Mood Disorders & Emotion Circuits Flashcards
After receiving contextual information from the brain and sensory inputs from the body, where does the hypothalamus control outputs?
Autonomic Nervous System & Pituitary Gland (HPA axis)
What kind of influence does the cortex exert on the hypothalamus? What does this mean?
The cortex exerts an inhibiting influence on the hypothalamus which means that the subjective expression of emotion requires the cortex, while the visceral expression of emotional behaviors involves descending pathways from the hypothalamus.
Parasympathetics have long _______ with ganglia near the _______ _______. Sympathetics have long _______ with ganglia near the ______ _____.
Parasympathetics have long pre-ganglionics with ganglia near the target organ.
Sympathetics have long post-ganglionics with ganglia near the spinal cord.
What NT do all pre-ganglionics use?
Cholinergic
What NT do post-ganglionics have?
Parasympathetic: Cholinergic
Sympathetic: Adregneric
What is the hypothalamic-pituitary-adrenal axis? (HPA)
The hypothalamus stimulates release of NT from the anterior pituitary which stimulates the adrenal cortex to produce glucocorticoids which activates the body’s stress response.
What are the limbic areas involved in emotion and mood?
Cingulate gyrus, ventral striatum=nucleus accumbens, hypothalamus, amygdala, hippocampus
What is the overall effect of fear circuits?
Overall effect = arousal, vigilance - enhanced memories (so that we remember what situation caused the danger)
What is the cue versus context?
snake –> amygdala triggers fear response
zoo –> cortex & hippocampus dampens down the fear
What area of the brain makes dopamine?
Substantia nigra & ventral tegmental area
What part of the brain makes norepinephrine?
Locus Coeruleus
What part of the brain make serotonin?
Raphe Nuclei
What are the reuptake enzymes?
DAT= dopamine transporter NET= norepinephrine transporter SERT= serotonin transporter
What is MAO?
monoamine oxidase for enzymatic degradation on intracellular presynaptic cell or synaptic cleft
What is COMT?
degrades catecholamines in synaptic cleft and pre- and post- synaptic cells
What are treatments for anxiety?
Non-drug 1. CBT 2. eye movement desensitization & reprocessing Drugs that Act on GABA pathways Antidepressants Beta-blockers
What is the diagnostic criteria for Bipolar Disorder?
Depression symptoms + mania symptoms
What are the structural changes seen in depression?
Decreased gray matter volume & functioning in the prefrontal cortex and hippocampus. Pyramidal neurons are smaller and loss of GABAergic interneurons. Hippocampal atrophy, increased activity in amygdala (bigger cell bodies & more dendritic branching). The Anterior cingulate cortex may be activated
What does lithium do in depression?
Lithium strengthens both pre- and post- synaptic activity of CA1 neurons. Pre-synaptically Li+ enhances BDNF release which enhances LTP and post-synaptically Li+ prolongs the opening of AMPA receptors
Why is the HPA axis over-stimulated in stress?
Under normal conditions, the hippocampus exerts an inhibitory effects on the hypothalamus, but chronically elevated glucocorticoids and severe traumatic stress can cause hippocampal atrophy. Therefore this allows excessive hypothalamic activation of the HPA axis
What is the genetic basis of depression?
We know that there is a genetic link, but we don’t know exactly what it is.
What are the treatments for depression?
- MAOI
- SSRIs
- Psychotherapy
- Ketamine
How does ketamine work to treat depression?
Increases Glu in cortex by blocking NMDA receptors on interneurons so decreasing GABA
Why are anti-seizure meds prescribed to patients with bipolar depression?
Bipolar is like epilepsy in that over time it results in increased frequency and increased severity of episodes. Drugs that increase GABA prevent these gradual events in the CNS by increasing inhibition overall.
What pathway does Li+ work on?
Lithium may act on GSK3 (synthase kinase 3 that is part of Wnt signaling pathway)
