Abstract
Dopamine (DA) dysregulation plays a central role in the pathophysiology of schizophrenia, as it relates most directly to the symptoms and to their treatment. This dysregulation has been well characterized by in vivo imaging studies in humans and comprises two main components, a striatal excess and a cortical deficit. Such an alteration can result from abnormal regulation of dopamine neuron activity by other systems. Recent evidence has pointed to the hippocampus as a main source of altered modulatory influence onto dopamine, possibly leading to the excess striatal activity. We review here the clinical and preclinical data, while relating the measures obtained from imaging to what we believe are their corresponding molecular equivalent. We then summarize the elements that have arisen from these lines of research into one overall integrative model.
| Original language | English |
|---|---|
| Title of host publication | Schizophrenia |
| Subtitle of host publication | Third Edition |
| Publisher | Wiley-Blackwell |
| Pages | 413-432 |
| Number of pages | 20 |
| ISBN (Print) | 9781405176972 |
| DOIs | |
| State | Published - Mar 8 2011 |
Keywords
- Antipsychotic drugs and their impact - on tonic dopamine neuron firing
- DA hypothesis of schizophrenia - first formulated by Rossum, observation that antipsychotics may block DA receptors
- Dopamine and cognition - suboptimal cortical dopamine transmission
- Dopamine and psychosis - increased striatal phasic dopamine release
- Dopamine and schizophrenia
- Dopamine neuron activity - and striatal dopamine dynamics
- Excess striatal dopamine underlying psychosis
- Schizophrenia, and multiple clinical features - ranging from positive symptoms
- Tissue dopamine and homovanillic acid
- Tyrosine hydroxylase immunolabeling
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