neuro exam 4

• what is tryptophan


  serotonin precursor
• what is conduct disorder


  persistent aggressive or antisocial behavior that disrupts the child's environment and impairs his or her functioning
• what is psychopathy


  lack of concern about performance, shallow, lack of remorse or guilt, callousness
• what is cognitive empathy


  representation of intentions and thoughts of another individual
• what is emotional empathy


  affective responses to emotional displays of other individuals and to verbal descriptions of the emotional states of others
• what parts of the brain are associated with psychopathy

  amygdala, insula, prefrontal cortex
• how are psychopathy and autism different

  psychopathy has an intentional aspect to the lack of interpersonal connections whereas people with autism don't have the awareness to create interpersonal connections
• Why would serotonin and oxytocin be involved in callous unemotional behavior


  oxytocin is involved in socialization and maternal feeling-- it increases socialization and involves the reward pathway
• what are risk factors for psychopathy


  early childhood adversity, exposure to violence, substance abuse, brain region abnormalities, genetics
• "disturbances in emotional responsiveness"

  does not respond to emotional situations normally -- less remorse not as much empathy, etc
• psychopathy medications


  lithium, phenytoin, serotonin re-uptake inhibitors
• why are psychologists hesitant to treat psychopaths

  not a lot of success
• what regions are involved in the social network

  NAc, amygdala, VTA, ACC, mPFC, insular cortex
• ACC role in autism


  mediates observational fear learning
• insular cortex role in autism


  sensory information
• mPFC role in autism


  social interaction, understanding and contextualization
• dopamine and serotonin in autism


  dyregulation does not associate reward with social interaction
• what often co-morbids autism


  ADHD, anxiety, depression, epilepsy
• environmental risk factors for autism


  advanced parental age, birth trauma, close together pregnancies
• passive vs active case finding in autism

  passive: checking records

  active: going into the community
• de novo mutations vs common genetic variations in ASD

  de novo: alterations in germ cells that are rare with large effects

  CGV: alterations that may interact with genetic and environmental factors that are more common with smaller effects
• Tuberous sclerosis


  a systemic disorder that leads to the development of tumors within various organs
• Fragile X


  most common genetic cause of mental retardation in which a defective gene results in a weak spot on the X chromosome which makes it susceptible to breakage
• what type of proteins are affected in ASD

  scaffolding proteins
• ASD medications


  risperidone and aripiprazole
• ASD medication drawbacks


  weight gain
• what is MDD


  persistent feelings of sadness, hopelessness, and a lack of interest or pleasure in activities
• what are the risk factors for depression


  traumatic experience, genetic makeup, abnormal function of HPA axis, inflammatory cytokines, hormonal imbalance, chronic stress
• brain areas involved in MDD

  reduced volume in PFC, loss of neurons and glia in the PFC and hippocampus, lack of synaptic plasticity, HPA axis
• what are glucocorticoids


  steroids responsible for the body's response to stress; chronic increase decreases synaptic number and function
• what is the mTORC1 pathway


  pathyway for synaptic plasticity and translation of synaptic proteins; neuronal sensor for activity; antidepressants stimulate the pathway
• What is BDNF

  protein that promotes growth and development of neurons; chronic stress and depression decrease the expression
• what is the impact of BNDF on Val66Met

  Val66Met blocks the processing and release of BDNF and causes atrophy of neurons in the hippocampus and PFC
• why is depression 2X more common in women

  hormonal fluctuations
• what is the role of insulin in depression

  insulin resistance causes a disruption in BDNF and mTORC1 pathway
• why not treat patients with BDNF

  it is too large to pass the blood brain barrier
• what mechanisms may underly the success of ECT therapies for depression

  able to induce rapid, synaptic activity, increase in BDNF expression in the hippocampus and PFC
• what problems are associated with SSRI therapies

  they take weeks to work
• what is ketamine

  dissociative anesthetic
• how does ketamine work as an antidepressant

  NMDA glutamate receptor antagonist and increases synaptic glutamate release; signals mTORC1 pathway