Assessment | Biopsychology | Comparative | Cognitive | Developmental | Language | Individual differences | Personality | Philosophy | Social |
Methods | Statistics | Clinical | Educational | Industrial | Professional items | World psychology |

Clinical: Approaches · Group therapy · Techniques · Types of problem · Areas of specialism · Taxonomies · Therapeutic issues · Modes of delivery · Model translation project · Personal experiences ·

---

Research has indicate that the neurochemistry in the brains of people with schizophrenia is different from that of controls and such activity has been hypothessied to have a causal effect on the condition.

Contents 1 Adrenochrome 2 Dopamine 3 Glutamate 4 Calcium channel abnormalities 5 Nicotine 6 See also 7 References 8 Further reading 9 Key texts 9.1 Books 9.2 Papers 10 Additional material 10.1 Books 10.2 Papers 11 External links

AdrenochromeEdit

Main article: Schizophrenia - Adrenochrome hypothesis

Megavitamin therapy advocates Abram Hoffer and Humphry Osmond claimed that adrenochrome is a hallucinogenic substance and may be responsible for schizophrenia^[1] and other mental illnesses. In what they called the "adrenochrome hypothesis", they speculated that megadoses of vitamin C and niacin could cure schizophrenia by reducing brain adrenochrome.^[2]

DopamineEdit

Main article: Schizophrenia - Dopamine hypothesis

Particular focus has been placed upon the function of dopamine in the mesolimbic pathway of the brain. This focus largely resulted from the accidental finding that a drug group which blocks dopamine function, known as the phenothiazines, could reduce psychotic symptoms.

An influential theory, known as the "dopamine hypothesis of schizophrenia", proposed that a malfunction involving dopamine pathways was therefore the cause of (the positive symptoms of) schizophrenia. This theory is now thought to be overly simplistic as a complete explanation, partly because newer antipsychotic medication (called atypical antipsychotic medication) can be equally effective as older medication (called typical antipsychotic medication), but also affects serotonin function and may have slightly less of a dopamine blocking effect. In addition dopamine pathway dysfunction has not been reliably shown to correlate with symptom onset or severity.

GlutamateEdit

Main article: Schizophrenia - Glutamate

Interest has also focused on the neurotransmitter glutamate and the reduced function of the NMDA glutamate receptor in schizophrenia. This has largely been suggested by abnormally low levels of glutamate receptors found in postmortem brains of people previously diagnosed with schizophrenia^[3] and the discovery that the glutamate blocking drugs such as phencyclidine and ketamine can mimic the symptoms and cognitive problems associated with the condition.^[4] The fact that reduced glutamate function is linked to poor performance on tests requiring frontal lobe and hippocampal function and that glutamate can affect dopamine function, all of which have been implicated in schizophrenia, have suggested an important mediating (and possibly causal) role of glutamate pathways in schizophrenia.^[5]

Calcium channel abnormalitiesEdit

Calcium channel abnormalities are currently being explored as a factor in schizophrenia. Related to this, three small studies have found some improvements on some measures, in schizophrenia with tardive dyskinesia, with the calcium channel blocking agent nilvadipine added to an existing antipsychotic regimen^[6]

NicotineEdit

Main article: Schizophrenia - Sensory gating

Sensory gating is thought to be disturbed in schizophrenia. Because the Nicotinic acetylcholine receptor mediate sensory gating, tobacco smoking , which excites nicotinergic receptors, ameliorates symptoms of auditory hallucinations in many patients with schizophrenia.

---

See alsoEdit

• Biological psychiatry
• Orthomolecular psychiatry

References Edit

1. ↑ Hoffer, A The Adrenochrome Hypothesis and Psychiatry. URL accessed on 2011-07-25.
2. ↑ Hoffer, A. and Osmond, H. The Hallucinogens (Academic Press, 1967).
3. ↑ Konradi C, Heckers S. (2003) Molecular aspects of glutamate dysregulation: implications for schizophrenia and its treatment. Pharmacology and Therapeutics, 97(2), 153-79.
   
4. ↑ Lahti AC, Weiler MA, Tamara Michaelidis BA, Parwani A, Tamminga CA. (2001) Effects of ketamine in normal and schizophrenic volunteers. Neuropsychopharmacology, 25(4), 455-67.
   
5. ↑ Coyle JT, Tsai G, Goff D. (2003) Converging evidence of NMDA receptor hypofunction in the pathophysiology of schizophrenia. Annals of the New York Academy of Sciences, 1003, 318-27.
   
6. ↑ Yamada K, Ashikari I, Onishi K, Kanba S, Yagi G, Asai M. (1995) Effectiveness of nilvadipine in two cases of chronic schizophrenia. Psychiatry Clin Neurosci. Aug;49(4):237-8

Further readingEdit

Key textsEdit

BooksEdit

PapersEdit

• Weinberger DR, McClure RK. (2002) Neurotoxicity, neuroplasticity, and magnetic resonance imaging morphometry: what is happening in the schizophrenic brain? Arch Gen Psychiatry. Jun;59(6):553-8.

Additional materialEdit

BooksEdit

PapersEdit

• Google Scholar

External linksEdit

This page uses Creative Commons Licensed content from Wikipedia (view authors).