Phys II exam 3 (final)

frontal lobe

functions in motor/efferent planning and execution, personality

parietal lobe

functions in sensory and sensory association

occipital lobe

functions in vision/processing, primary visual cortex lines calcarine sulcus

temporal lobe

varied functions- processing sound, recognizing faces, language processing; medial part of lobe involved in emotion, memory, and learning

cortical neurons

receive signals (granular cell layer IV), communicate with other cortical neurons, send large output fibers (pyramidal/betz cells layer V)

3 types of cortex in cerebrum

neocortex- 90% of human cortex, 6 layers of cells; archicortex- 3 layers of cells (hippocampal formation); paleocortex- 4-5 layers of cells (olfactory cortex)

layers of neo cerebral cortex

1- molecular layer, 2- external granular layer, 3- external pyramidal layer(association,commisural fibers to other areas of cortex), 4- internal granular layer(main input layer), 5- internal pyramidal layer (main output layer, down spinal cord), 6- polymorphic layer

granular neurons

higher cortical function of association areas, intracortical processing via layers 1, 2, and 3, extensive processing of sensory info, extensive communication via small intracortical neurons,

cerebral association areas

prefrontal: planning, parieto-occipital-temporal: sensory, limbic: emotion

primary centers

where fibers originate or end at

parieto-occipito-temporal association area

interprets incoming sensory information- somatic sensation (more parietal), visual (more occipital), auditory, and olfactory; provides meaning behind sensory stimuli, sub-areas: spatial coordinates, language comprehension(wernicke’s), visual language (reading), naming objects

spatial coordinates

sub-area of parieto-occipital-temporal association area, provides ability to localize and process own body parts, sounds, and visual stimuli

wernicke’s area

sub-area of parieto-occipito-temporal association area, provides ability to comprehend language, most important area for higher intellectual function because experiences are converted into thoughts and memories (which utilizes other areas), located in dominant hemisphere (left side 95% people), loss/damage results in fluent/global aphasia

visual language (interpretive) area

sub-area of parieto-occipito-temporal association area, angular gyrus- located between primary visual cortex and wernicke’s area, relays visual information of written words to wernicke’s, allows for ability to read, damage causes difficulty interpreting written words (can’t read) but can still understand auditory language

area for naming objects

sub-area of parieto-occipito-temporal association area, interprets both auditory and visual information, names learned through auditory input while qualities learned through visual input

prefrontal association area

integrates sensory information with deeper meaning, can also involve motor output- thought processes, motor planning, working memory; higher intellectual function (less than wernicke’s) found via injuries- elaboration of thought, ability to take multple sources of information and analyze them, ability to plan a course of action- mentally and physically (motor planning)

damage to prefrontal association area

decreased ambition/planning, loss of purpose/depression, loss of ability to solve complex problems, inability to multitask, inappropriate social responses, easily distracted, decreased aggressiveness

working memory

sub-area of prefrontal association area, keeps track of multiple pieces of information, allows for deeper understanding- makes planning possible, alteration of conscious action (reflexes), consider consequences, solve complex problems, remembering something as long as we’re using it

communication area

sub-area of prefrontal association area, the distinct ability humans have to communicate that animals do not, involves sensory and motor function- coordination pathway

communication pathway of communication area

primary auditory/visual cortices → wernicke’s area → prefrontal association area → broca’s area → primary motor cortex

limbic association area

concerned with emotion, motivation, and behavior; part of a complete/larger limbic system, provides context for emotion, communication with many areas of cortex and deeper brain structures, houses area for recognition of faces

area for recognition of faces

associated with limbic association area, made of 2 connected portions- occipital and temporal; occipital portion- involved in communicating with primary visual cortex, temporal portion- involved in communication with limbic system; __ultimately responsible for relaying specific facial visual stimuli to limbic system for emotional meaning;__ damage causes prosopagnosia (inability to recognize faces)

thoughts

not limited to a specific isolated region but spans cerebral cortex, thalamus, limbic system, & reticular formation; can be generally summarized as pleasure, displeasure, pain, comfort, basic sensation; must be contextualized and localized

memory

3 categories- short-term, intermediate, and long-term; sensitization of consequential details and habituation of monotonous details; types are declarative and reflexive

memory sensitization/facilitation

facilitation/enhancement of synaptic pathways for consequential input (emotional, positive, negative, pain, pleasure), allows continued strength of sensory/memory pathway

memory habituation

inhibition of synaptic pathways by blocking calcium channels for inconsequential information (monotonous details), loss of signal strength over time

declarative (explicit) memory

conscious- things you can consciously recall, includes- details of important experiences, surroundings, time, causes, meaning, conclusions; contains episodic memory(personal experiences, ‘my car was slow’) and semantic memory(factual information, ‘my car was white’)

reflexive (implicit) memory

subconscious- can’t recall everything just able to do it, includes- motor activities, learned skills (riding a bike), hand-eye coordination (can’t teach), emotional responses

short-term memory

lasts seconds to a max of a few minutes, may be converted to longer term via consolidation if theres is repetition or meaning associated (phone numbers, etc), mechanisms- circuits of reverberating neurons, only lasts as long as you’re actively thinking about it

consolidation of memories

converted short-term memory to long-term memory because there was something meaningful about it, requires repetition and rehearsal; can be negatively effected by concussions or general anesthesia

intermediate memory

lasts several minutes-weeks, eventually lost unless consolidated into long-term memories, mechanism- temporary chemical or physical changes at synapses, pre-synaptic facilitation of sensory pathway by facilitator pathway

molecular habituation

progressive closure of calcium (Ca+) channels at sensory axon terminal

molecular facilitation

serotonin released by facilitator pathway causes a cascade at sensory axon terminal, ends up blocking potassium (K+) channels, potassium unable to leave cell temporarily result in prolonged action potentials

long-term memory

structural changes have occurred- increased number of neurotransmitters are able to be released, increased neurotransmitter vesicles and release sites, changes in dendritic spines- increased # of receptors, stronger synapses; memories have been consolidated multiple times (short-term → intermediate → long-term), able to last entire lifetime, can be selectively recalled by conscious mind (declarative memory)

long term potentiation

regulated by glutamate receptors NDMA and AMPA, repeated high intensity stimulation (meaningful & important stimuli), results in stimulation of AMPA receptors letting in Na+ and NMDA receptors letting in Na+ and Ca++

influx of Ca++

theorized to trigger cascade within postsynaptic neurons that leads to increased # of AMPA receptors (increased response to stimuli)

codified memories

similar information is grouped, new and old information has to be sorted

hippocampus

one of most important destination sites for reward & punishment underscores importance of meaning and emotion behind memory storage; ‘physical location’ for long term memory storage- due to being destination of reward/punishment signals, located in most medial portion of temporal lobe cortex

papez circuit

classic circuit involving hippocampus and structures of limbic system, involved in learning, memory, and emotion; hippocampus → fornix → mammillary bodies of hypothalamus → mammilo-thalamic tract → thalamus → cingulate gyrus of limbic lobe

anterograde amnesia

damage to hippocampus, fail to make new memories, loss of capability to store new declarative memories in long term memory, past memories are typically intact

retrograde amnesia

damage to hippocampus or thalamus, loss of recent memories, thalamus must be important in the retrieval of past memories

left brain dominance

95% of people have this side dominant, wernicke’s area at birth is 50% larger, Broca’s area- almost always dominant on this side, hand skills area- 90% of people dominant on this side

non-dominant hemisphere

right in most people, important for everything except language- music, art, non-verbal communication, visual patterns, spatial relations

corpus callosum

large structure responsible for bidirectional communication between majority of cerebral hemispheres; sound, language, and right field of view processed on left side

anterior commisure

small structure responsible for communication between anterior temporal lobes, amygdala part of limbic system (emotional connections)

subconscious mind

major responsibilities of the reticular formation and limbic system

reticular activating system (RAS)

receives signals from lateral hypothalamus (orexin releasing neurons), activation of cerebrum occurs in 2 ways- generalized or specific

generalized reticular activating system

direct stimulation of background neuronal activity throughout brain; bulboreticular facilitory area- located in pons and midbrain, project to thalamus (distributed widely from thalamus), neurotransmitter- acetylcholine signals that last only milliseconds

specific reticular activating system

activation of neurohormonal systems that facilitate or inhibit specific areas of cerebrum through hormone-like neurotransmitters; neurohormonal signals- nuclei of RAS release several different neurotransmitters; neurotransmitters- some are inhibitory some are stimulatory; signal duration- persist for minutes-hours (long-lived impact on brain)

stimulatory neurohormonal signals

stimulatory- norepinephrine (originates in locus ceruleus, diffuse area of activity), acetylcholine (originates in gigantocellular neurons); located in upper pons into mesencephalon, damage results in coma

What may result in a coma

when RAS is compressed and/or damaged limiting and/or cutting off stimulatory neurohormonal signals to the brain

inhibitory neurohormonal signal

serotonin- originates in raphe nuclei, primarily acts on diencephalon, also inhibits pain in spinal cord; located in lower pons into medulla, damage results in no sleep

stimulatory and inhibitory neurohormonal signal

dopamine- originates in substantia nigra, primarily acts on caudate and putamen of basal nuclei, also stimulatory in hypothalamus and limbic system (emotion & motivation)

consequences of stimulatory drugs on brain activity

caffeine- counteracts adenosine receptors which facilitate sleep, increases excitability of neurons by reducing threshold

consequences of inhibitory drugs on brain activity

anesthetics- decreases excitability of neurons by increases threshold via making neurons less responsive to excitatory agents

sensory function of RAS

reticular formation receives incoming information (pain) and sends to the thalamus & cortex, sensory input stimulates RAS → strong stimulation of thalamus & cortex → positive feedback loop between RAS and cortex

thalamus

each area of cerebral cortex corresponds to specific area here, it allows for reverberation of signals- positive feedback, could help establish memories by activating back and forth signals (positive feedback loop)

limbic system

entire neuronal circuitry that controls emotional behavior and motivation, originally described as border structures that separate deeper regions from cortex & cortical association areas, complicated system of structures that each have their own unique function, consists of hypothalamus, hippocampus, and amygdala

hypothalamus

potentially most important 4 grams in your entire body, control headquarters for- limbic system, endocrine system, autonomic (vegetative) control; involved in 2-way communication with all other regions of limbic system, sends output signals to 3 locations- reticular area, thalamus & cortex, and pituitary gland

hypothalamus and limbic system

important areas- lateral hypothalamus, ventromedial nucleus, periventricular nuclei; reward & punishment centers and role in learning & memory- most of the decisions we make come down to anticipated reward or punishment, if reward or punishment center is not activated the experience is hardly remembered

stimulation/lesions of lateral hypothalamus

stimulation- gives urge to eat and drink, strong stimulation- associated with rage (hangry); lesion- no urge to eat or drink, loss of drive

stimulation/lesion of ventromedial nucleus

stimulation- relaxation and feeling of fullness; lesion- excessive eating and drinking, easily agitated

periventricular nucleus/zone of hypothalamus

stimulation- associated with fear and shame, animals quickly learn to turn stimulation off to avoid the feelings it evokes

reward centers

lateral nuclei, ventromedial nuclei, can lead to addictions, weak stimuli gives sense of reward, strong stimulus gives sense of punishment

punishment centers

periventricular zone of hypothalamus, central gray area surrounding aqueduct of sylvius (midbrain), when stimulated animals show signs of displeasure, fear, punishment, pain, terror, and physical illness

amygdala in limbic system

key for receiving sensory information related to emotion and survival, heavily involved in fear responses (life or death), those with smaller amygdala consider less fear repercussion (“Tom Cruise has a small amygdala”), originated as part of olfactory cortex, abundant connections with hypothalamus

hypothalamus controlling cardiovascular regulation

increase in arterial pressure & heart rate= stimulation of lateral and posterior hypothalamus, transmitted through vasomotor center in upper medulla; decrease in arterial pressure and heart rate= stimulation of preoptic area of hypothalamus, transmitted through vasomotor center in lower medulla

hypothalamus temperature regulation of increased blood temperature

stimulates __preoptic area__ of hypothalamus, increase in temperature increases activity, __mechanism to cool down via sympathetics- peripheral vasodilation and sweating__

hypothalamus temperature regulation of decrease blood temperature

stimulates __preoptic area__ of hypothalamus, decreased temperature decreases activity, __mechanism to warm up- peripheral vasoconstriction, increased thyroid hormone, shivering__

hypothalamus body water regulation

thirst center- stimulates sensation to drink via stimulation of lateral hypothalamus; increases reabsorption of water in kidneys via stimulation of- supraoptic nucleus of hypothalamus, pituitary to secrete ADH (antidiuretic hormone); dehydration- osmoreceptors sense increased Na+ concentration → project to supraoptic nucleus → ADH released by posterior pituitary → increased water absorption in kidneys

hypothalamus regulation of eating and hunger

increase in desire to eat/search for food- stimulation of lateral hypothalamus by ghrelin(↑ hunger); decrease in desire to eat/search for food- stimulation of vetromedial nucleus of hypothalamus by leptin (↓hunger, ↑ fat storage), insulin (↑ glucose levels in blood), and vagus nerve (stretch in stomach/GI)

hypothalamus endocrine function

controls on anterior pituitary- hormonal control mechanism, various releasing and inhibitory hormones into blood, blood supply to pituitary comes from hypothalamus; control of posterior pituitary (neurohypophysis)- neurological control mechanism, produces 2 hormones (neuropeptides oxytocin and ADH) that are released by posterior pituitary gland

HPA axis (hypothalamic pituitary adrenal)

Hypothalamus- master regulator of homeostasis (endocrine and autonomic); Pituitary Gland- master endocrine gland (direct control by hypothalamus- CRH) and releases 9 hormones (adrenocorticotropin ACTH, acts on adrenal glands); __Adrenal Glands__- stress response glands stimulated by ACTH, __releases cortisol (glucocorticoids)__ + many other hormones __from cortex__ (stress hormone), releases catecholamines (epinephrine, norepinephrine) from medulla

cortisol

decreases inflammation- has immune consequences (why you get sick after being very stressed), up-regulated alpha-1 adrenergic receptors (vasoconstriction, ↑BP), stimulates gluconeogenesis (amino acids→glucose= ↓ muscle), decreased glucose utilization (insulin resistance & ↑blood glucose), mobilization of free fatty acids

cortisol levels

measured in blood or saliva, highest in morning in healthy adults (5-25mcg/dL) then steadily lowers to be lowest overnight (

immune consequences of cortisol

anti-inflammatory, blocks early stages of inflammation (↓ inflammatory signaling, ↓ capillary permeability, ↓migration & phagocytosis of WBCs, ↓ lymphocyte proliferation (T-cells), ↓ IL-1 & fever), rapid ↓ of inflammation if it had already started and instead begins healing- ↓ immune activity in tissue but ↑ resources (amino acids) for repair

pharmacology of cortisol

useful for significantly reducing overactive immune system displayed in autoimmune diseases and hypersensitivities; long list of potential side effects- ↑ blood clotting, avascular necrosis, osteoporosis, tendon rupture

Electroencephalogram (EEG)

from millions of neurons firing synchronously, currently impossible to directly measure small group or single neuron activity; used for diagnosis/evaluation of epilepsy (rapid spiking waves), sleep disorders, understanding overall activity of brain (coma, drug overdose/intoxication, brain damage)

4 typical patterns of brain activity

Alpha waves, beta waves, theta waves, delta waves

Alpha brain waves

Low frequency and low voltage, seen in a calm, relaxing, meditation, resting awake state

Beta brain waves

Higher frequency, low voltage, pattern of an adult active brain- activating frontal and parietal lobes, active, alert, awake, and thinking; present in REM sleep

Theta brain waves

Low frequency, high voltage, frequently seen in kids developing brains, seen during emotional distress

Delta brain waves

Very low frequency, very high voltage, brain activity present during slow-wave sleep

Sleep

State of unconsciousness that the person can be aroused from

Coma

State of unconsciousness a person cannot be aroused from

2 types of sleep

REM rapid eye movement, slow-wave sleep

REM sleep

25% of sleep time, characterized by bouts of increased brain activity (beta waves- resembles active brain), bouts occur every 90 minutes and last 5-30 minutes, associated with dreams, Antonia- temporary paralysis (hyperpolarization of motor neurons), more difficult to wake up from, increased activity (high BP, metabolic rate, respiratory rate)

Slow-wave sleep

Extremely restful sleep, bouts last longer than REM sleep (larger % of sleeping time), 1st bout finished after 1 hour, decreased activity- 30% decrease in BP, metabolic rate, and respiratory rate

How we fall asleep

Active inhibitory process- lower reticular areas (raphe nuclei), inhibit activating centers

Melatonin

Released by pineal gland after (indirect) stimulation by suprachiasmatic nucleus of hypothalamus (light-dark cycle); SCN → paraventricular nucleus → inhibits sympathetic nervous system → decreased superior ganglion activity → decreased pineal gland activity; peak secretion occurs in children prior to puberty; reduced to 60% of peak levels after 25-40, reduced to 20% peak levels after 90

What does blue light inhibit?

Pineal gland activity

Serotonin

Released by raphe nuclei, fibers connect thalamus, hypothalamus, lambic system and cerebral cortex; if formation is blocked animal couldn’t sleep but if raphe nuclei was stimulated they fell asleep right away

Sleep deprivation associated with

Poor cognition, poor physical performance, poor overall health; lack could affect- neural maturation, facilitation of learning/memory, cognition, clearance of metabolic waste (beta-amyloid), conservation of energy

Sleep apnea

Sleep disorder characterized by pauses in breathing or insufficient breathing, interruptions of cycle cause fatigue, 2 types- obstructive and central

Obstructive sleep apnea

Most common, collapsible airways of pharynx, associated with URTI, obesity, teeth/jaw dysfunction

Central sleep apnea

Imbalanced respiratory control centers (medulla- nucleus of solitary tract), receives sensory information from- peripheral chemoreceptors, baroreceptors, stretch receptors in lungs, relays to pneumotaxic and apneustic centers of pons and medulla

Narcolepsy

Inability to regulate sleep wake cycle, ‘blurred lines’ between wake and sleep, degeneration of orexin releasing, now considered to be a neurodegenerative disease

5 jokey features of narcolepsy

Daily sleepiness, cataplexy, inability to move at start/end of sleep, vivid hallucinations, fragmented sleep

Seizures/epilepsy

Focal (partial) is isolated to small localized area, generalized is widespread, diffuse, and has bilateral affected areas

Generalized tonic-clinic (grand Mail) seizure

Loss of consciousness, affects all areas of brain, alternating tonic (tightness), alternating clinic (spasmodic - convulsions); features- biting tongue, possible cyanosis, loss of control of bowel and bladder, lasts 3-4 minutes, state of confusion afterwards