Behavioral Neuroscience FINAL exam

neurolinguistics

neural mechanisms mediating comprehensin, production, and acquistion of language

language circuit steps

1. hear/see language

2. signal sent to posterious language area (PLA)

3. signal sent to association/memory areas

4. back to PLA

5. signal sent to wenicke’s area

6. signal sent via arcuate fasciculus to broca’s area

7. signal sent to insular cortex and/or primary motor cortex (Speech or write)

8. signal sent to cerebellum if needed

9. further downstream

aphasia

impairment in language comprehension/production by brain damage

alexia

inability to read

agraphia

inability to write

broca’s aphasia

inarticulate speech and difficulties using and understanding grammatical device - damage in medial left frontal lobe

agrammatism

difficulty in comprehending grammatical devices, such as verb endings and word order

anomia

difficulty in finding the appropriate word to decribe something

articulation difficulty

mispronunciation of words often altering sequence of sounds

wernicke’s aphasia

poor speech comprehension and fluent, but meaningless - damage in the left temporal lobe

pure word deafness

ability to hear and speak and usually to read and write without being able to comprehend meaning of speech

anosognosia

lack of self-awareness regarding disability, easiliy frustrated when others don’t understand

engram

physical representation of what has been learned (memory)

equipotentiality

capacity of intact brain areas to carry out memory functions of other lost (via destruction) areas

bilateral medial temporal resection

almost complete destruction of hippocampus

organic amnesia

memory loss resulting from brain damage

retrograde amnesia

difficulty retieving old memories

anterograde amnesia

difficulty forming new memories

morris water maze

inescapable tub filled w murkey water containing rest platform just below the surface

nature vs nurture

importance of biological predispositions (nature) and environmental influences (nurture) as deteminats of human behavior and ability

behavioral genetics

how genotype interacts w/ environment to determine behavioral attributes

heritability

amount of variability in a trait that is attributable to hereditary factors

selective breeding

breeding animals possessing a desirable characteristic

family study

investigation of an attribute within a household as a function of kinship

twin study

compare MZ twins vs DZ twins

adoption study

adoptees compared to biological parents vs adoptive parents

correlation coefficient (R)

calculated value ranging from +1 to -1 reflecting strength and direction of a relationship between 2 variables

heritability coefficient

numerical estimate, ranges from 0 to 1 of amount of variation in an attribute due to hereditary factors

H² = (rMZ twins - rDZ twins) x 2

nonshared environmental influence

people living together do not share, making them different from one another

NSE = 1 - rMZ twins reared together

shared environmental influence

people living together share and make these individuals similar to one another

SE = 1 - (H² + NSE)

gottesman’s limit setting model

range of ability is determined by genes, but actual value of ability is determinded by environment (range of reactions)

epigenetics

heritable changes in gene expression that do not involve changes (mutations) to underlying DNA sequence

parkinson’s disease

degenerative neurological syndrome - profound movement deficits

neurodegenerative disease

disease by progressive neuronal atrophy

posture distrubance

inabilitu to counteract gravity w/ muscles (walking impaired)

tremors

repetitive rhythmic motions, seen while at rest (pill rolling)

rigidity

stiffness due to increased muscle tone in flexor and extensore muscles causing limbs to move in specific rigid steps

akinesia

poverty of movement, motionless, speech, and writing affected

lewy body

abnormal, toxic greggate of protein w/ dense a-synucein core

a-synucein

membrane protein involved in dopamine transmission

basal ganglia

subcortical nuclei. mediating voluntary movement, posture, and autopiolet for well-learned movements

basal ganglia pathway steps

• main output → globus pallidus

  • inhibits thalamus

• main input → caudate and putamen

  • receives movement signal from cortex

  • signals GP to stop inhibiting particular movement

• degeneration of 75% substantia nigra (SN) and nigrostriatal pathway

  • dopamine → L-DOPA

• SN projects to striatum via nigrostriatal pathway and excites putamen

• cell death in SN

  • decrease activity of putamen =

  • increase acitvity in GP

  • decrease in movement

huntington’s disease

rare neurological syndrome - abnormal movements and cognitive deficit

hyperkinesis

uncontrollable twitching and jerking of body

atheotosis

stream of slow, involuntary writhing contractions and twisting of the body

huntingtin gene

gene codes for a protein whose mutation is implicated in HD

11-24 = normal >39 = disease

schizophrenia

psychosis - disturbances of thought, language, behavior (0.5-1.5% prevalance) (1:1 M:F ratio)

delusions

false beliefs despite disconfirming evidence (Grandeur + persecution)

neologisms

new words; often combonations of words

hallucinations

sensory perceptions not directly attributatble to environmental stimuli (voices)

negative symptoms

absence or reduction of normal thoughts, feelings, and behaviors

positive symptoms

production of abnormal phenomena

lack of insight

inability to recognize that thought is disturbed

loosening of associations

continual shifting of thoughts without any apparent logic (incoherent speech)

flat affect

lack of emotional expression

diathesis-stress model

psychopathologies (disease) are a result of a biological predisposition and environmental trigger (stessor)

viral hypothesis

exposure to a virus in utero affects genes + neurodevelopment causing schizophrenia

hypofrontality

loss of activity in frontal lobe, related to negative symptoms

hallucination activity located in…

parahippocampol gyrus and auditory cortex

modified dopamine hypothesis

schizophrenia caused by excess mesolimbic dopamine activity (positive symptoms) and subsequent dopamine underactivity in cortex (negative symptoms)

neuroleptic

drug used to treat psychoses - dopamine antagonist

extrapyramidal symptoms (EPS)

movement and muscle disorders

long-term potentiation (LTP)

increase in readiness of a postsynaptic neuron to fire after repeated stimulation by presynaptic neuron - mediated by two hippocampal glutamate receptors

what are the two glutamate receptors

1. NMDA (n-methyl-D-aspartate(

2. AMPA (a-amino-3-hydrixy-5-methyl-4-isoxazolepropionic acid)

long-term potentiation pathway stpes

1. removal of magnesium block on NMDA

• release of mucho glutamate → stimulates AMDA → depolarization → Mg2+ removed

2. activation of protein kinases in post-synaptic cell

• Ca+ influx through open NMDA receptors activates protein kinase

• alter functionality +strengthens synapse

3. enhanced release of glutamate

• second messenger required

• nitric oxide

  • synthesis by kinases

  • diffuses out and enters presynaptic cell

  • stimulates glutamate release

protein kinase

enzyme odifies proteins via chemically adding phosphate groups to them via phosphorylation

glutamate post synaptic changes

• more AMDA receptors

• decrease in membranes electrical resistance

glutamate presynaptic changes

• increase release of glutamate

• growth of addional terminal buttons

primary motor cortex

elicits movement

posterior parietal cortex

intention to move a body part

supplementary motor cortex

planning and organizing movements

premotor cortex

receives information about the target to which the body is directing its movement,+ information about body’s current position & posture

prefrontal cortex

important for considering the probable outcomes of movements

antisaccade task

voluntary eye movement from one target to another

lateral corticospinal tract

controls muscles in the lateral parts of the body, such as hands and feet

medial corticospinal tract

controls muscles in the medial parts of the body, including trunk and neck

Alzheimer’s Disease

irreversible dementia - memory impairment, intellectual deterioration + involuntary movements, + psychosis

agnosia

disturbance in visual recognition

aphasia

disturbance in language production + comprehension

apraxia

disturbance in motor activity despite intact motor function

executive function deficit

impaired ability to plan organize, + engage

proteopathy

disease state caused by structuraly abnormal proteins, affect neurons

BAPtists viewpoint

AD due to formation of extracellular plaques composed of a fragment of amyloid precursor protein - eventually kill neurons

alzheimers disease steps

1. amyloid precursor protein (APP) sticks through neuron membrane

2. enzymes cut APP into fragments of protein, including B-amyloid

3. B-amyloid fragments come together in clumps to form extracellular plaques that affect neurons

TAUists view point

AD due to accumulation of phosphate on tau (t) proteins composing microtubules, leading to intracellular neurofibrillary tangles when microtubules collapse- evenutally kill neurons

CTE (chronic traumatic encephalopathy)

degenerative brain disease found in athletes w/ history of repetitive brain traum

hypofrontality

decreased cerebral blood flow in prefrontal cortex when performing executive functioning task

cholinergic hypothesis

degeneration of cholinergic activity causes deterioration in cognitive function seen in AD

major depressive disorder

episodes of severe depression that do not alternate w periods of mania

monomine hypothesis

depression caused by low levels of serotonin + norepinephrine

antidepressants

medications relieve symptoms of depression + anxiety, reduces receptor supersensitivity

monomine oxidase inhibitor

block actions of MAO. potential overdose, toxicity, lethal food interactions

tricyclic antidepressants

inhibit reuptake of NTS, mostly epinephrine + serotonin. side effects + fatal overdose

SSRI ( selective serotonin reuptake inhibitor)

drug prevents reuptake of serotonin. latency 5-30 days

receptor sensitivity hypothesis

depression result of pathological alteration, supersensitivity, up regulation, in receptor sites following under stimulation by monoamines

supersensitivity

compensatory increase in receptr sensitivity following prolonged under stimulation; causes up regulation—pproduction of new receptor sites

neurotrophic hypothesis

depression result of stress induced affects on intracellular mechanisms decrease neurotrophic factors, such as BDNF

brain derived neurotrophic factor BDNF

protein promotes survival + functions of neurons, encourages growth + differentiation of new neurons + synapses

neurotrophic hypothesis steps

1. chronic stress leads to decrease in expression of BDNF in hippocampus

2. increases in glucocorticoids, decrease neuron survival

3. hippocampal atrophy

4. impaired feedback + exerbation

transcortical sensory aphasia

impaired comprehension + sematic paraphasia, but fluent, grammatically-correct speech—damage to posterior langauge area