Neuro Exam 3

Sympathetic vs Parasympathetic

Sympathetic- flight or fight, mobilize glucose stored (release stored energy), decrease digestion, increased bp and heart rate, divergence, anxiety disorder

Parasympathetic- rest and digest, increase digestion, stop sweating, pupils constrict, distributed processing

Cortisol

stress hormone - released from adrenal cortex because of communication from secretory hypothalamus

aids in metabolism and use of stored energy - can cause oxidative stress (stress that causes a protein to misfold - ex: plagues in brain)

long term exposure can cause exocytosis (cell death)

PTSD

long term sympathetic state- brain starts to shrink in mass because of increased cortisol levels over long periods of time

Oxytocin

increase bonds within groups and ethnocentric behavior

released from posterior pituitary gland

Vasopressin (ADH)

sodium gets high in blood and body needs to retain water - ADH tells kidney to not excrete and to retain as much fluid as it can, inhibit urine production

blood hypertonic- retain, get thirsty

blood hypotonic- low sodium, excrete as much water and increase the Na in blood

Hypothalamus

homeostasis - keep body in regulated steady state

secreting hypothalamus releases neurohormones through blood stream

hypothalamus → pituitary gland → neurohormones

3 components of neuronal response

Humoral- how much salt in blood

Visceromotor- muscular - blood goes to organs - shivering, hair stands up when cold, sweating, panting when hot

Somatic- voluntary motor- cold=stand up and move, hot=jump in pool

Lateral hypothalamus

initiates motivation to actively seek or generate warmth - homeostasis

Prandial state

Anabolism - intestines full, nutrients broken down in gut into glucose and glycogen and ketone and fatty acids - triglycerides go into blood and become adipose tissue

energy stored as glycogen and triglycerides

Postabsorptive state

catabolism - breaking down complex macromolecules

intestines empty and glycogen gets released from liver - triglycerides broken into: ketones, fatty acids, and glucose = now can use energy

Lipostatic hypothesis

keeps body at certain set point

period of starvation- body weight drops, eat normal food, retain more glycogen, body returns to normal weight - leptin drops and starvation response

forced feeding- gain weight,retain back to normal eating, weight declines back to set point

Leptin

spikes= decreases appetite, increase energy expenditure

Anorexia

lesion lateral hypothalamus - related to leptin signaling

Obesity

lesion ventromedial hypothalamic - related to leptin signaling

Elevated leptin levels

activates arcuate neurons that release aMSH and CART (anorectic peptides- diminish appetite and increase energy expenditure)

arcuate nucleus, connects areas of hypothalamus - cause humoral, spinal cord affected (jitters), lateral hypothalamus (starved)

fire off paraventricular nucleus → activates sympathetic nervous system → stimulates release of ACTH and thyrotropin → turns off eating behavior

Decreased leptin levels

arcuate neurons release NPY and AgRP (counteract the CART and aMSH) from arcuate nucleus→ and stimulate lateral hypothalamus (eat more) → NPY and AgRP inhibits secretion of TSH and ACTH

oxygentic peptides-make you want to eat more, located in arcuate nucleus

neurons stimulating feeding behavior

lateral hypothalamic peptides - make us feel good

melanin-concentrating hormone (MCH) and orexin

Cephalic

smell good food, food is in head - ghrelin is released, hungry !

Gastric

stomach fills up - signals brain by vagus nerve

works with CCK released by intestines in response to certain foods and tells brain when full

Substrate

food is in intestines and broken down to distribute energy throughout the body, storing

insulin released by B cells of pancreas - insulin is highest in this phase

Ghrelin

released when stomach is empty

activates NPY and AgRP in arcuate nucleus

Dopamine reward circuit

high calorie = more reward neurons fire off

dopaminergic axons in the ventral tegmental area projecting to the forebrain

parkinson’s disease typically have a damages ventral tegmental area and do not get the same thrill from eating

dopamine depleted animals

lack motivation to seek food but enjoy it when available

Serotonin

low: postabsorptive period

rise: anticipation of food

spike: during meals

high calories elevates mood and rise blood tryptophan and brain serotonin

Volumetric drinking

hypovolemia: decrease in blood tone

receptors detect drop in bp → sends message vagus nerve → nucleus of solitary tract → hypothalamus → stimulates subtomical organ which releases angiotensin and decrease blood flow to kidneys (stop peeing)

Osmotic/tonic thirst

Hypertonicity- increased concentration Na in blood

neurons of OVLT stimulate → lateral hypothalamic area activate → magnocellular neurosecretory cells → releases vasopressin (ADH)

Diabetes insipidus- loss of vasopressin, lots of pale watery urine

Temperature regulation

anterior hypothalamus - cause humoral and visceromotor responses

fall in temp- TSH is released by anterior pituitary, stimulates thyroid gland

cheat sheet

genotype differences

X chromosome (1500) is much larger than Y (50)

genetic disorder- have to have bad transcript on both chromosomes - females less likely to have it, but can be carrier

X linked disease- much more common in males

SRY gene

on Y chromosome, sex determining region - encodes TDF (testis determining factor) causes genetic areas to develop testicles

TDF= not released=female. the default pathway is female

gender is determined at union

hormones and sex

sex hormones- steroids

endocrine glands- release sex hormones

pituitary gland- regulated endocrine glands

male hormone= testosterone (androgens), female hormone=estradiol (estrogens)

Aromatase

only difference of testosterone and estrogen hormone

Protein vs steroid hormones

protein- do not pass through cell membrane, bind surface receptors

steroid- pass through cell membrane which allows to change genetics of cell (alter DNA) and bind cytoplasmic receptors - alter membrane excitability, sensitivity to neurotransmitters, neurotransmitters released

hormone difference in cycles

Men- levels fluctuate daily, twice a day; rise when first wake up and rise in the middle of the afternoon

Woman- levels fluctuate, 28 day cycle

Gonadotropins

signaled by hypothalamus and released by anterior pituitary

males- LH produces testosterone, FSH aids in sperm maturation

female- LH and FSH cause estrogen secretion (follicular phase and luteal phase)

Sexual response cycle

Arousal, plateau, orgasm, resolution

cerebral cortex- tells us what is attractive/what we want in mate

spinal cord- mediates sexual response of genitals

spinal cord injury and sexual response

ganglions come out of the sympathetic chain in the sympathetic ganglion - ganglion near parasympathetic - operates independently of spinal cord- therefore still sexual response even though they cannot feel it

parasympathetic vs sympathetic in arrousal

parasympathetic- engorgement (blood goes to genitals),

sympathetic- orgasm

Neurotransmitters within sex

relax smooth muscle

acetylcholine, vasoactive intestinal polypeptide (VIP), nitric oxide (NO)

nitric oxide- relaxes smooth muscle to help for engorgement in males

mammals mating strategy

polygyny- male mates with many females

polyandry- female mates with many males

monogamy- one mate per person

prairie vs meadow voles

prairie- solid family values, monogamous, more oxytocin (female) and vasopressin (male)

meadow- asocial and only want sex, fewer receptors

Male and female brains differences

only 2-3 nuclei are different

Males- onuf’s nucleus help with urinating or defecating- extra sphincter and coded to ejaculate, sexually dimorphic nucleus (SDN) in rats or INAH in humans is two times larger

Females- smaller brain because smaller body, denser corpus callosum and more communication between the sides of the brain

homosexual males- INAH size of female

cognition differences male vs female

relation between cognition and hormones

males better with spatial reasoning, woman are better with language reasoning

woman get low estrogen levels (menopause) spatial reasoning improves

Prostaglandins

involved in tissue damage, pain, and fever

synthesized from arachidonic acid via COX enzyme

inhibit COX enzyme- males no longer want to mount females and allow to be mounted by other males

females to COX enzyme- start to look like males

Mismatches between genes and hormones

androgen insensitive genetic males- defective androgen gene and an X chromosome, genetically XY, phenotype XX (look female, female behavior etc) : no ovaries but undescended testicals

congenital adrenal hyperplasia genetic females- abnormally large adrenal glands, genotype: XX, more male phenotype (look more male)and produce more testosterone

activational effects of sex hormones

cause temporary modifications in brain organization, structural changes in neurites

men- rise in testosterone (want sex), fall in testosterone (no sex)

females- rise in estrogen (ovulation) increases sexual interest

estradiol surges = more receptors in hippocampus and reach more surface area = rat has peak fertility = increase in density

estradiol may have some neuro protective effects

James-Lange theory

emotion = response to physiological change in body

see snake = emotional expression first then experience fear (sweating, heart rate, before brain relates to something fearful) - do not have to have experience have physiological reaction

Cannon Bard Theory

emotions independent of emotional expression

see snake= need to be afraid - attach to things we know and are fearful of - then physiological change - need experience to know if you should be afraid

unconscious emotions

stimulus can have emotional impact without any conscious awareness - (stick tongue out and get smacked in head, stop sticking out tongue)

amygdala becomes active and changes the way we process information

Brocas limbic lobe

involved in emotion and emotional expression - cortex forming a ring around corpus callosum

cingulate gyrus, medial temporal lobe (limbic system), hippocampus

Papez circuit

limbic structures - links cortex with hypothalamus

starts at neocortex when seeing/processing something - gives us reasoning and controls response → cingulate cortex- emotional experience - connects with emotional memory → hippocampus connects the experience and expression→ hypothalamus- emotional expression- look of fear, happiness and releases neurohormones → anterior nuclei of thalamus- sensory related

Abnormal emotional expressions

Rabies infection - hyper emotional expression - infection targets the hippocampus and gets extra stimulated

Lesion anterior thalamus - leads to spontaneous laughter or crying not associated with an emotion

Single emotion concepts

we have diverse emotions - can be happy but also feel anxiety, mixed emotions

things that are relatively minor from a stimulus standpoint that cause a great response or the opposite

Temporal lobe and emotion

Kluver Bucy syndrome - take temporal lobe out and decreased fear and aggression, decreased vocalizations and facial expressions

hypersexuality, placidity, hyperorality (put inappropriate things in mouth), disordered eating

temporal lobe becomes damaged from stroke, trauma, encephalitis

Amygdala and fear

bilateral amygdalectomy reduces fear and aggression - anger, sadness, and disgust may be affected - inability to recognize fear in facial expressions, unable to concentrate and low energy

normal people- amygdala kicks off for fearful faces compared to happy/neutral faces and kicks off from learned fear

Predatory vs affective aggression

Predatory- attack towards head or neck, no sympathetic activity, attack to kill, quiet, no eye contact - elicited by stimulating lateral hypothalamus - medial forebrain bundle → ventral tegmental area

Affective- attract attention, bigger and stronger but tries to avoid violence, high levels of sympathetic - elicited by medial hypothalamus - dorsal longitudinal fasciculus → periaqueductal grey

hypothalamus and aggression

removal of cerebral hemispheres but not hypothalamus - sham rage = aggressive behavior without stimulus - can be reversed with lesions in hypothalamus

can happen from strokes

Serotonin and aggression

block serotonin = increase aggression

too much serotonin = cause aggression

physiological sweet spot - SSRI good drug to block reuptake and make your own source to keep it in range

Electroencephalogram (EEG)

device on head that records brain rhythms and measures generalized cortical activity

recognizes burst activity of neurons (afferent axons) in pyramidal cells in dendrites of the cortex

diagnose: epilepsy, sleep disorders, ICU patients, neurosurgery

recording brain waves

voltage fluctuations measured by finding the difference between positive and negative charges = wave, wave gives current

tiny fluctuations of AP firing on afferent axons in the pyramidal cells of the cortex = make into wave and wave gives current

Irregular vs synchronized

Irregular- dense, low amplitude wave

synchronized- slower wave but higher amplitude, low frequency - everything is firing together in an organized burst

Magnetoencephalography (MEG)

recording magnetic signals generated by neural activity - shows sources of activity better than EEG - but can’t give detailed images of fMRI

fMRi and PET show blood flow differences and the changes in brain matabolism of glucose

Beta

dense, lowest amplitude, irregular - awake and moving around - uses lots of areas of the brain

Alpha

quiet, waking state - sitting in a chair, dozing off

Theta

more regular and spaced out, really drowsy - light sleep, tossing and turning - K complexes and spindles

stage 1+2

Delta

very regular, high amplitude and slow waves - deep sleep - disconnected from outside sensory world

stage 3+4, 4 is the longest stage of sleep

REM sleep

looks like beta - brain is very active

stage 5 - heart rate increases, piloerection

sleep releases hormones that

shut off the thalamus - paralysis so you don’t act out dreams

thalamus is active during REM

low hormone = sleep walking

Walter freeman

neuro rhythms coordinate with burst activity and bind together the pyramidal cells to burst together at identical times = waves of sleep

more synchorounous the waves = less conscious control

Seizures

usually respond well with meds

Generalized- entire cerebral cortex - electrodes exploding with activity - high amplitude, high frequency - lose consciousness

Partial- circumscribed cortex area (ex: arm or visual)

Absence- less than 30 sec of generalized - not disruptive to motor but yes cognition - misdiagnosed as ADD

old passive sleep theories

toxin- body produces toxins that accumulate, toxins build up and gets drowsy, so sleep to process toxins

ischemia- standing all day and blood pools to legs and lower body = makes us tired and want to sleep

synaptic fatigue (Pablo)- produce neurotransmitters and once the body has spend it all you need to sleep to reproduce neurotransmitters

Cleighton- natural state is sleep and only wake for needs (hunger, bathroom)

Bremer- brain is resting while asleep which isolates body from sensory experience - thought the thalamus was not active

three functional brain states

people talkin about sleep

Sigmund Freud- dream functions, wish fulfillment, conquer anxieties - doesn’t do much

Allan Hobson and Robert McCarley- activation synthesis hypothesis - need to synthesis proteins - true

Avi Karni- certain memories require strengthening period for REM sleep - true

diffuse modulatory neurotransmitter systems

norepinephrine and serotonin- very important in waking cycle and REM cycle

when falling asleep= decrease the firing/inhibited

Cholinergic neurons

enhance REM events - active during waking - turn off in most of sleep cycle

control rhythmic behaviors of the thalamus and sends burst activity to inhibitory neurons (GABA)

thalamus burst in activity controls the cortical EEG which blocks the sensory input which keeps us from acting out

Reticular Activating System

in midline of brain, if stimulated people get burst activity and start to sleep, more stimulation= wake up and be alert

gives signals for us to sleep but has to be active for us to be awake

Sleep promoting factors

Muramyl dipeptide- from CSF and goes away in REM sleep

Interleukin-stimulates the immune system - sleep deprived = get sick

Adenosine- amino acid that gets released when inhibitory system activates and body paralysis

Melatonin- hormone produced by pineal gland, helps with circadian rhythm

Gene expression in sleep

half a percent of genes are either awake or sleep states - certain genes are triggered by sleeping - neuro plasticity related gene

no sleep= no memories, no new proteins, no healing

Circadian Rhythms

daily cycles of light and dark

need to be active= physiological and biochemical highest

can drift from lack of zeitgebers

Zeitgebers

environmental time cues - light and dark cycle

no environmental cues of light and dark = drift out of 12 hour phase and into 24 hours

Suprachiasmatic Nucleus

regulates the circadian rhythm -each SCN has a rhythmic message that has a firing rate that varies with the circadian rhythm - genes cause this to happen not tetrodotoxin

photoreceptor synapses directly on SCN neurons - photoreceptor is a ganglion cell in the retina that contains melanopsin (slowly excited by light)

SCN sends out efferent to the hypothalamus, midbrain, diencephalons - uses GABA

each cell has a clock gene that changes mRNA which causes us to sleep and wake

Creativity

understanding the fundamental rules for meaningful utterances

Form

language is formed for an arrangement of difference sounds from a limited range in a predictable sequence

Content

language requites a combination of phonemes and the connection of words

Use

language is used as a mean of social communication

language in brain

Parietal-occipital-temporal association cortex- links several sensory modalities

Pre-frontal cortex- planning responses

Parietal lobe (left)- locate lots of language function

Brocas vs Wenickes’s area

Brocas- motor area of the frontal cortex that allows our mouth/tongue to move speech

Wernicke’s- understanding of speech

Wada procedure

used to determine hemisphere dominant for speech (typically left- rarely right side)

gives an anesthetic that shuts down speech so they can see where the speech centers are so they don’t damage them in brain surgery

Stages of language in lil kids

6 months - babbling

1 year- one word sentences - (mom, dad, yes, no)

1.5 years- 30-50 words, adjectives, nouns, verbs

2 years- 2 word speech - 50-several hundred words

2.5 years- 3 or more word sentences, multiple combinations, grammatical errors, good comprehension

3 years- full sentences, few error around 1000 word vocabulary

4 years- close to adult speech

Brocas aphasia

Lesions: Left posterior inferior frontal

Verbal output: Non-fluent - use filler words (bro, like, um)

Repetition: Impaired- cant repeat a word you tell them to

Comprehension: Normal - gets frustrated because they know what they want to say but can’t

Naming: Marginally impaired- cannot name object even if they know what its used for

Associated Signs: Right hemiparesis, Right homonymous hemianopia, apraxia of left face and limbs

Wernicke’s aphasia

Lesions: Left posterior superior temporal

Verbal output: Fluent- words messed up but they do not realize

Repetition: Impaired

Comprehension: Impaired- do not realize what they are saying is wrong

Naming: Impaired

Associated Signs: Difficulty with occupational engagement

Conduction Aphasia

Lesions: left parietal - arcuate fasciculus is damaged

Verbal output: fluent

Repetition: impaired

Comprehension: normal

Naming: impaired (paraphasic)

Associated Signs: Right hemisensory deficit, apraxia of all limbs and face

Global Aphasia

everything verbal is impaired and outcome is not good

Lesions: left frontal temporal perietal

Verbal output: nonfluent

Repetition: impaired

Comprehension: impaired

Naming: impaired

Associated Signs: Right hemiparesis, right hemisensory, right homonymous hemianopsia

Anomic Aphasia

Lesions:left posterior inferior temporal or temporal-occipital region

Verbal output: fluent

Repetition: normal (anomic)

Comprehension: normal

Naming: impaired - can tell everything about the object but cannot get the correct word

Associated Signs: none

Transcortical motor

similar to brocas but bigger and effects the motor production and right hemiparesis - hard to tell the difference

Lesions: Left medial frontal or anterior border zone

Verbal output: nonfluent

Repetition: normal

Comprehension: normal

Naming: impaired

Associated Signs: right hemiperesis

Sensory

similar to Weirnkes but can repeat normally

Lesions: left medial parietal or posterior border zone

Verbal output: fluent

Repetition: normal

Comprehension: impaired

Naming: impaired

Associated Signs: Right homonymous hemianopia

mixed aphasia

Lesions: left medial frontal parietal or complete border zone

Verbal output: nonfluent

Repetition: normal

Comprehension: impaired

Naming: impaired

Associated Signs: Right hemiparesis, right hemisensory defect

Wernicke Geschwind Model

it over simplifies and takes speech into a sutomotor response- makes the assumption that speech is just like writing and you’ll have the same problems with speech and writing but thats not true

Split brain procedures

opposite side acts as if it wasn’t there; conflicting behaviors and brief stimuli only went to one hemisphere

left hemisphere language dominance- right visual field repeated easily - left visual field has difficulty verbalizing - unable to describe anything to left of visual fixation point

Right vs left hemisphere

right- can perceive the left side of body, drawing, puzzles, holistic

left- can perceive both sides of the body, language, logical, objective - left planum temporal is larger than right