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{{ClinPsy}}
  
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Early research into biological factors in depression centered upon monoaminergic theories with particular focus first on [[norepinephrine]] and later [[serotonin]].
⚫
[[Chemical imbalance (mental health)]]
  
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This work followed a number of pharmacological observations following the use of various compounds eg:
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*Reserpine, an early antihypertensive, caused depression in some patients and depleted monoamine stores in rat brain;
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*Iproniazid, a drug studied as an antitubercular agent, elevated depressed mood and inhibited [[monoamine]] degradation by the [[enzyme]], [[monoamine oxidase]];
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*[[Imipramine]], a tricyclic compound originally studied as an [[antipsychotic]],had marked [[antidepressant]] effects and blocked the reuptake of norepinephrine (and to some extent serotonin) into [[presynaptic neurons]].
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These observations led researchers to argue that norepinephrine activity was decreased in depressive disorders and elevated in manic or excited states.
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This was idea was further developed by [[Schildkraut]]’s [[catecholamine hypothesis of depression]]
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Other researchers proceeded by comparing groups of normal and depressed people and identified a number of differences in depressives.
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*Elevated [[corticotropin-releasing hormone]] (CRH);
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*Elevated [[acetylcholine]] activity;
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*Increased [[Gamma-aminobutyric acid]] (GABA) levels;
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*Excessive [[glucocorticoid]] activity in psychotic major depression;
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*[[Hippocampal]] volume loss,perhaps reflecting the effects of excessive [[glucocorticoids]] on[[neurogenesis]] .
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On the basis of these differences hypotheses have been developed for the causal role of a number of mechanisms in depression these include:
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  ⚫
[[Chemical imbalance (mental health)|Chemical imbalance theory of mental health]]
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*[[Depression and beta-endorphin]]
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*[[Depression and Brain-derived neurotropic factor]]
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*[[Depression and catecholamines]]
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*[[Depression and norepinephrine]]
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*[[Depression and dopamine]]
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*[[Depression and GABA]]
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*[[Depression and dynorphin]]
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*[[Depression and L-dopa]]
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*[[Depression and serotonin]]
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*[[Depression - 5-Hydroxytryptophan|Depression and 5-Hydroxytryptophan]]
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===Key texts – Papers===
 
===Key texts – Papers===
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*Schatzberger,AF, Garlow, SJ and Nemeroff,CB, Molecular and cellular mechanisms in depression.[http://www.acnp.org/Docs/G5/CH72_1039-1050.pdf Full text]]
   
   
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[[Category:Depression]]
  
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[[Instructions_for_archiving_academic_and_professional_materials]]
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'''Neurochemistry of depression: Academic support materials'''
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*[[Neurochemistry of depression: Lecture slides]]
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*[[Neurochemistry of depression: Lecture notes]]
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*[[Neurochemistry of depression: Lecture handouts]]
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*[[Neurochemistry of depression: Multimedia materials]]
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*[[Neurochemistry of depression: Other academic support materials]]
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*[[Neurochemistry of depression: Anonymous fictional case studies for training]]
   
   
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[[Category:Depression ]]
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{{Psych-stub}}
  
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[[Category:Neurochemistry]]
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[[Category:Neurochemistry of depression]]

Latest revision as of 11:57, 12 December 2008

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Early research into biological factors in depression centered upon monoaminergic theories with particular focus first on norepinephrine and later serotonin.

This work followed a number of pharmacological observations following the use of various compounds eg:

  • Reserpine, an early antihypertensive, caused depression in some patients and depleted monoamine stores in rat brain;
  • Iproniazid, a drug studied as an antitubercular agent, elevated depressed mood and inhibited monoamine degradation by the enzyme, monoamine oxidase;
  • Imipramine, a tricyclic compound originally studied as an antipsychotic,had marked antidepressant effects and blocked the reuptake of norepinephrine (and to some extent serotonin) into presynaptic neurons.

These observations led researchers to argue that norepinephrine activity was decreased in depressive disorders and elevated in manic or excited states. This was idea was further developed by Schildkraut’s catecholamine hypothesis of depression

Other researchers proceeded by comparing groups of normal and depressed people and identified a number of differences in depressives.

On the basis of these differences hypotheses have been developed for the causal role of a number of mechanisms in depression these include:


Chemical imbalance theory of mental health


  • Depression and beta-endorphin
  • Depression and norepinephrine
  • Depression and dopamine
  • Depression and GABA


See also

Bibliography

Key texts – Books

Additional material – Books

Key texts – Papers

  • Schatzberger,AF, Garlow, SJ and Nemeroff,CB, Molecular and cellular mechanisms in depression.Full text]


Additional material - Papers

External links

Instructions_for_archiving_academic_and_professional_materials

Neurochemistry of depression: Academic support materials

  • Neurochemistry of depression: Lecture slides
  • Neurochemistry of depression: Lecture notes
  • Neurochemistry of depression: Lecture handouts
  • Neurochemistry of depression: Multimedia materials
  • Neurochemistry of depression: Other academic support materials
  • Neurochemistry of depression: Anonymous fictional case studies for training
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