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What are the mechanisms of habituation and sensitization?
- Habituation is a decrease in response to a repeated, harmless stimulus (like ignoring your nagging sibling) via homosynaptic depression, reducing neurotransmitter release at the sensory-motor synapse
- sensitization is an increase in response, often to a threatening event, involving heterosynaptic facilitation where arousal (like adrenaline) boosts neurotransmitter release at multiple synapses, making the system more responsive overall
Short term vs long term memory...
- Short-term is about 10 seconds
- long term is theoretically for infinity but retrieval issues and interference can mess this up.
What are the aspects of working memory?
- phonological loop
- visuospatial sketchpad
- central executive
visuospatial sketchpad
- holds visual and spatial information
phonological loop
stores auditory information including words
central executive
directs attention toward one stimulus or another and determines which items to store in W.M.
What area does spatial memory utilize and whats an example?
- Uses the hippocampus, can be shown as in the Morris water maze test with rats
- hippocampus and limbic structures are important for consolidation, and LTM are reflected as changes in the cortex.
How does memory effect the cortex?
- there is some kind of metabolic process or change at the synapse of neurons that contributes to learning and memory
- Neurons that fire together WIRE TOGETHER RAHHHH!!!!
What is long-term potentiation (LTP)?
- an increase in a cell's firing potential after brief, rapid stimulation. Believed to be a neural basis for learning and memory
- Long lasting improvement in communication between neurons
- shown as an increase in dendrite surface area, receptors, and neurotransmitters
What is a Hebbian synapse?
synaptic connection that strengthens when the presynaptic neuron and the postsynaptic neuron are active at the same time
“cells that fire together, wire together”
What are the roles of AMPA and NMDA receptors in LTP?
- AMPA receptors handle the "how much" (strength), and NMDA receptors handle the "when" (coincidence for plasticity).
- they modulate sodium and calcium influx into the cell.
Glutamate Synapses
- Glutamate is a neurotransmitter (and amino acid)
- Glutamate is an ionotropic fast acting neurotransmitter
How do AMPA receptors mediate neural communication?
- Directly related with Na+ (sodium)
- Glutamate bonds with AMPA receptors and opens sodium channels
- causes Depolarization aka EPSP
How do NMDA receptors mediate neural communication?
- these are bigger ion channels
- Mg++ (magnesium) blocks these larger receptors, but the inside of the cell being more positive from EPSP or AMPA effects, kicks the Mg++ out of the channel letting more sodium into the cell, and more importantly, Ca++ because calcium is larger and needs these larger ion channels to get in.
What enzyme is formed by Ca++ and required for making more AMPA and NMDA receptors?
- CaMKII
- Also makes more dendrite branches = more synapses
- move receptors to better positions and make them more responsive
- like a neural house keeper or stage hand. CaMKII is necessary for LTP to occur
What is LTD (long term depression)?
- opposite of LTP
- Prolonged decrease in response at a synapse
- low frequency stimulation
- use it or lose it, shown in memory disorders like Alzheimer's
What is Wernicke-Korsakoff Syndrome?
- Degenerative brain disorder associated with alcoholism
- Thiamine is an amino acid we get from foods only, so alcoholics often are deficient in this.
- Thiamine is necessary for glucose metabolism, without it, the brain gets no fuel.
- patients will make up things to fill memory gaps
- cell loss or shrinkage of hypothalamus and frontal lobe
What are possible causes of Alzheimers disease?
- Genetics, environmental factors, chromosomal abnormalities, abnormal protein folding
What is the basic function of Alzheimers?
- Protein clumping of plaques (Amyloid) and tangles (Tau) are too big for microglia to degrade or dispose of
- creates issues and interference in neural communication and function.
Possible Alzheimer treatments...
- Acetylcholine: stimulates receptors and increases ACh release
- Antioxidence to prevent free-radicals, found in foods like berries
- Immunization: primes immune system to fight off amyloid or tau but its hard to know who will establish Alzheimers later in life and who wont.
Why do some people have a split brain procedure?
- to stop chronic and severe seizures by separating the hemispheres of the brain and reducing the widespread effect of the inappropriate action potential storm.
What areas does the left hemisphere specialize in generally?
- Language
- Analytics
- Sequences
What areas does the right hemisphere specialize in generally?
- Spatial
- patterns
- Emotion
- Prosody (patterns or cadence of poetry or music)
What are the weaknesses of a split brain patient?
- Two hemispheres are acting independently so opposing signals can be sent to each hand, aka less control over movement
- Information does not cross easily from one hemisphere to the other
- can struggle with language and identifying object from different sides of visual field.
How is language of split brain patients effected?
Because language is primarily a left hemisphere function, a split brain patient can only write "hat" with their right side of the body and only point to identify the object with the left side.
Why is the left hemisphere dominant in language?
- deep in your temporal lobe, the "Planum Temporale", seems to be a bit larger in the left hemisphere in 65% of people
- people with dyslexia dont have this asymmetry
What is Aphasia?
- A disturbance in the production or comprehension of speech caused by brain damage like stroke
What is the first type of Aphasia called?
- Broca's Aphasia
- Broca's patient could only say "tan" due to damage of the Broca's area of the brain in the frontal lobe.
Nonfluent aphasia
- Anomia: difficulty finding the word
- Difficulty with articulation
- Aggramaticism: problems with function words like "to be or not to be"
- Can write fine so patients often carry a note pad
Wernicke's Aphasia aka Fluent aphasia
- Discovered by Carl Wernicke
- Due to lesions in the temporal lobe
- Speech is still articulate but meaningless
- Poor speech comprehension
- Disruptions of: word recognition, comprehension of words, ability to put thoughts into words
What is pure word deafness?
- cannot comprehend speech sounds
- due to damage to left temporal lobe
- Cannot recognize rapidly changing complex sounds
- Damage to: Wernicke's area, next to primary auditory cortex
What is Transcortical sensory aphasia?
- Damage to area posterior to Wernicke's area
- Cannot comprehend or produce meaningful speech
- CAN repeat what they hear
What is conduction Aphasia?
- Damage to arcuate fasculus, the direct path from Wernicke's to Broca's areas
- poor repetitions, particularly of nonwords
- Comprehension is intact
Wernicke's vs Broca's area...
- Wernickes (speech comprehension)
- Broca's (speech production)
what is william's syndrome?
- A genetic condition
- strengths: well developed language and music skills, social, empathetic, strong face processing abilities
- Broca and Wernicke areas are intact
- Weaknesses: cardio vascular problems, very low IQ, poor spatial cognition, drawing abilities are not good either
- Neuropathology: reduced posterior parietal and occipital lobe
- brain size is generally smaller
- neuropathology is generally consistent with behavioral/cognitive profile
What are the symptoms of depression?
- more common in women
- feelings of worthlessness
- loss of joy
- little energy
- changes in food and sex apetite
- sleep difficulties, leading to a snowball of other issues and increasing symptoms
What is the link between stress and depression?
- 50% of women with recurrent depressions show signs of overactivity in the HPA Axis
- Hypothalamic-pituitary-adrenal axis !
- increased CRF and Cortisol and cause reduction in hippocampus size, which could impact learning and memory
What brain areas are involved or effected by depressive disorder?
Damage or dysfunction of:
- Hippocampus (learning and memory)
- Prefrontal cortex (regulation of emotion)
- Overactive Amygdala (emotion, fear)
How does MAO inhibitors work?
- Inhibits production of an enzyme that breaks down monoamine (serotonin, dopamine, and norepinephrine)
- thus an increase in monoamine
- Originally used to treat tubercilosis patients discovering euphoric effects.
What are side effects of MAO:
Cheese effect: increase blood pressure and heart rate, caused by ingesting cheese because MAOIs block the enzyme needed to break down these foods. A spike in norepinephrine can lead to headaches, and even stroke or death.
What are tricyclic antidepressants? How do they work?
- Block the reuptake of serotonin and noradrenaline
- increase concentration of serotonin in the synaptic cleft (more huz at the function #ratio)
- older medication that is more general and has more side effects than SSRI
What are SSRI ?
- selective serotonin reuptake inhibitors
- more specific that Tricyclic antidepressants
- Prozac, Zoloft, Paxil
- Not addictive, still has withdrawal if suddenly stopped
What do MAOI, Tricyclic, and SSRI Antidepressants all have in common?
- they are all monoaminergic agonists: meaning they increase the amount of neurotransmitter activity by blocking uptake or blocking enzymes from breaking down neurotransmitters.
Bipolar Symptoms aka manic-depressive
- Mania and Depression
- Depressive episodes are longer than mania
- Effects sexes almost equally
- Mania: Euphoria, lots of energy, and delusion, little sleep
Causes of depression and Bipoalr
- Genetic: high degree of heritability
- Environmental: hormones (ex. post partum) or stress from HPA axis and sympathetic nervous system.