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Depression & bipolar
Uni of Notts, Neurobiology of disease, second year, topic 6
| Term | Definition |
|---|---|
| Core depression symptoms (9) | Low mood, anhedonia, appetite changes, sleep changes, fatigue, guilt, poor concentration, psychomotor changes, & suicidal ideation or attempt |
| Diagnostic requirements of major depressive disorder | ≥5 of 9 symptoms for at least 2 weeks, including low mood &/or anhedonia |
| Manic episode | ≥1 week of elevated/irritable mood plus ≥3 symptoms like grandiosity, reduced sleep, pressured speech, impulsivity, & distractibility present most of the day for most days |
| Characteristics all bipolar subgroups share | All involve episodes of mania or hypomania |
| Monoamine hypothesis of depression & bipolar (Schildkraut, 1965) | Depression results from monoamine functional deficit, while mania results from monoamine functional excess |
| Experimental evidence of monoamine hypothesis | Reserpine depleted monoamines & caused depressive symptoms; Iproniazid (MAO-B inhibitor) increased monoamines & improved mood |
| Flaws of monoamine hypothesis | It doesn’t explain delayed antidepressant effects, treatment resistance, why drugs like cocaine aren’t antidepressants, & why some antidepressants don't even affect monoamines |
| How HPA changes in depression | Higher activation increasing CRH in CSF & cortisol in bodily fluids; & impairs negative feedback, leading to chronic stress signalling |
| Structural endocrine changes in depression | Enlarged pituitary & adrenal glands/cortex |
| How antidepressants affect HPA | Some restore negative feedback regulation |
| How depression affects hippocampal volume | Associated with ~10% reduced hippocampal volume |
| Neuroplasticity hypothesis of depression (& how antidepressants support it) | Mature neurons undergo atrophy, reducing connectivity. Antidepressants increase BDNF, promoting dendritic spine growth & synaptic plasticity |
| Neurogenesis hypothesis of depression | Fewer new neurons & precursor cells are formed |
| How inflammation is linked to depression | Higher cytokines, chemokines, & acute phase proteins (inflammatory markers) are associated with depressive symptoms |
| How cytokine-altering illnesses support the inflammation hypothesis (& a counterargument) | Diseases/drugs affecting cytokines can trigger depressive symptoms. However, disorders causing inflammation & pain may also cause depressive symptoms on their own |
| How CBT helps depression | Breaks negative cycles between thoughts, mood, behaviours, & physical functioning |
| How SSRIs treat depression, why they're first-line antidepressants, & why they have side effects | Block SERT to increase synaptic serotonin with safer side effects & lower overdose toxicity (good in suicidal patients) but by increasing all serotonin pathways, some may oppose each other leading to side-effects |
| How tricyclic antidepressants work & their downsides | Block serotonin & noradrenaline reuptake but also block histamine, muscarinic, & α1 receptors → more side effects |
| How SNRIs work & their downsides | Inhibit serotonin & noradrenaline reuptake but may raise blood pressure |
| Mirtazapine | Enhances noradrenaline/serotonin signalling & causes sedation that may help sleep (sleep disturbances form positive feedback with depression) |
| Unforseen dangers of MAOIs | They prevent tyramine (from cheese) breakdown, causing hypertensive crisis via excess noradrenaline release |
| Why SSRIs take weeks to work | 5-HT1A autoreceptors initially reduce serotonin firing until they desensitise, while BDNF-driven plasticity takes weeks |
| Ketamine treatment | NMDA antagonism increases glutamate signalling through AMPA pathways, activating mTOR & BDNF plasticity pathways |
| Vagus nerve stimulation | Implanted electrodes near collarbone stimulate the vagus nerve to treat resistant depression |
| Psychedelic therapy | 5-HT2A agonism may rapidly alter neural connectivity & mood |
| How lithium functions in bipolar & its downsides | Reduces dopamine/glutamate signalling & increases GABA activity but has a narrow therapeutic window (~0.6–1.2 mmol/L); toxicity can cause renal/neuro effects such as extreme seizure |
| Valproate & its downsides | Blocks voltage gated Na+ channels, increases GABA synthesis, & stabilises mood but can lead to developmental & cognitive defects of unborn children if taken during pregnancy |
Created by:
Denny12
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