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11 Cards in this Set

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MDD Neurotransmiter hypotheses
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
MDD brain imaging
KEY: Reduction in gray matter volume in hippocampus & prefrontal cortex!!!!


KEY: reduction in GLIAL CELL DENSITY AND NUMBER ergo cannot repair damaged neurons
Bipolar Neurotransmitter hypothesis
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
Bipolar brain imaging
↑ 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!!!
Panic Disorder Neurotransmitter hypothesis
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!
Panic Disorder Imaging
Panic may originate in an abnormally sensitive fear network which includes:
Prefrontal cortex
Insula
Thalamus
Amygdala
Amygdalar projections to brainstem and hypothalamus
SAD neuroimaging
OVERACTIVE AMYGDALA

Anxiety disorders might be characterized by hyperactivity of subcortical emotion-processing areas and hypoactivity of cognitive processing/“top-down control” areas
OCD neurotransmitter
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
OCD neuroimaging
OCD involves imbalance between direct and indirect pathways, leading to relatively greater excitation of the circuit, and resultant stereotyped behavior
Schizophrenia neurotransmitter
1) Dopamine: excess Dopamine

2)Glutamate: excess glutamate --> leads to neuron death

3)Gaba: HYPO-GABA
Schizophrenia Brain imaging
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