Basic Science Of Depression And Anxiety Flashcards
Cognitive abnormalities such as impaired memory and feelings of hopelessness, worthlessness, and guilt come from
Hippocampus and prefrontal cortex
Mediates anhedonia (inability to experience pleasure) and decreased motivation
Nucleus Acumbens
Ventricular enlargement, increased CSF, and periventricular hyperintensity have been seen with
Depression
We also see reduced volume in caudate and basal ganglia, hippocampus, frontal cortex, and gurus rictus with
Depression
People that are at high risk for MDD have a thinner
Right lateral cortex
However, people who actually have MDD have a thinner
Left medial cortex
Smaller hippocampal volume may predispose to
PTSD
Smaller preventable anterior cingulate cortex volume may result from
PTSD
Activated head of the caudate, anterior cingulate gurus, and orbitofrontal cortex are neuronal activity correlates for
Obsessive-Compulsive Disorder (OCD)
Relates to Tourette’s and Huntington’s
-The same pathways are affected resulting in hyperactivity of motor function
OCD
Have fewer GABA receptors which results in increased activity in the amygdala and frontal cortex
Panic Disorder
Thus, what can we use to treat panic disorder?
Benzos, barbituates, alcohol, and steroids
Depression represents a decreased availability of either
5-HT, NE, or both
Typically shows decreased 5-HT, dopamine, and NE
Depression
Characterized by increased dopamine
Mania
Typically shows decreased GABA, increased NE, and altered 5-HT
Anxiety
What percentage of depression patients are treatment resistant?
30-46%
Problems in the glucocorticoid release feedback mechanism cause
Mood disorders
Mediate the neuroanatomical changes during stress and antidepressant treatment
Brain-Derived Neurotrophic Factor (BDNF)
Enhances dendritic branching and synapse number
BDNF
Can be affected by stress and neurotrophic should as well as other stimuli that have anti-depressant like effects
Neurogenesis
Stress and drug abuse inhibit
Neurogenesis
Neurogenesis is required for antidepressant actions. Thus lack of neurogenesis may result in
Depression-like behavior
In healthy people, when we inject dexamethasone, you will not release
Glucocorticoids
When injected with dexmethasone, still release glucocorticoids
Depressed Patients
Says that there are reduced levels of GABA which cause depression
GABA hypothesis
GABA levels are reduced in CSF and plasma and fewer GABAergic neurons in
Depression
Reduced glutamate neurotransmission causes
Depression
Inhibits NMDA receptors but increases AMPA receptor levels and thus has strong antidepressant effects
Ketamine
63% of SSRI resistant patients respond to
Ketamine Treatment
Patients with autoimmune diseases or treated with recombinant interferon often suffer from
Depression
Blocking cytokines pathways in mice has
Antidepressant phenotype
Increases his tone and DNA methylation causing reduced transcription of genes involved in antidepressant effects
Stress
Histone acetylation promotes transcription so histone deacetylase (HDAC) inhibitors act as
Antidepressants
Used to induce a grand meal seizure which increases sensitivity and number of 5-HT receptors and increases neurogenesis
Electroconvulsive Therapy (ECT)
The major side effect of ECT is
Retrograde amnesia
