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Mental disorders
Anxiety Disorders
Alzheimer’s-type Dementia

Help The Serotonin Surprise Depression and the Birth and Death of Brain Cells Antidepressants and Brain Cell Growth
La mémoire qui flanche Depression: Beyond Serotonin
Time-of-Day-Dependent Enhancement of Adult Neurogenesis in the Hippocampus
Original modules
History Module : Neurogenesis Neurogenesis

Many experiments have shown a close connection between reduced neurogenesis in the hippocampus and elevated glucocorticoid levels induced by stress.

In rats, ablation of the adrenal glands that secrete glucocorticoids increases neurogenesis in the dentate gyrus of the hippocampus. This effect can be reversed by the injection of a glucocorticoid such as corticosterone. Similarly, the continued administration of corticosterone can prevent neurogenesis in the dentate gyrus of normal rats.

Some situations that are naturally stressful for animals also have a negative impact on neurogenesis. For example, exposing a rat to the scent of one of its natural predators, such as a fox, will reduce the growth of new neurons in the rat's dentate gyrus. The same thing happens when rats are subjected to a psycho-social stress, such as when two rats of the same sex are placed together in the same cage.

Research : Fred Gage Research : Elizabeth Gould Link : Surviving stress

The hypothesis that the rate of formation of new neurons (neurogenesis) in the hippocampus might have some connection with depression is still recent. It has been widely criticized, and even its defenders concede that a decline in neurogenesis in the hippocampus is certainly not the only neuronal change that occurs in depression.

But a number of facts seem to point surprisingly clearly to a role for neurogenesis in depression, and the weight of this evidence is hard to ignore:

  • Stress, which often leads to depression, reduces neurogenesis in the hippocampus.
  • Antidepressants that improve patients' moods increase the rate of formation of new neurons in the hippocampus.
  • When antidepressants are administered to animals, it takes two to three weeks before the rate of neurogenesis increases, and then another two weeks before the new neurons become functional. This is just about the same amount of time that it takes for antidepressants to start having an effect on a patient's morale.
  • If an antidepressant is given during a period of chronic stress, it prevents the decline in neurogenesis.
  • Exercise, which improves morale in depressed people, also promotes neurogenesis in the hippocampus.
  • Electroshock treatment has these same two effects.
  • Lastly, in numerous autopsies of people who suffered from depression, their hippocampi were found to be smaller than normal.

Section of the dentate gyrus of the hippocampus, showing newly formed cells. These are the darker cells in the subgranular zone (SGZ), and they have been labelled with 5-bromo-2-deoxyuridine (BrdU), an analogue of thymidine.

The histogram shows that various antidepressant treatments increase the number of new labelled cells. The treatments tested include electroconvulsive shock (ECS), the MAOI tranylcypromine (TCP), the SSRI fluoxetine (FLU), and the selective norepinephrine reuptake inhibitor reboxetine (REB).

Even those authors who have called attention to these converging observations freely admit that it is far from certain that reduced neurogenesis in the hippocampus is the primary factor in triggering depression. It seems more likely that after patients have fallen into a depression, the decline in neurogenesis helps to keep them there, or at least makes it harder for them to develop the new mental constructs that they would need to come out of it.

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