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Depression antidepressants and the shrinking hippocampus, symptoms of extreme fatigue and headaches - PDF Review

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A lecture delivered in the West Midlands by Dr Imran Waheed, Consultant Psychiatrist, on The Neurobiology of Depression. Researchers have found that repeated depressive episodes can cause a critical brain component to shrink over time.
People who suffer from recurrent depression could find a critical part of their brain responsible for forming memories shrinking over time, according to a new study. Fifteen research institutes from around the world, including those from the United States, Europe and Australia, combined the results of their own data on the hippocampuses of depressed and healthy people. They found that 65 percent of the depressed subjects suffered from recurrent depression, and that these people also had a smaller hippocampus, which is responsible for forming long-term memories and connecting them with emotions. He added that the study’s findings meant that people who suffered from depression at an earlier age were more at risk, since it meant that those who began suffering the effects of depression, which include social withdrawal and reduced performance at school or work, were likely to suffer more episodes in future. In addition, researchers also found that the hippocampuses of people who were taking antidepressants were larger, implying that the drugs could have a protective effect. For a long time, the only biological theory which attempted to explain clinical depression and how antidepressants counteract it was the monoamine hypothesis. The literature on stress, neurogenesis, and antidepressants, is impressive and growing rapidly. To establish whether neurogenesis is involved in antidepressant action, you need to to manipulate it – for example, by blocking neurogenesis and seeing if this makes antidepressants ineffective.
Anyway, some of the rats were injected with antidepressants during the final two weeks of the stress procedure. The crucial finding is that the white and the black bars are all pretty much the same height. But as we saw earlier, MAM did not stop antidepressants from protecting rats against stress. The most interesting aspect of this paper, to my mind, was an essentially unrelated new finding. As you can see in the drawings above, stress (the middle column) caused shrinking and stunting of the dendrites in pyrimidal neurones from three areas relative to the unstressed rats (left), while those rats recieving antidepressants as well as stress showed no such effect (right). Neuroskeptic:As to your comment about immediate effects, subjectively, most people I know that use SSRIs say they experience very immediate effects of blunted emotions and reduced drive(sex, competition, etc) in general. Neuroskeptic is a British neuroscientist who takes a skeptical look at his own field, and beyond. In this photo, a woman holds a packet of the antidepressant drug Prozac, also known as fluoxetine, in Leicester, central England February 26, 2008.
The findings have implications for the long-term health of those who suffer from the disease, especially for children and young adults.

They examined the brain magnetic resonance imaging results of 8,927 people, of whom 1,728 had major depression. People who had only experienced one depressive episode were found to have a normal-sized hippocampus. During the early 1960s, it was noticed that early antidepressant drugs, such as imipramine, all inhibited either the breakdown or the removal (reuptake) of chemicals in the brain called monoamines, including serotonin.
The authors gave lab rats a six-week Chronic Mild Stress treatment, a Guantanamo Bay-style program of intermittent food deprivation, sleep disruption, and confinement.
The black bars represent animals who were given injections of methylazoxymethanol (MAM), a cytostatic toxin which blocks cell division (rather like cancer chemotherapy). This second graph shows the number of hippocampal cells expressing KI-67, a protein which is a marker of neuroproliferation. Stress was found to reduce the volume of several areas of the rat’s brain, including the hippocampus and also the medial prefrontal cortex (mPFC).
Well, for one thing, it doesn’t prove that antidepressants work by increasing dendritic branching. It might well do, but this was a study in rats given huge doses of antidepressants (by human standards), so we really don’t know whether the findings apply to humans. In neuroscience, theories never live or die on the basis of single experiments (unlike in physics).
It’s funny how the staunchest monoamine bashers are often the most fervent neurogenesis acolytes. I think the fact that MDMA (ecstasy) causes an instant mood boost indicates that immediately increasing serotonin can have an impact on mood. His blog offers a look at the latest developments in neuroscience, psychiatry and psychology through a critical lens. The damage to the brain comes from recurrent illness,” Ian Hickie of the University of Sydney, who led the study’s Australian arm, told the Guardian.
This led many to conclude that antidepressants improve mood by raising monoamine levels, and that depression is probably caused by some kind of monoamine deficiency.
Chronic stress has various effects on rats, including increased anxiety and decreased time spent grooming leading to fur deterioration. This graph shows the effects of stress and antidepressants on the rat’s behaviour in the Forced Swim (Porsolt) Test. Further work found that antidepressants increase expression of NCAM1, a protein which is involved in dendritic growth. Cheekily, the authors come close to implying this in their choice of title for the paper, but the published evidence shows no direct evidence for this.

But it does suggest that the much-blogged-about neurogenesis hypothesis is not the whole story.
Perhaps the SSRI effect on neuronal dendritic spine morphology is mediated by the immune system.It is now known that microglia activity affects dendritic spine morphology.
The findings are right there in the title, but a little history is required in order to appreciate their significance.
For various reasons (not all of them good ones), it was later decided that serotonin was the crucial monoamine involved in mood, although for several years another, noradrenaline, was favored by most people.
Neurogenesis, the birth of new cells from stem cells, occurs in a couple of very specific regions of the adult brain, including the elaborately named subgranular zone (SGZ) of the dentate gyrus (DG) of the hippocampus. It had no effect on most other tests, although it did seem to make the rats more anxious in one experiment. MAM (black bars again) reduced neurogenesis, and in particular, it completely blocked the ability of antidepressants to increase it. Importantly, the authors found that following stress, the mPFC did not shrink because neurones were dying or because fewer neurones were being born, but rather because the existing neurones were changing shape – stress caused atrophy of the dendritic spines which branch out from neurones.
To find out, you would have to show that blocking the effects of antidepressants on dendrites also blocks their beneficial effects. The hippocampus is not an area generally thought of as being involved in mood or emotion, and damage to the human hippocampus causes amnesia, not depression. They found that this made two antidepressants (fluoxetine, aka Prozac, and imipramine) ineffective in protecting the animals against the detrimental effects of chronic stress.
The second pair of bars, representing the stressed rats who got placebo injections, is a lot higher than the first pair of bars representing rats who were not subjected to any stress. I suspect this is what the authors are now working hard to try to do, but they haven’t done so yet. Given that the purpose (if any) of adult neurogenesis remains a mystery, it’s entirely possible that neurogenesis has nothing to do with depression and mood. There are so many differences between the two experiments that there could be any number of explanations – the current study used rats, while Santarelli used mice, for one thing, and that could well be important. The other four pairs of bars are pretty much the same height as the first pair; these are rats who got antidepressants, showing that they were resistant to the effects of stress. Whatever the reason, this result suggests at the least that neurogenesis is not the only mechanism by which antidepressants counteract the effects of stress in animals.

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