What is the Origin of Long-Term Depression (LTD)?

The term originated in the field of neurophysiology, discovered in the early 1980s as a counterpart to Long-Term Potentiation (LTP). It describes the persistent weakening of synapses following certain patterns of electrical stimulation. Its inclusion in the hormonal domain reflects the established neuroendocrine interface, recognizing that hormones are powerful neuromodulators of synaptic function.

What is the Mechanism of Long-Term Depression (LTD)?

LTD is typically induced by low-frequency stimulation and involves a decrease in the postsynaptic response to a constant presynaptic signal. The cellular mechanism often includes the internalization of postsynaptic receptors, particularly NMDA and AMPA receptors, reducing the cell's sensitivity to neurotransmitters like glutamate. Hormones such as cortisol, when chronically elevated, can disrupt the molecular pathways underlying LTD, impairing the brain's ability to prune unnecessary neural connections and contributing to cognitive dysfunction.

Long-Term Depression (LTD) ∞ Area

Long-Term Depression (LTD)

Meaning

Long-Term Depression (LTD) is a specific neurophysiological phenomenon referring to a long-lasting decrease in the strength of synaptic transmission between two neurons, often observed in the hippocampus and cerebellum. In the context of hormonal health, it represents a form of neural plasticity that is critically modulated by circulating hormones like estrogens and glucocorticoids. This reduction in synaptic efficacy is essential for processes like memory clearance and adaptive behavioral change.