MAOIs in the contemporary treatment of depression.

Prozac, a common antidepressant of the SSRI type, elevates serotonin levels in the brain.

The Chemistry of Depression - Neurotransmitters and …

Preclinical studies showing that central administration of somatostatin can alter sleep patterns, appetite, locomotor activity, and cognition have created interest in investigating somatostatin's role in mood disorders. The clearest evidence for involvement of somatostatin in psychiatric illness has come from studies of major depression. A consistent decrease has been reported in CSF somatostatin concentrations in depressed individuals. In primates, CSF somatostatin has been reported to undergo circadian variation, with concentrations varying 10% over 24 hr with the highest concentrations observed at night (6). Although the reported differences between depressed and normal patients are substantially greater than 10%, this circadian variation emphasizes the need for attempts at CSF sampling at uniform times. Although Rubinow et al. (72) did not find any time-of-day differences in patients, he did note large differences (increases and decreases) in subjects who were sampled in both morning and evening. Research over the past 15 years on a number of neuropeptides in CSF have revealed that they are almost exclusively of central origin, although the actual sites are unclear (65, 66). Decreases in CSF somatostatin concentrations are proposed to be the result of decreased neuronal synthesis and release. Whether this is a primary or secondary effect of the illness is unknown (see below).

The role of dopamine and norepinephrine in depression and antidepressant treatment.

The Chemistry of Depression - Neurotransmitters and More

Berger et al. also found that a super-shortening of REM latency in endogenous depressives occurred following administration of the long-acting oral muscarinic agonist, RS86 (3), when compared to normals and to eating disorder patients. Possibly related to all of the above findings, Berger et al. (4) also found that physostigmine-induced arousal and awakening from sleep more frequently occurred in affective disorder patients than in normals.

Do you know of any tests to see which neurotransmitter is off and causing the depression I have? A.

Schittecatte et al. (102) have also demonstrated that human depressives are subsensitive to the REM sleep suppressing effects of clonidine, thereby supporting the -adrenergic subsensitivity postulated to exist in depressives on the basis of neuroendocrine challenge studies (1). It is not clear at this stage whether the clonidine subsensitivity is a direct reflection of changes in the -noradrenergic system or merely a consequence of the supersensitivity proposed to exist in the balancing cholinergic systems. It could be very illuminating to obtain both clonidine and cholinomimetic challenge data in the same subjects (107).

As of January 2014, I am not convinced that testing for neurotransmitter levels adds to the clinical treatment of a patient.


Glutamate Neurotransmitter And Depression | …

Cooke (1976) studied the effect of fluoride (200 mg/litre) on common sunflower () seeds grown in sand culture. No effect on total dry weight was observed; however, there were significant reductions in leaf growth. Keller (1980) grew Norway spruce () cuttings in sand and watered with 100 mg fluoride/litre during winter until bud break. Watering with sodium fluoride significantly depressed the carbon dioxide uptake of shoots. Although the previous year’s needles did not show signs of injury, most of the new needles were killed immediately after flushing with fluoride. Exposure to fluoride significantly increased the susceptibility of plants to sulfur dioxide in subsequent fumigation experiments. Zwiazek & Shay (1987) grew jack pine () seedlings in sand culture at 3 or 15 mg fluoride/kg dry weight. Wilting was the first sign of fluoride injury and occurred in approximately 50% of plants after 25–26 h at 15 mg fluoride/kg and 2–6 h later in only 7% of plants exposed to 3 mg/kg. Fluoride-induced injuries to mesophyll and guard cells were similar to those caused by drought and included the appearance of lipid material in the cytoplasm during early stages of injury, suggesting cell membrane damage. Plants exposed to 3 mg/kg for up to 168 h showed significant reductions in water content. Respiration was significantly reduced after 24 h, but not after longer exposure times, while photosynthetic oxygen release was significantly reduced at 48 and 91 h but had recovered after 168 h (Zwiazek & Shay, 1988a). Zwiazek & Shay (1988b) reported that 3 mg fluoride/kg significantly reduced growth (as measured by fresh weight) and acid phosphatase activity and increased total organic acid content of jack pine () seedlings.

Glutamate Neurotransmitter And Depression

In a study on the neurotoxicity of sodium fluoride in rats (Mullenix et al., 1995), changes in behaviour were monitored in groups of Sprague-Dawley rats after exposure to fluoride at three different experimental stages. A number of behavioural patterns were examined, and pairs of control and experimental animals were observed at the same time. Some of the statistical methods were not fully described. In the first group, dams were administered subcutaneous injections of 0.13 mg sodium fluoride/kg on gestation days 14–18 or 17–19, 2–3 times daily. Nine weeks after delivery, they were examined, and measures of time–structure changes were depressed in exposed animals compared with controls. The second group was exposed to 0, 75, 100, 125 or 175 mg fluoride/litre in their drinking-water for 6 or 20 weeks immediately after weaning. The top group was discontinued because of mortality and dehydration, and the second top group showed significant deficits in body weight. Plasma fluoride was elevated over controls in all groups, and low-level behavioural effects from noise were correlated with plasma fluoride levels but not dose. Some specific behavioural changes compared with controls were reported for 100 and 125 mg/litre females and 125 mg/litre males, but there was considerable variation in the controls, and data for some dose groups were not reported. Plasma fluoride did not show a dose–response trend. The third group was given 0 or 100 mg fluoride/litre in drinking-water for 5–6 weeks. Testing after 10 weeks was reported to show a depression in low-level behavioural effects in females but not males. It is difficult to interpret the results of this study without more detailed analysis of the data, some of which are not presented; consequently, the significance of these data remains uncertain.