Final answer:
Pruritus can be influenced by the balance of excitatory and inhibitory neurotransmitters, particularly glutamatergic and GABAergic systems. Directly blocking glutamatergic transmission is inadequate due to homeostatic synaptic plasticity. Treatments targeting specific NMDA receptor subunits have been explored but are limited by side effects in humans.
Step-by-step explanation:
Factors Affecting Pruritus and Neuronal Regulatory Mechanisms
Pruritus, or itching, can be modulated by various neuronal mechanisms. Glutamatergic transmission is one pathway implicated in pruritus. However, simply blocking this transmission is not a straightforward solution due to the complexity of homeostatic plasticity in synapses. This indicates a natural balance to prevent over or under activity that could disrupt neural function. Additionally, excitotoxicity caused by excessive glutamate and calcium influx can also aggravate pruritus.
Regulation of neuronal activity and pruritus also involves the balance between excitatory and inhibitory neurotransmitters, with the GABAergic system playing a crucial role in maintaining this balance. Disruptions in the excitatory-inhibitory balance, often observed in neurological disorders, can lead to altered pruritus sensations. Treatments targeting the NMDA receptor subunit composition have been explored to manage pruritus, particularly the NR2B subunit with compounds like CP-101,606. Yet, such treatments' applicability in humans remains limited due to side effects. The complex interplay of neurotransmitters in regulating neural activity suggests that a multifaceted approach is required to manage pruritus effectively.