Hippocampus

Memory Consolidation

Turning the day's experience into durable memory, which happens during deep and REM sleep. This is the step that breaks first when sleep breaks, and it is why memory complaints on these compounds usually trace back to sleep.

G Protein-Coupled Estrogen Receptor

A membrane estrogen receptor separate from ER-alpha and ER-beta. It responds in seconds, which is why some estrogen effects in the brain appear far too fast to be explained by gene transcription.

NMDA Glutamate Receptor

The receptor that carries the calcium current behind learning. It is also the route by which too much glutamate kills the cell, so the same channel that writes memory is the one that destroys the neuron when it stays open too long.

Excitotoxic Injury

Death by over-stimulation. Glutamate opens calcium channels, calcium floods in past what the mitochondria can hold, and the cell triggers its own destruction. It is the final common path for a large share of neuronal death, and it is the exact process estrogen defends against.

Local Brain Estrogen Synthesis

The brain makes its own estradiol from testosterone, in neurons and astrocytes, independently of what the testes supply. This single fact is why a blood estradiol reading does not tell you what the brain has, and why an aromatase inhibitor is a different kind of intervention from simply having low testosterone.

Verbal Memory

Recall of words, names and conversation. Studied in testosterone trials in older men with mixed and generally small results, which is worth stating plainly: this is one of the few cognitive measures here with any controlled human data at all, and the data does not show a large effect.

Working Memory

Holding and manipulating information over seconds. The cognitive measure most sensitive to lost sleep and to raised cortisol, which makes it the one most likely to move on these compounds and the one least likely to be noticed as a cognitive effect.