Emotion, mood, learning, memory Flashcards
3 neuromodulatory systems
- serotonin (5-HT)
- dopamine
- acetylcholine (Ach)
which part of the brain releases serotonin
raphe nuclei
how are raphe neurons activated
by novel, unexpected, but innocuous sensory stimuli
what is serotonin involved in
arousal and the control of sleep-wake cycles
where is dopamine produced
substantia nigra
dopamine function
movement initiation
disease related to lack of dopamine
Parkinson’s disease
what happens when dopamine reaches the frontal lobes
provides “reward” and reinforces adaptive behaviors
how can dopamine be activated artificially
electrical stimulation of ventral tegmental area
how is dopamine related to ADD? what does this suggest?
increasing dopamine and norepinephrine with Ritalin improve ADD
- suggests these NTs play a role in selective attention
acetylcholine functions (2)
- supply to frontal lobes and hippocampus is important in memory
- supply to thalamus and striatum for movement initiation
2 disorders associated with depleted Ach
- Alzheimer’s
2. Parkinson’s
limbic system
ancient part of brain with many homeostatic functions
7 functions of limbic system
- body temperature
- water balance
- appetite, metabolic rate, growth
- sex drive, menstrual cycle, birth reflexes
- emotional behavior
- motivation and reward
- memory
what is the command center of the limbic system
hypothalamus
hypothalamus
“head nucleus of the ANS”
6 things resulting from stimulation of hypothalamus
- thirst
- anorexia
- bulimia
- sexual behavior
- rage
- pleasure
which part of hypothalamus senses blood osmolarity
supraoptic nuclei
which part of hypothalamus secretes ADH
posterior pituitary
ADH
vasopressin that increases water reabsorption in kidney collecting tubules
3 causes of depression
- genetic predisposition
- stressful life events
- last biochemical imbalance
which chemicals are particularly related to depression
serotonin, noradrenaline, dopamine
4 chemical treatments for depression
- tricyclics
- monoamine oxidase inhibitors
- SSRI’s
- lithium
tricyclics
non-selective biogenic amine re-uptake inhibitors
MAO inhibitors
non-selective biogenic amine breakdown inhibitors
SSRI
selective serotonin re-uptake inhibitors
what is lithium specifically used for
manic-depressive disorders
lithium
affects second messenger system and cell membranes
is depression tightly correlated with biogenic amine levels
no, long-lasting changes in cell membrane receptors channels are also implicated
how is drug dependence created
drugs that affect limbic reward centers can produce dependence
tolerance
chronic use of a drug leads to upregulation of enzymes that break down the drug
associative learning
conditioned stimulus becomes associated with an unconditioned stimulus
non-associative learning
sensitization or habituation to a repeated stimulus
operant conditioning
associate a behavior with a reward
3 types of learning
- associative learning
- non-associative learning
- operant conditioning
hypothesized mechanism of short-term memory
cyclical electrical activity in neural circuits
hypothesized mechanism of long-term memory
molecules changes in neuronal cell membranes and synapses
3 types of working memory
- episodic
- visuo-spatial
- phonological
phonological memory
recent words and sounds
visuo-spatial memory
recent sights and locations
2 types of long-term memory (and 4 sub-types)
- declarative
- a) semantic
- b) episodic - procedural
- c) stimulus-response behaviors
- d) motor skills
where is short-term episodic memory located
frontal and parietal lobes
where is phonological memory located
temporal lobe
where is visuo-spatial memory located
occipital lobe
where is declarative memory located
temporal lobe, hippocampus, amygdala
where is procedural memory located
basal ganglia, cerebellum
where does transfer from STM to LTM occur
likely in temporal lobes
- reward system involving hypothalamus is also implicated
caudate nucleus function
consolidating stimulus-response associations
Korsakoff’s syndrome
complete anterograde amnesisa due to hippocampus damage
Alzheimer’s disease
degeneration of memory-holding neurons due to amyloid precursor proteins causing “excitotoxicity”
simplified explanation of Alzheimer’s
neurons damaged by over-excitation
3 neuronal mechanisms
- reverberating circuit
- molecular change
- synapse strengthening
reverberating circuit
neural circuit “holds” a memory by continual cyclical activation
molecular change
2nd messengers change gene expression of proteins in the cell membrane, to change the neuron’s responsiveness to “search and recall” signals
2 examples of 2nd messenger molecules
- nitric oxide
2. cGMP
how are 2nd messengers activated
when an event input is associated with a relevant context input
synapse strengthening
2nd messengers change gene expression at output synapses, causing permanent structural alterations in them, which increase neuron output