GABAergic Signaling describes the process of inhibitory neurotransmission mediated by Gamma-Aminobutyric Acid (GABA), the most prevalent inhibitory neurotransmitter in the adult central nervous system. This signaling pathway is essential for regulating neuronal excitability, controlling muscle tone, and promoting states of relaxation and anxiolysis. Its function is intimately involved in modulating the body’s stress response and is a critical component of neuroendocrine regulation.
Origin
The term is a neurobiological and pharmacological construct, combining the acronym for the chemical messenger, GABA, with the suffix ‘-ergic,’ which denotes a process that is activated by or acts upon the specified substance. This standardized nomenclature is used to classify various neurotransmitter systems within the nervous system.
Mechanism
GABA is released into the synaptic cleft and primarily acts by binding to the ionotropic GABA-A receptor located on the postsynaptic neuron. Receptor binding causes a conformational change that opens an intrinsic chloride ion channel, allowing negatively charged chloride ions to flow into the neuron. This influx hyperpolarizes the cell membrane, effectively inhibiting the neuron from firing an action potential and thus providing a dampening effect on neural and associated hormonal activity.
Progesterone protocols can combine with other hormonal therapies to enhance cognitive support by balancing neurosteroid actions and systemic endocrine function.
Increased anxiety during hormonal protocols often stems from temporary neuroendocrine system recalibration, impacting neurotransmitter balance and stress axis regulation.
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