Section I. The cholinergic system.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to John Smythies.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
This paper reviews the possible role of catecholamine o-quinones (oQs) in the genesis of Parkinson's disease (PD). This disease is characterized by damage caused to the pigmented catecholaminergic cells in various areas of the brain. The pigment involved is neuromelanin that is the end product of catecholamine oxidation by the o-quinone route. Evidence is presented regarding the overproduction in PD of these catecholamine oQs that damage the electron chain in the mitochondria leading to cell death. The roles of glutathione S-transferase and reactive oxygen species in this are also surveyed. A review of all known biochemical properties of these o-quinones is included. The hypothesis is put forward that an important factor in the genesis of PD may be the overload by environmental toxins of enzymes such as glutathione S-transferase that also detoxify catecholamine oQs.
This paper reviews the current status of the adrenochrome theory of schizophrenia. An account is first given of all the experiments in which adrenochrome was reported to induce psychotomimetic effects in normal volunteers. Then the evidence is presented that adrenochrome may actually occur in the brain as a metabolite of adrenaline in the C2 group of adrenergic neurons in the medulla, together with an account of current ideas of the function of these neurons in higher limbic functions. Lastly the recent evidence is reviewed that the gene for the enzyme glutathione S-transferase is defective in schizophrenia. This enzyme detoxifies adrenochrome.