Brain and Behavior Test 4 Study Guide Stress and Health 1 What is a stressor 2 What is allostasis A stressor is anything that throws the body out of allostatic balance Allostasis is the range of measures appropriate for situation sleep vs bungee jumping 3 What are the 3 stages of a stress response 1 Alarm SNS activation 2 Resistance decreased SNS activity increased HPA activity cortisol and other hormones for maintaining prolonged alertness and increased immune function to fight infections and to heal wounds 3 Exhaustion NS and immune system are spent person is tired inactive and vulnerable to illness 4 What is the role of the sympathetic NS in the stress response 5 What is the HPA and what is it s role in the stress response The HPA is the hypothalamus pituitary gland and the adrenal cortex The hypothalamus makes CRH corticoptropic releasing hormone pituitary makes ACTH adrenocorticotropic adrenal secretes cortisol increase in blood sugar and metabolism The role of the HPA is activated with prolonged stress it is beneficial in the short term and detrimental in the long term acute activation of HPA boosts immune system and even improves memory 6 Why do you feel terrible during finals week Powerful inescapable temporary stress can lead to your body reacting with illness with increased immune activity body increases production of natural killer cells cell helps with fighting infection immune system gets tired more susceptible to illness 7 What are some effects of long term stress hippocampal damage reproductive effects decreased libido in women can inhibit mestrual cycle ovulation in women decreased sexual performance in men decreased immune function prolonged sickness syndrome increased blood sugar causes pancreas to release glucagon kidney damage Learning and Memory 1 What is an engram and what were Lashley s critical mistakes in looking for the engram Engram is a physical representation of a memory Lashley s mistake was he thought certain areas of cortex effected performance but it was really the size of the lesion TWO FALSE ASSUMPTIONS memory is in cortex all memories are physiologically the same 2 What are implicit memory and explicit memory What brain regions are important for each Explicit Memory remembering events episodic memory and knowing facts semantic memory Deliberate recall of info that one remembers as a memory brain regions hippocampus nearby cortical areas and medial diencephalon Implicit Memory skills and habits emotional associations and conditional reflexes the influences of recent experiences on behavior w o necessarily realizing that one is using memory brain regions striatum motor areas of cortex and cerebellum amygdala and cerebellum Both are types of long term memory 3 What are some differences b t short term memory working memory and long term memory What brain region is important for working memory Short term memory working memory small capacity fades quickly unless rehearsed once forgotten its gone where you parked your car Long term memory ex phone number and recalling school teacher infinite capacity lasts indefinitely could be forgetting and then recalled with appropriate cues Brain areas important in working memory is dorsolateral prefrontal cortex 4 What were some of HM s impairments what could he still do HM lost declarative explicit memory and spatial memory He still had intact procedural memory type of implicit and intact working memory 5 With regard to memory what are some functions of the hippocampus declarative explicit memory spatial memory consolidation short term can lead to long term 6 What other brain regions are important in learning and memory and what type of learning do they subserve cerebellum for learning a conditioned response and also for motor learning skills and cognitive stuff too parietal lobe if damaged don t spontaneously elaborate on memories temporal lobe damage causes semantic dementia prefrontal cortex learning reward and punishment and working memory 7 What is a Hebbian synapse Hebbian synapse is a synapse that increases in effectiveness because of simultaneous activity in pre and postsynaptic neurons 8 What is LTP What receptors are necessary LTP is long term potentiation LTP is a burst of stimulation from axons For example 100 excitations per second for 1 4 seconds onto dendrites can result in potentiated strengthened synapses for minutes days or weeks Glutamate receptors needed are AMPA and NMDA 9 What are some presynaptic changes that occur in LTP What are some postsynaptic changes that happen in LTP presynaptic changes retrograde transmitter from dendrite to axon terminal usually nitric oxide Decreased threshold for producing APs increased release of neurotransmitter expansion of axon and release of NT from more sites along axon postsynaptic changes more NMDA receptors in postsynaptic membrane 10 What is evidence that there is a functional connection between LTP and actual learning drugs that block LTP block retention of learned material drugs that facilitate LTP facilitate learning LTP increases certain proteins and blocking those proteins weakens memories IN PEOPLE partial NMDA agonist so ramp up excitability of synapses given with behavioral treatment for PTSD learn faster Alzheimer s Disease and other Dementias 1 What are some cognitive and non cognitive symptoms of dementia What are the 4 A s of demenita Impairment in memory and cognition accompanied by decreased ability to relate function at home work or social settings noncognititve symptoms delusions suspicions hallucinations agitation and depression 4A s of dementia amnesia loss of memory agnosia loss of ability to recognize objects apraxia loss of knowledge about how to do things aphasia loss of speech 2 What are some symptoms of Alzheimer s Disease AD deficits in explicit and implicit memory gradual progression to more serious memory loss language problems depression sleeplessness loss of appetite etc sundowning state of increased agitation activity and negative behaviors which happen in the day through the evening hours 3 What is the difference b t early onset and late onset AD Which one has a stronger genetic contribution Early onset AD people less than 40 years old gene on chromosome 21 gene for ApoE4 which breaks down beta amyloid other genes on other chromosomes linked to more of these cases Late onset AD over 60 years old some genes that increase risk but only account for small percent of cases Half of patients have no known relative with AD 4
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