We use cookies to distinguish you from other users and to provide you with a better experience on our websites. Close this message to accept cookies or find out how to manage your cookie settings.
To save content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about saving content to .
To save content items to your Kindle, first ensure no-reply@cambridge.org
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about saving to your Kindle.
Note you can select to save to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
The dopamine hypothesis has been the major pathophysiological theory of
psychosis in recent decades. Molecular imaging studies have provided
in vivo evidence of increased dopamine synaptic
availability and increased presynaptic dopamine synthesis in the striata of
people with psychotic illnesses. These studies support the predictions of
the dopamine hypothesis, but it remains to be determined whether
dopaminergic abnormalities pre-date or are secondary to the development of
psychosis. We selectively review the molecular imaging studies of the
striatal dopaminergic system in psychosis and link this to models of
psychosis and the functional subdivisions of the striatum to make
predictions for the dopaminergic system in the prodromal phase of
psychosis