depression

Question 1

Symptoms and causes

Answer 1

Genetic predisposition, pain, trauma, and grief are common causes. multifactorial.

Psychologic symptoms include anhedonia, negative effect (e.g., fear, suicidal thoughts), and despair

Can have physiological symptoms such as sleep disturbance, loss of appetite/libido/energy, unexplained pains.

Also leads to social symptoms, with neglected self care, loss of interests/hobbies, and inability to properly function in work and social settings.

Question 2

SSRIs mechanism and function, and binding sites.

Answer 2

Inhibit SERT, which brings 5-HT back into the neurone. Prolongs the 5-HT in the synaptic cleft, and increases tonic EC [5-HT].

Citalopram binds to central site, but can also bind to an allosteric site.

Desensitisation of the 5-HT-1A/5A autoreceptors reduces their negative feedback of the 5-HT system.

Question 3

Glutamate hypothesis of depression

Answer 3

Sees changed [glutamate] in plasma and CSF in depression.

Ketamine found to be atypical antidepressant.

May be mediated by mGluRs and NMDARs link to synaptic plasticity.

Question 4

Neuroplasticity hypothesis, BDNF, and neurological changes to brain anatomy

Answer 4

Changes in volume, connectivity and neurogenesis in different regions of the brain lead to the onset of depression.

A meta-analysis saw reduced grey matter volume and reduced white matter integrity, some regions are unusually active, while others were found to be unusaully inactive.

Largely believed to be due to the role of BDNF, and its regulation of neuroplasticity and (hippocampal) neurogenesis.

Believed that SSRIs may partially function by upregulating BDNF, SSRIs found to also directly bind to TRKB (BDNF receptor)