Depression

Question 1

anterior cingulate cortex

Answer 1

• Rostral and caudal
• Abnormal function during major and bipolar depressive phases most associated with the rostral subdivision
• Patients with depression have higher activity in the anterior cingulate cortex
• More likely to be successfully treated with monoamine therapy

Question 2

vmPFC

Answer 2

• Projects to hypothalamus and periaqueductal gray
• Mediate the visceral autonomic activity associated with emotion
• Emotional or affective functions
• Patients with bilateral vmPFC lesions had lower levels of depression

Question 3

diPFC

Answer 3

• Receives input from sensory cortices
• Dense interconnections with premotor areas, lateral parietal cortex
• Distinct connectivity
• Cognitive or executive functions
• Bilateral dlPFC lesions had higher levels of depression

Question 4

Hippocampus

Answer 4

• One of the biggest regions involved in depression

- Studies indicate reduced volume of hippocampus in individuals with depression

Question 5

Hypothalamic-pituitary-adrenal axis HPA

Answer 5

• fear response
• longer term effects
• Leucocortorids

Question 6

Monoamine Hypothesis

Answer 6

• Dopamine, norepinephrine, adrenaline, serotonin
• The Mono Amine Oxidase MAO breaks these transmitters down
• Depression is associated with reduced monoamine activity
• Monoamine based antidepressants are the biggest line of treatment
• Takes SSRI’s up to 6 weeks to work on treating depression

Question 7

Neurogenesis

Answer 7

• Adult neurogenesis in the dentate gyrus is treatment of depression
• Neurogenesis hypothesis of depression postulated that decrease in new granule cells related to pathophysiology of depression and recovery of neurogenesis is related to treatment
• Hippocampal atrophy, neurogenesis, and depression are related
• Chronic stress found to atrophy of apical dendrites, suppression of adult neurogenesis
• Corticosterone and cortisol HPA response, increases stress

Question 8

HPA Axis

Answer 8

• Stress activates the axis causes the PVN (paraventricular nucleus) to release CRH and AVP
• This causes the anterior pituitary to release ACTH (adrenal cortico hormone)
• ACTH causes adrenaline release by the adrenal cortex
• Glucocorticoids are stress responses, diverts energy from non essential to muscles and heart for flight or fight response, longer response
• Adrenal medulla release adrenaline which if the right away fear
• This takes long because the chemical signal from the brain down to the pvn and etc
• Adrenalin and glucocorticoids from the adrenal cortex mobilize energy for action
• The hippocampus exerts negative control over this system to inhibit the PVN and its release of CRH and AVP

Question 9

Stress and Depression

Answer 9

• The hippocampus has high levels of glucocorticoids receptors
• Chronic activation of the HPA axis leads to chronic activation of the glucocorticoid and mineralocorticoid receptors
• Leads to decrease in action on hippocampus and an inability for the hippocampus to negatively feed back on the HPA axis
• SSRI’s increase hippocampal neurogenesis
• But blocking neurogenesis does not cause depression but neurogenesis is necessary for recovery using SSRIs
• HPA axis does cause atrophy and depression
• When you recovery you form hippocampal connections to amygdala, nucleus accumbens, and prefrontal cortex
• Down regulating bdnf is related to depression hpa and hippo

Question 10

Resilience

Answer 10

• Refers to the capacity of an individual to avoid negative social, psychological, and biological consequences of extreme stress
• increased VTA firing rate is associated with increased depression
  
  • Increased bdnf in nucleus accumbens (opposite of hippo)
  • Resilient mice escaped this vulnerability by downregulating the excitability of the vta by increasinG the number of K+ channels in the VTA
• Increased PAG transcription factor associated with reduced depression
  
  • Blocks release of substance P and increasing production of transcription factor