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11 Cards in this Set
- Front
- Back
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MDD Neurotransmiter hypotheses
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1. Monoamine deficiency hypothesis
a. Result of the deficiency of monoamines (serotonin, dopamine, norepinephrine) b. Acute increases in monoamines produce secondary neuroplastic changes (transcriptional/translational) 2. Amino acid neurotransmitter system dysregulation a. Glutamate dysfunction plays a role in the pathophysiology of MDD (chronic stress --> excess glutamate --> hyperactivation of NMDA receptors--> death of neurons and glial cells 3. Neuroendocrine dysregulation increase cortisol →less negative feedback → toxic effects on hippocampus |
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MDD brain imaging
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KEY: Reduction in gray matter volume in hippocampus & prefrontal cortex!!!!
KEY: reduction in GLIAL CELL DENSITY AND NUMBER ergo cannot repair damaged neurons |
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Bipolar Neurotransmitter hypothesis
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Hypothalamic-pituitary-thyroid axis dysregulation
Hypothalamic-pituitary-adrenal axis dysregulation Loss of sensitivity of glucocorticoid receptors --> impaired feedback inhibition in HPA axis --> elevated levels of corticosteroids Cortisol may lead to increase in inflammatory cytokines and disrupt immune response |
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Bipolar brain imaging
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↑ lateral ventricular volume with successive manias
Thinning of dorsolateral PFC with increased illness duration ↓ gray matter volume of anterior cingulate cortex ↓ activity in the lateral orbital prefrontal cortex in mania ↑ activity in the anterior cingulate in mania ↑activity in amygdala SAME AS MDD!!! |
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Panic Disorder Neurotransmitter hypothesis
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1) SEROTONERGIC DYSFUNCTION
↓ 5HT1A receptor binding in cingulate cortex & raphe nucleus (PET).. Hence, SSRIs treat panic disorder--> Serotonin has INHIBITORY effects on locus ceruleus, hyopothalamus, and periaqueudctal gray region 2) NORADRENERGIC THEORY Locus coerulues (that makes norepi) have increased noradrenergic transmission If stimulate locus coeruleus in animals will give fear response! If give patients an alpha antagonist they have more panic attacks, but don’t know for sure Panic disorder associated with increased activity and sensitivity of noradrenergic system 3) (GABA) - Benzodiazepine Receptor System Similarly the GABA system = inhibitory system Benzodiazepines bind to GABA-A receptor and decreased binding to this receptor lead to panic disorder Ergo felt there are FEWER GABA-A RECEPTORS --> LESS GABA -->PANIC! |
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Panic Disorder Imaging
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Panic may originate in an abnormally sensitive fear network which includes:
Prefrontal cortex Insula Thalamus Amygdala Amygdalar projections to brainstem and hypothalamus |
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SAD neuroimaging
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OVERACTIVE AMYGDALA
Anxiety disorders might be characterized by hyperactivity of subcortical emotion-processing areas and hypoactivity of cognitive processing/“top-down control” areas |
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OCD neurotransmitter
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1) Serotonin Hypothesis: given SSRI work,assume has to do with low serotonin (no support for this)
2) Glutamatergic Involvement: Association with glutamate transporter gene SLC1A1 Increased caudate glutamate by MRS Elevated CSF glutamate |
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OCD neuroimaging
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OCD involves imbalance between direct and indirect pathways, leading to relatively greater excitation of the circuit, and resultant stereotyped behavior
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Schizophrenia neurotransmitter
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1) Dopamine: excess Dopamine
2)Glutamate: excess glutamate --> leads to neuron death 3)Gaba: HYPO-GABA |
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Schizophrenia Brain imaging
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Enlarged Ventricles
Shrunken Temporal Gyri Decreased white matter tracts Increased cortical cell density & LOW HIPPOCAMPAL VOLUME New theory: OLIGODENDROCYTES are greatly reduced in prefrontal cortex |
