a range of symptoms including tremors, rigidity, bradykinesia, and tardive dyskinesia.
Additionally, Parkinson's Disease (PD) involves the degeneration of dopaminergic neurons in the Substantia Nigra, leading to an imbalance in neurotransmission affecting glutamate and GABA. This can also lead to excitotoxicity, where excessive neurotransmitter activity causes damage to neurons. Treatment options in PD and other diseases explore the modulation of glutamate receptors and dopamine receptors to manage symptoms.
In the context of schizophrenia, a dysfunction in cognitive function associated with excessive glutamate release overstimulates AMPA receptors, contributing to excitotoxic effects and neuroanatomical changes. For both schizophrenia and PD, exploring pharmaceutical compounds targeted toward specific receptor subtypes, such as the NR2B subunit of the NMDA receptor, may offer a strategy to manage symptoms while reducing side effects.