Unit 4: Brain and Behavior Flashcards
EEG
Measurement of electrical activity from surface of scalp to measure activity of cerebral cortex
Synchronous
EEG signal is large, same timing
Asynchronous
EEG signal is small, timing is off
MEG
Detects tiny magnetic signals produced by synchronously active neurons, better at localizing sources of neural activity in brain
4 EEG rhythms
- Beta-awake and alert
- Alpha-awake and resting
- Theta-sleeping
- Delta-deep sleep
Synchronous activity led by one of two things
- Central pacemaker (thalamus)
2. Collective behavior among cortical cells
Zeitgebers
Environmental cues that entrain circadian cycles (primary cue: sunlight)
Internal Circadian Clock
SCN in hypothalamus
Where are higher frequency (beta) waves mainly located?
Cortex
Where are lower frequency (delta) waves mainly located?
Thalamus
Transcriptional-translational feedback loop
- BMAl1 and CLOCK promote transcription of per and cry genes
- Bind together and inhibit transcription of own genes
- Degrade
- Allows BMAL1 and CLOCk to promote per and cry transcription again
EOG
Records eye movements during REM
EMG
Detects muscles activity
4 stages of sleep
- Theta waves
- Spindles and K complexes
- Occasional delta waves
- Predominantly delta waves
Recuperation
Sleep is needed to restore homeostatic balance lost during the day
Adaption
Sleep is the result of an internal timing mechanism, evolved to conserve energy and to protect us from dangers of the night
Effects of sleep deprivation: in support of theory
- Bad mood, reduced cognitive abilities, and sleepiness
- Reduced immune function, increased BP, lower body temp
Effects of sleep deprivation: inconsistent with theory
- Unimpaired logical and critical thinking
- Retained physical strength and motor performance
- Recovery sleep is relatively short
Anterior hypothalamus
Sleep
Posterior hypothalamus
Wake
Rostral reticular formation
Wakeful
Caudal reticular formation
Sleep
Anterior sleep area in hypothalamus (VLPO)
Inhibits targets using GABA as its NT
Posterior awake center (lateral hypothalamic area)
Excited targets using orexin
Rostral RF areas
LC, 5-HT, Ach, HA
Human sleep regulated by 2 basic neural processes
- Sleep need-homeostatic process
2. Sleep urge-circadian process
3 types of drugs that affect sleep
- Hypnotic-increases sleep
- Anti-hypnotic-decreases sleep
- Chronotbiotic-alters circadian rhythm
2 types of sleep disorders
- Insomnia
2. Hypersomnia
Process of homeostasis
Sensory transduction of variable, detecting changes from optimal range, integrated response (humoral visceromotor & somatic) to restore parameter back to optimal (negative feedback)
3 zones of hypothalamus
- Periventricular
- Medial
- Lateral
4 regions of hypothalamus
- Mammillary region
- Tuberal region
- Supraoptic region
- Preoptic region
3 components of response from hypothalamus to maintain homeostasis
- Humeral
- Visceromotor
- Somatic motor
Humeral
Releasing hormones
Visceromotor
Adjusting the balance of sympathetic and parasympathetic outputs of the ANS
Somatic motor
Motivating appropriate behaviors by the somatic motor system
Paraventricular nucleus
Initiates humoral and visceromotor responses
Lateral hypothalamus
Motivates the somatic motor response, contains 2 main types of outputs (uses MCH and other uses orexin)
2 lobes in pituitary gland
- Anterior-synthesizes and secretes hormones in response to hormones released by hypothalamus
- Posterior-stores and secretes hormones
What does the ANS do?
Influences function of internal organs
Physiological mechanisms if hot or cold
- Decrease or increase metabolism
- Sweat or shiver
- Increase or decrease blood flow to skin
Behavioral mechanisms if hot or cold
- Find a cool or hot place
- Become less or more active
- Sleep or fluff fur (more or less clothes)
- Stand alone or together
2 advantages of high body temperature
- Mobile all year long
2. Protection from fungal infections
Where are the most important neurons for temp homeostasis found?
Clustered in preoptic and anterior hypothalamic nuclei (receive input from anterolateral tract and respond to changes in blood temp)
Where are neurons for the 3 responses to temperature changes produced?
Humoral and visceromotor: neurons in paraventriclar nucleus
Somatic motor: initiated by neurons of lateral hypothalamus
2 types of thirst
- Osmotic-eating salty foods
2. Hypovolemic-losing fluid volume
Nuclei that conserve water (2)
- Supraoptic
2. Paraventricular
What generates desire to drink? (2)
- Preoptic nuclei
2. Lateral hypothalamic area
What is water conservation controlled by?
Release of ADH from paraventricular and supraoptic neurons via posterior pituitary
What does ADH enable?
Enables kidneys to reabsorb water and thus excrete a concentrated urine
Baroreceptors
Type of mechanoreceptor sensory neuron that is excited by stretch and inhibited by relaxation of blood vessel
What does renin do?
Hypovolemia causes kidneys to release it, which leads to synthesis of angiotensin II, which causes constriction of blood vessels to increase BP
Lateral lesions of hypothalamus cause…
Anorexia
Lesions of ventromedial hypothalamus cause…
Obesity
Arcuate nucleus
“Master area” for control of appetite
2 sets of neurons in arculate nucleus
- Sensitive to hunger signals (low leptin)-release AgRP and NPY onto PVN and lateral hypothalamic area
- Sensitive to satiety signals (high leptin)-release alphaMSH and CART into same targets
High orexigenic signals, low satiety signals
Food consumption happens
Low orexigenic signals, high satiety signals
Food consumption is inhibited
Hormone in stomach
Ghrelin (hunger)
Hormone in intestines
CCK (satiety), stimulates vagus nerve and closes exit of stomach
Hormone in blood
Insulin, low=hunger, high=satiety
High ghrelin
Low CCK, insulin, & gastirc tension
Activates NPY/AgRP (hunger) containing neurons
High CCK, insulin, & gastric tension
Activates alphaMSH and CART (satiety) containing neurons
Hedonic effects modulated by…
Dopamine (ventral tegmental area) & serotonin (Raphe nucleus)
Mesocorticolimbic pathway
(ventral tegmental area and nucleus accumbens) is major “reward” pathway for ICSS and natural rewards
7 main areas of cortex for language
- Primary visual cortex
- Primary auditory cortex
- Angular gyrus
- Wernicke’s area
- Arcuate fasciculus
- Broca’s area- like secondary motor cortex
- Primary motor cortex
Wernicke-Geschwind Model: spoken language
Auditory cortex –> Wernicke’s area
Wernicke-Geschwind Model: words written
Visual cortex –> angular gyrus –> Wernicke’s area –> arcuate fasciculus –> Broca’s area –> motor cortex
Broca’s (nonfluent) Aphasia
Expressive aphasia, normal comprehension but poorly articulated speech, writing difficulties
Wernicke’s (fluent) Aphasia
Receptive aphasia, poor comprehension and meaningless, fluent speech, writing difficulties
Dejerine
Reading aphasia, damage to left angular gyrus, inability to read (alexia) and write (agraphia), but no difficulty speaking or understanding speech, damage in pathways from visual coretx
Conduction Aphasia
Damage to arcuate fasciculus, fluent speech (Broca’s area is working) but there is error awareness with attempts to correct them (Wernicke’s area working), poor repetition of unfamiliar words
Effects of cortical damage: anterior lesions
Expressive aphasia
Effects of cortical damage: posterior lesions
Receptive aphasia
Sign language: damage to frontal cortex
Can impair making of gestures (nonfluent)
Sign language: damage to temporal cortex
Can impair understanding of gestures (fluent)
Bilingual brains
Thicker language areas in temporal and frontal cortex, shifting languages activates frontal, temporal, and basal ganglia (helps secondary motor cortex aka Broca)
Mutations in FOXP2 gene
Verbal dyspraxia- inability to produce the coordinated muscle movements needed for speech
What does the FOXP2 gene encode?
Transcription factor that affects development of Broca’s area, motor cortex, basal ganglia, and cerebellum
KIAA0319
Gene associated with dyslexia, chromosome 6 and 18
Dyslexia patients have lower activation in…
Angular gyrus, but over-active Broca’s area
LTM: Declarative memory
Explicit-what: broken into semantic and episodic, medial temporal lobe
LTM: Procedural memory
Implicit-how: includes motor skills, basal ganglia & cerebellum
Retrograde amnesia
Memory loss for events before trauma
Anterograde amnesia
Inability to form new memories after trauma
Semantic memory
General world knowledge, anterior pole of medial temporal lobe
Episodic memory
Life events, hippocampus and (mostly ) rhinal cortex
3 major structures in part of medial temporal lobe caudal anterior pole
- Amygdala
- Hippocampus- spatial
- Rhinal cortex
Where is short term memory held?
Telencephalon- including prefrontal and parietal cortex
Lateral intraparietal cortex (LIP)
Guides eye movement to locations of objects of interest
Cell assembly
Internal representation of an object consists of all the cortical cells activated by the external stimulus (Hebb)
Learning and memory is a 2 stage process
- Acquisition of ST memory
2. Consolidation of LT memory
How is memory stored in the network?
Through a unique pattern or ration of activity across the neuronal assembly
Advantages of distributed network (2)
- No single neuron represents specific memory (population type coding)
- Graceful degradation of memories with gradual neuron loss
What transmitter is most often at modifiable synapses?
Glutamate
LTP
Strengthening of synaptic connections
Hippocampus consists of 2 thin sheets of neurons
- Dentate gyrus
2. Ammon’s horn (CA3 & CA1)
Input specificity
When one pathway into synapse is stimulated weakly, it produces insufficient postsynaptic depolarization to induce LTP
Cooperatively in LTPs
In order to achieve necessary depolarization to elicit LTP, one input must fire fast enough to produce temporal summation of its EPSPs or a set of weak inputs must cooperate to produce spatial summation
Associativity in LTPs
LTP can be elicited at synapses that are
activated by weak, low-frequency, stimuli if their
activation is temporally concurrent with an LTP inducing stimulus at another set of synapses on the same cell
3 phases of LTP
- Induction
- Expression (“early LTP”)
- Stabilization (“late LTP”)
Rise in postsynaptic Calcium activates what 2 protein kinases?
- Protein kinase C
2. CaMKII
LTD is site specific
Homo-synaptic LTD, only on spines getting glutamate (and Calcium)
Glutamate receptor trafficking
Egg carton model, AMPA receptors are replaced maintaining same number
Protein PSD-95
Comprises slot protein
Where is bidirectional synaptic plasticity found?
Area IT (inferotemporal cortex)- stores visual info including familiar faces
Blocking NMDA receptors with antagonists
No learning in inhibitory avoidance expts & prevented learning of location of escape platform (for rats)
Knockout CaMKII or NMDA receptors
No learning/ reduced learning
Metaplasticity
Rules of synaptic plasticity change depending on the history of synaptic or cellular activity (modification threshold slides up or down)
NR2A
Admits less Calcium
NR2B
Admits more Calcium
Synaptic scaling
Adjustment of absolute synaptic effectiveness that preserves the relative distribution of synaptic weights
Why is phosphorylation not a viable LT consolidation mechanism? (2)
- Phosphorylation is not permanent
2. Protein molecules are not routinely replaced
ST and LT phases of memory depend on different molecular mechanisms (2)
- ST (early LTP): kinases
2. LT (late LTP): protein synthesis
Molecular Switch Hypothesis
Kinases that can auto-phosphorylate could stay “on” all the time (ex: CaMKII)
Protein kinase M zeta
Involved in regulating AMPA receptor number, involved in mRNA translation and promotes its own synthesis for a time
Protein ZIP
Temporarily inhibits function of PKMzeta and can erase memories
CREB-1
LT memory consolidation, gene transcription activator, phosphorylated by protein kinase A (which is activated by cAMP)
