PSYC414 Lecture Notes - Lecture 20: Dysbindin, Neuregulin, Rgs4
![](https://new-preview-html.oneclass.com/P39wlKzyDB5qj2bZ5WLejdnRobAW4M0g/bg1.png)
5/10
Developmental genes associated w/ risk for schizophrenia
❖ RGS4- regulator of G protein signaling 4 protein
o Metabotropic receptors – defect in this gene has effects on second –messenger;
can’t work properly
❖ DISC 1 – disrupted in schizophrenia 1 (cell proliferation, axonal migration)
o All this occurs really young; in embryo/after and during the first few years of life
o Increase in number of neurons, synapses, axons, etc. as we get older these ween
out
o If disrupted, neurons all over the place
❖ DTNBP1 – dystrobrevin-binding protein 1 (neural plasticity)
o Be flexible and learn new things is disrupted
❖ NRG1- neuregulin 1 (neural growth, proliferation)
o Early neural growth
❖ DAOA- D-amino acid oxidase activator- helps degrade D-serine
o D-Serine is a co-agonist for NMDA receptor)
o Too much activity developmental lasting effects
❖ COMT- Catechol-O-methyltransferase
o DA, NE, etc. enzyme that metabolizes DA
o Not working = too mcuch dopamine
❖ Genes are not regulated properly in development that leads to schizophrenia
Gray matter loss
❖ When you start seeing symptoms of schiz.
❖ Loss in PFC, temporal lobe, frontal/parietal cortex
Etiology of schiz.
❖ Early stage
❖ Genetic predisposition & gene expression
o Hereditary – one twin has it, runs in families, etc. have a certain gene structure
o + environmental insults including viruses, toxins, poor nutrition, birth
complications
▪ chaotic home life, mother having an infection during pregnancy (i.e., flu)
❖ neurodevelopmental abnormalities from conception to early adulthood including
neuron formation, migration, synaptogenesis, pruning, apoptosis
o stress, interaction w/ environment changes neuron development, migration
patterns may be off, synapses may be less/fewer/off, pruning = excessive; during
childhood we have an abundance of neurons, they start to prune back unless are
find more resources at oneclass.com
find more resources at oneclass.com
Document Summary
Developmental genes associated w/ risk for schizophrenia. Rgs4- regulator of g protein signaling 4 protein: metabotropic receptors defect in this gene has effects on second messenger; can"t work properly. Disc 1 disrupted in schizophrenia 1 (cell proliferation, axonal migration: all this occurs really young; in embryo/after and during the first few years of life. Increase in number of neurons, synapses, axons, etc. as we get older these ween out. Dtnbp1 dystrobrevin-binding protein 1 (neural plasticity: be flexible and learn new things is disrupted. Nrg1- neuregulin 1 (neural growth, proliferation: early neural growth. Daoa- d-amino acid oxidase activator- helps degrade d-serine: d-serine is a co-agonist for nmda receptor, too much activity developmental lasting effects. Comt- catechol-o-methyltransferase: da, ne, etc. enzyme that metabolizes da, not working = too mcuch dopamine. Genes are not regulated properly in development that leads to schizophrenia. When you start seeing symptoms of schiz. Loss in pfc, temporal lobe, frontal/parietal cortex.