The most common class of drugs used to help schizophrenia,
neuroleptics, work by blocking and disabling
the dopamine receptors in the brain (7).
The prevailing opinion on the mechanism of estrogen in schizophrenia is
that it works in a similar way.
A study done on rats that had been dosed with a
psychotic drug showed that the dissociation constant
Kd of the binding of a dopamine receptor ligand
was 2.8 times higher in a group treated with estrogen, which showed that
the receptors treated with estradiol had
less of an affinity to the ligand. These researchers concluded that
estrogen treatment reduced the sensitivity of the dopamine receptors, blockading
them like neuroleptics. This is supported by the fact that, like
estrogen, neuroleptics also reduce the worst symptoms and can delay relapses,
but don't seem to reduce the lifetime risk of developing the disease (4).
Another researcher reported that estrogen had an
effect on dopamine activity in the nucleus accumbens
by in a way slowing down the process; inhibiting the release of dopamine,
as Hafner et al suggested, and also, she claimed, by prolonging the uptake
process of extra dopamine to the receptors. The idea is that by slowing
the process, estrogen, like neuroleptics, would return dopamine sensitivity
to the receptors and would normalize the amount of dopamine in the system
(5).
Only a few studies have specifically targeted estrogen's
interaction with dopamine, so it is still largely uncertain as to whether
estrogen directly affects dopamine activity as these scientists suggest.
Other research suggests that estrogen may take another route to delay schizophrenia.