Biopsych Exam 3

Front 1

Non-associative learning

Back 1

habituation
How? due to a decrease in motor neuron action potentials
Why? NT release by sensory neurons decreases
Why? less Ca ++ enters Sensory Terminal buttons
sensitization

Front 2

habituation

Back 2

ignoring of an irrelevant stimulus, decrease in strength of reaction due to repeated stimulus

Front 3

sensitization

Back 3

heightened attention to the environment increase in responding due to an aversive stimulus
How? due to an increase of Ca ++ in Sensory terminal buttons
Why? tail sensory neurons active interneurons that synapse on siphon sensory ternimnal buttons
How? cause more Ca ++ enters sensory terminal buttons causing more NT release
name of process is presynaptic facilitation

Front 4

Associative learning

Back 4

learning relations either between: stimuli [classical conditioning] or stimuli and responses [operant conditioning]

Front 5

Classical or Pavlovian Conditioning

Back 5

CS- neutral stimulus
US - stimulus which produces reflex
UR- reflex or automatic response
CR - reflex elicited by CS because CS association with the US

Front 6

Pavlovian Condition in Aplysia

Back 6

CS - light touch on siphon- no reaction
US - shock on tail - large gill withdraw reflex (UR)
pairing of CS and US >> light touch (CS) now causes reflex (UR)

Front 7

Neural Mechanism

Back 7

same as sensitization
tail-shock-activated interneuron facilitation PLUS the temporal relation (pairing) of CS and US

Front 8

Activity-Dependent Enhancement Model

Back 8

Discrimination Training
CS + paired with US
CS - not paired with US

Front 9

Second Messenger Effects in Sensitiztion

Back 9

Remember G-protein linked receptors (metabotropic receptors)
attached to a signal protein, with a G protein inside
-when activated part of the G protein breaks off inside post synaptic cell and triggers the synthesis

Front 10

Second Messenger cyclic AMP
short term facilitation

Back 10

short-term facilitation:
1. Cyclic AMP activates the enzyme:
2. Protein Kinase A which closes K+ channels
3. Increases length of action potentials
4. This causes more Ca ++ influx
5. Causing more NT release

Front 11

Second Messenger cyclic AMP
long term facilitation

Back 11

more permanent changes
1. Cyclic AMP activates the enzyme:
2. Protein Kinase C which induces structural changes in the cell
-increases vesicle formation
-increased zones of NT release on the membrane

Front 12

Hebb Theory of Consolidation of Existing Pathways

Back 12

synaptic strength increases with use
-applied to short-term memory
-applied to long-term memory
--process requires co-occurance
: activation of pre- and post- synaptic membranes at the same time--this leads to permanent neural changes

Front 13

Implications of Learning and Memory

Back 13

There is no new synthesis of neuronal pathways
-learning occurs at the convergence of pre-existing pathways
-memory may be a result of co-occurence and stimulus convergence

Front 14

LTP

Back 14

Long-Term-Potention
a brief period of repeated, intense elec. stim. to pre-synaptic neurons has long-lasting effects on the post-synaptic neurons

Front 15

Qualities of LTP are like memory

Back 15

1. Stimlulus specificity
2. Long-term retention
3. repetition leads to longer retention

Front 16

Neural Mechanism of Memory

Back 16

1. Hippocampus involved in memory formation
2. LTP can be produced only in hippocampus
3. NMDA glutamate receptors involvement in LTP
--- if they are blocked, normal transmission happens but not LTP
--- Co-occurence required for full activation of NMDA receptors
Process involves Ca ++ influx into the post synaptic cell activating protein kinases to induce LTP

Front 17

Cases of human Amnesia

Back 17

Clive Wearing
H.M.
-bi lateral medial temporal lobectomy
-- retrograde amnesia before damage
-- anterograde amnesia since damage
-- short-term memory
--recent long term memory
-- implicit memory
--explicit memory since damage
R.B.
-Ischemia produced damage
--symptoms similar to HM but less severe
--later autopsy reveal CAI damage

Front 18

What brain damage causes amnesia?

Back 18

1. Hippocampus hypothesis
2. HIppocampus-plus-amygdala hypothesis
3. medial-temporal cortex hypothesis
-- entorhinal cortex
-- perirhinal cortex
-- perihippocampal cortex

Front 19

Brain Areas that Contribute to Memory

Back 19

Rhinal Cortex, Hippocampus, Amygdala, Inferotemporal Cortex, cerebellum and striatum [caudate and putamen], prefrontal cortex, mediodorsal nucleus, basel forebrain

Front 20

Non-invasive administration of drugs

Back 20

1. oral-ingestion
2. inhalation
3. mucous membranes

Front 21

Invasive administration of drugs

Back 21

Injection
-subcutaneous [skin, fatty tissue]
-intramuscular
-intravenous

Front 22

Must enter the CNS

Back 22

by passing through the blood-brain barrier

Front 23

Once in various effects

Back 23

large changes to neural membranes [mess with receptor sites]
specific action on NTs
specific action on receptors

Front 24

Drug Action stopped

Back 24

liver filtering, excreted: sweat, breath, urine...

Front 25

Tolerance shifts the does response curve

Back 25

same dose >> less effect
same effect > needs larger dose

Front 26

Metabolic tolerance

Back 26

decrease of the amount of drug reaching target cells

Front 27

functional tolerance

Back 27

adaptive neural changes
decrease in drug ability to have an effect

Front 28

drug tolerance affected by

Back 28

user's behavior [contingent tolerance]
environmental factors [conditioned tolerance]

Front 29

contingent tolerane

Back 29

exposure alone does not lead to tolerance

Front 30

conditioned tolerance

Back 30

situationally specific tolerance
overdoes in novel environements
alcohol's hypothermic effect

Front 31

withdrawal sypmtoms

Back 31

sudden elimination- yields opposite effects
caused by same physiolocigal mechanism

Front 32

physical dependence theory

Back 32

reason for addiction: to avoid withdrawal

Front 33

positive-incentive theory

Back 33

reasons for addiction: to gain pleasurable effects

Front 34

activation of brain "reward" centers

Back 34

mesotelencephalic dopamine system
main pleasure neurontransmitter
2 main pathways
--midbrain >>basal ganglia [substantia nigra >> striatum ((caudate nucleus and putamen))]
--midbrain>>limbic system>>cortex
[ventral tegmentum >> septum and hippocampus amygdala >> prefrontal cortex

Front 35

Methods used to identify reward centers of the brain

Back 35

ICSS intracranial self-stimulation studies
drugself administration studies
place- preference studies

Front 36

self-administration

Back 36

only works when done into dopamine pathways nowhere else

Front 37

drug injection

Back 37

into dopamine pathways lead to place preference

Front 38

electrical stimulation

Back 38

more rewarding under influence of other drugs

Front 39

when dopamine pathway function is stopped

Back 39

drug reward reduced

Front 40

self-administration of drugs leads to

Back 40

increased amount of dopamine in brain

Front 41

commonly abused drugs and addictive component

Back 41

tobacco-nicotine
alcohol
marijuana THC
cocaine - blocks cetacholamine reuptake
opiates - mimics endogenous opiates
caffeine