intro to neuro exam 4

learning

change in behavior as a result of experience

memory

ability to recall or recognize based on previous experiences, implies mental representation or memory trace

declarative memory

things you know that you can tell others

nondeclarative memory

procedural; things you know that you can show by doing

immediate memory

ability to hold ongoing experiences in mind for fractions of a second

working/short-term memory

hold information in mind for seconds to minutes to achieve a goal, requires attention l

long-term memory

retaining information for days, weeks, life

memory consolidation

occurs between working and long-term memory, requires rehearsalam

amnesia

partial of total loss of memory

retrograde amnesia

deficit in recalling previous information

anterograde amnesia

deficit in learning new information

patient HM had _ amnesia after having his _ removed and he was of the surgery but he had memories, he retained the ability to form new memories (procedural learning)

anterograde, hippocampus, unaware, older, implicit

patient HM is an example of a _ (non-declarative) memory because he learned how to do the task without having (declarative) memory of learning it

procedural, conscious

korsakoff’s syndrome is caused by a _ (vit B1 deficiency) due to prolonged intake of large amounts of     , characterized by both   , and     amnesia; however patients are generally   to suggestions they have a memory problem; most patients show   and   activity in the frontal lobe of the   

thiamine, alcohol, retrograde, anterograde, indifferent, atropy, decreased, cortex

patient KC cannot retrieve _ memory due to accidental damage to cortex; his damage accounts for his amnesia, but not for loss of episodic memory

personal, hippocampal, anterograde

semantic memory

generalized declarative memorye

episodic memory

detailed autobiographical memory

brain-imaging studies show that _ and memories are processed and stored in different locations

semantic, episodic

patient KC can recall facts about himself but has _ memory of any events that included him → amnesia

no, episodic

patient JK suffered from _ disease which is the dysfunction of the basal ganglia; demonstrated in motor tasks or types of memory that seemed ; perfectly intact an memory → must be in different places

parkinsons, disruption, implicit, episodic, declarative, storage

hippocampal place cells are neurons that _ firing rates when a mouse walks/runs through a specific point in a previously learned maze; each new circumstance leads to a new neural     of space;     representations and sequences of activity are thought to be learned in hippocampal    ; involves     strengthening at    /    synapses

increase, representation, spatial, circuits, synaptic, CA1, CA3

synapses in learning cause relatively _ change in behavior that results from experience and is mediated by changes in synapses but neurogenesis

permanent, structural, not

neuroplasticity

nervous system’s potential for neurophysical or neurochemical change that enhances its adaptability to environmental change and its ability to compensate for injury

memory traces are stored in the brain through: changes in or of synapses and changes in strength → LTP

structure, number, synaptic

long-term potentiation (LTP)

changes in synaptic strength; long-lasting, activity-dependent, synaptic enhancement

hippocampal LTP: stimulate collaterals and record neurons: low frequency pulse evokes and after high frequency stimulation response is and it will increase the EPSP amplitude

schaffer, CA1, EPSPs, potentiated

LTP mechanism with single stimulus: stim → release     into synaptic cleft → binds to glutamate receptors on     dendrites

glutamate, CA1

AMPA

depolarizes membrane though Na+ influx

NMDA

normally blocked by magnesium

LTP mechanism for tetanus: depolarization to results in being expelled from receptor → acting on NMDA receptors opens / channel → triggers the activation of that cause the synthesis of proteins and insertion of new receptors

-35mv, magnesium, NMDA, glutamate, Na+, Ca2+, Ca2+, protein kinases, AMPA

evidence for LTP as a memory mechanism:

• induced within    

• long-   

• labile consolidation period (sensitive to    )

• induced at     frequencies

• correlates with maze learning

• drugs that block learning block     

• enriched environments promote     and    

seconds, lasting, disruption, physiological, LTP, learning, LTP

long-term depression (LTD)

long-lasting reduction in synaptic efficacy, small increase in Ca2+ activates protein phosphatases to dephosphorylate proteins that normally yield LTP

LTP and LTD may be responsible for sculpting the NS to respond to

• LTP strengthens critical for

• LTD weakens that interfere with performance

environment, synapses, performance, synapses

mass action principle

degradation of learning and memory depends on the amount (not the type) of cortex destroyed

dementia

progressive decline in mental function, memory and intellectural skills; defined as memory impairment plus: aphasia, apraxia, agnosia, or problems with executive functioning; age-related

aphasia

language problems

apraxia

complex movement problems

agnosia

problem identifying objects

senile plaques

extracellular, B-amyloid (exists as a molecular fragment of a large protein found in normal brain)

tau tangles

intracellular, abnormal accumulation of tau

alzheimers disease

neuronal cell loss and changes in neuronal morphology, specific loss of ACh-containing neurons, decreased brain weight, atrophy of the cortex, enlarged ventricles

nucleus basalis

produces ACh

best course of treatment for AD

try to compensate for the loss of cholinergic neurons and inhibit the degradation of ACh

which condition must be met to induce LTP?

all of the above

• glutamate must be released from the presynaptic terminal

• glutamate must open the postsynaptic AMPA receptors

• postsynaptic membrane must be depolarized to -35mV

  • Mg2+ block must be expelled from NMDA receptors to allow Ca2+ influx

which of the following is false regarding LTP?

drugs that block learning, enhance LTP

the proposed circuit involved in the rewarding and reinforcing effects of abused drugs incorporates many neuroanatomical structures but does not include the

cerebellum

pyramidal motor pathway

voluntary movement, “fake smile”

voluntary facial paresis

can’t fake a smile because of lesions in the motor cortex and brainstem

extrapyramidal motor pathway

emotional, automatic movement, duchenne smile

emotional facial paresis

can’t smile emotionally

papez circuit

proposed circuit for emotional processing, projects to hypothalamus

what is the papez circuit missing?

amygdala and frontal cortex (emotional centers)

hypothalamus

neuroendocrine function through connects with pituitary gland

hypothalamus and emotions: _ expression of emotions though activation of     system with expression of     and     defensive behaviors→ changes in    ,     ,      

autonomic, sympathetic, innate, conditioned, heart rate, temperature, sweating

“sham rage”

removed both cerebral hemispheres of animals → animals acted enraged → occurred spontaneously

the hypothalamus coordinates the and motor components of emotional behavior

visceral, somatic

hypothalamus is and for the coordinated rage response

necessary, sufficient

necessary

without the hypothalamus, no rage responsesu

sufficient

with the hypothalamus, but no cortex, there is a coordinated response

amygdala

missing piece of the emotional puzzle, responsible for relating sensory stimuli with emotional experience, site of associative learning

connectivity between and higher areas are required for higher order processing of and ultimately

amygdala, cortical, emotions, behavior

bilateral lesions of the amygdala

• physically unable to    

• cannot     fear in facial expressions

• does not have a concept of    

• does have     response that does     depend on the amygdala

• can follow group fear     due to voices and body language in others

feel fear, recognize, personal space, startle, not, responses

some emotional response are but most emotional response are this they depend on

innate, learned, experience

emotional learning

construction of implicit memories linking a situation or event to an emotional body state, can be conscious but is often subconscious

fear conditioning

innate reflex is modified by associating the normal trigger with an unrelated stimulus

fear conditioning mechanism:     paired with a     → experience of shock is relayed as pain (   ) → associated is learned by strengthening of the auditory inputs through     → leads to better activation of     circuits by the tone → enhances     responses

CS, US, negative reinforcement, LTP, amygdala, survival

fear conditioning and memory require brain regions → require for fear but not and not required for fear learning but required for

different, amygdala, memory, hippocampus, memory

nigrostriatal (dorsal striatum) DA projections

motorm

mesolimbic (ventral striatum) DA projections

reward

mesocortical DA projections

alertness, executive functions

emotional processing by the system guides behavioral choices by signaling impending and

limbic, reward, punishment

DA signaling in Nac is important for reinforcement of movements → DA signaling increases to perform these behaviors again in the future → DA inputs to NAc = emotional circuit

behavioral, motivation, reward

the reward synapse

VTA to NAc

VTA

source of DA sending projections to NAc

NAc

receives DA inputs from VTA

all addictive drugs produce an increase of

dopamine

basal ganglia

increases motor output to produce an overall increase in behavior

the hippocampus

tells the NAc our context

prefrontal cortex

provides NAc with options for behavior

rats will work to electrically stimulate the pathway → blockade of DA receptor signaling in the NAc will these behaviors

DA, eliminate

DA neurons in the VTA change their     patterns during     learning

activity, reward

nicotine

• binds to receptors on VTA neurons causing

• increases release onto VTA neurons

• both effects DA release

ACh, depolarization, glutamate, increase

cocaine and amphetamine

• block DA into VTA axon terminals → increasing the effect of DA

reuptake

opiates

• bind to opioid receptors on axon terminals of     interneurons

• opiates are     and decrease     release

• this     VTA neurons and increases DA release

GABAergic, inhibitory, GABA, disinhibitsad

addiction

• corruption of DA system

• drugs     increase DA levels in situations that would usually have     levels of DA

• affects    /    of reward

• reinforce addictive behavior by increasing DA at the     time/circumstance

artificially, lower, perception, processing, wrong

D2 receptors + Anhedonia

• addicts were found to have     D2 receptor expression and baseline DA release

• changes cause a    response to natural rewards such as food and sex

• addicts don’t feel    unless they have DA levels increased by drugs

lower, blunted, normal

lateralization of function

certain cognitive processes or behaviors are more dominantly controlled by one hemisphere of the brain rather than another

broca’s area

left frontal love, speech production and grammatical structure

wernicke’s area

left temporal lobe, language comprehensiona

arcuate fasciculus

connects broca’s and wernicke’s, repeating and integrating spoken language

primary auditory cortex

temporal lobe, processes sounds

angular gyrus

parietal lobe, reading, writing and connecting visual information to language

aphasia

a disorder that impairs a person’s ability to process language but does not affect intelligence

most common cause of aphasia

strokeb

broca’s aphasia

• motor, aphasia

• disruption of production and

• problems with written, spoken, “signed”

• patients cannot produce , but can understand it

• patients are acutely of their problem

expressive, language, organization, language, speech, aware

wernicke’s aphasia

• sensory/    aphasia

• language produced, sounds normal, but much of it makes no     

• many patietns seem to be completely     of their problem

receptive, sense, unaware

brain mechanisms:

• spoken word → → wernicke’s area (contains sound of ) → comprehend word

• thought → → broca’s area (stores programs for words) → facial area of cortex → cranial nerves →

A1, images, words, heard, wernicke’s area, motor, speaking, motor, speak

conduction aphasia → damage to

• patients have problems producing appropriate to language even though language is

• characterized by poor repetition

• patients seem to lose their train of

arcuate fasciculus, responses, understood, speech, thought

evidence for both general and localized brain function:

• most aphasics have a mixture of     and     problems

• clinical syndrome’s usually involve     that spread beyond     regions

• substantial recovery of     after damage

expressive, receptive, damage, localized, language

role of right hemisphere

• prosody →     of speech

  • includes the rhythm, timing, emphasis, volume, pitch to convey     and     emphasis

coloring, emotion, grammatical