2 Flashcards

Question

Features of neurons

Answer 1

Common features of neurons: Cell body Dendrites Axon Cell body • Cell body; contains nucleus and other organelles. Ex. Mitochondria for ATP Dendrites - branches upon which incoming fibers make connections (at synapses) with other neurons receiving stations for excitation or inhibition Dendrites- receiving area- information transfer happens between neurons at the synapses Branches of dendrites lined with receptors- get excited or inhabited Axon- releases the signal out to the synapses Many receptors throughout the brain Axon- conducts electrical signals away from cell body to synapses

Answer 2

Transmission occurs from the presynaptic cell to the postsynaptic cell Flow of information: Synapse dendrite soma  axon  synapse Transmission between neurons- happens at axon- axon makes neurons different- transmit info in form of AP Happens from the presynaptic cell synapsing with the dendrites of another cell AP- generated at axon hillock Neurons that need the info to transfer fast- myelin sheaths made by glial cells Terminal buttons- neurotransmitter release receptor at synapse to the dendrites info goes to cell body, AP is generated at axon hillock travels to terminal button and synapse wth another dendrite

Answer 3

Dendrites are covered with short dendritic spines Dendrites and their spines are constantly modified and canchange rapidly in response to changes in synaptictransmission: #, size, shape, etc. Dendritic spine- inc surface area, constantly modified- change rapidly based on info in brain and neurotransmitters, the dendrites themselves change in #- inc or Dec, Chang in size and shape Disorders- have different amount of dendritic spines Drugs of abuse- change dendritic spines- may be key to drug addicted state

Answer 4

Axons transmit electrical signals from the axon hillock (at the soma) to the terminals. A neuron usually has one axon, but it may branch to form axon collaterals. Terminal buttons have synaptic vesicles containing neurotransmitter chemicals. Axon hillock- goes down to terminals- usually have one axon- can form collaterals the terminal buttons release- dopamine, gaba Rrelease from synaptic vesicles Most axons are wrapped with myelin sheath, a fatty insulating coating created by layers of glial cells: Schwann cells Oligodendroglia Fatty insulated cells made by Schwann cells in the periphery, Oliginderia- myelinated nerves in the spinal cords and brain Both are glial cells- protect neurons Multiple sclerosis caused by determined myelin sheaths= less communication

Answer 5

Node of Ranvier = break in myelin sheath  increases speed of AP conduction Breaks in the sheath= nodes of fancier- AP jump along= spreads up Myelin breaks down- nerotransmission doesn’t happen as well Schwann cells: form myelin sheaths in peripheral nervous system (PNS); wrap only one axon; release growth factors and promote regeneration of damaged axons Oligodendroglia: form myelin sheaths in central nervous system (CNS); wrap many axons Astrotes: provide structural support for neurons and help maintain ionic balance in the extracellular environment; take up excess NTs- maintain homeostasis- take up excess transmitters Microglia: remove dying cells by phagocytosis at sites of nerve damage; responsible for immune response- waste removal, immune response All glial cells important May contribute to disorders

Answer 6

Soma (cell body) performs most metabolic functions. The nucleus contains pairs of chromosomes. Chromosomes = strands of DNA; gene = section of chromosome coding specific proteinComplementary RNA made by transcription factors: nuclear proteins that bind to DNA, transcribing it to make RNA-Experiences can affect gene transcription Protein translation in cytoplasmic ribosomes. More interested in neurons but glial do cause abnormalities Cell body- metabolic functions, energy production Nucleus- has chromosomes- genes- read by mRNA to make proteins0 very important Transcription can be modified- dna doesn change much- expression of genes changes- transcription factors- gets read by enzymes after mRNA to make proteins- experiences and stressors- effect gene transcription= epigenetics

Answer 7

Epigenetics: control of gene expression by chromosome modifications that do not affect the DNA code. Ex. DNA Methylation: attachment of methyl groups to a gene reduces its expression (blocks translation). Epigenetics- change gene expression not gene itself DNA methylation- methyl attached to gain= blocks transcription- doesn’t turn into protein Acetylation of chromatin(dna wrapped around his tones)- can be changed when added acetylate - makes it unwind DNA= more likely to be transcribed Chang expression of dna Trauma, drug use, causes acetylation- changing expression of genes When chromatin tails acetylated, charges open up chromatin (part B)  allows transcription factors to bind  increases transcription Methylation of histone tails (part C)  pulls chromatin tighter  prevents transcription factor binding  reduces transcription Opens chromatin- allows transcription to bing Methylation- maes it harder to read May explain the differences not caused ny genes- differences in twin- how experiences change behaviour

Answer 8

Axoplasmic transportUses cytoskeleton: network of microtubules and neurofilaments that provide shape and structure to the cell. Microtubules form a track that proteins travel along by the action of motor proteins. Proteins that are made in the soma neeed to be transported Uses or cytoskeleton Help form a path for proteins- Alzheimer’s- microtubules get tangled causing tangled neurons

Answer 9

Proteins in the Cell Membrane Receptors: cell membrane proteins -initial sites of action of neurotransmitters (NTs), hormones, and drugs. Enzymes: catalyze biochemical reactions Transporters: for charged molecules (Ex. amino acids, glucose, metabolic products) Many proteins - many are receptors= where chemicals bind to Enzyme- help w biochemical reaction Transporters- help them get across cell membrane

Answer 10

 more negative ions (and amino acids) inside the cell, and more positive ions outside. Distribution f ions in neuron when at rest Difference in charged ions and proteins= more negative inside then outside Neurons can get only so positive before reach AP(0-50)

Answer 11

Allowed H & H to set the membrane potential (clamp it) at any level, and simultaneously measure underlying permeability changes (current flowing across membrane) Used voltage lamp on squid’s Set membrane potential to level amd stimulate axon and observe ion channel

Answer 12

Most ion channels are gated, but some K+ channels are not (=leaky); K+ moves freely K+ moves into the cell because it is attracted to the negatively charged particles (electrostatic pressure) K+ moves back out of cell when its concentrationrises (down its concentration gradient) In open channel- potassium called it of neuron- slowly

Answer 13

Equilibrium potential for potassium (EK): when the two forces are balanced. The membrane potential is still more negative inside (~-58 mV). When two forces are balanced- potassium wont move(-58)- these. Forces generate action potential Equilibrium reached when ions are balanced Interior- high concentration of negative charge Ions cant diffuse across membrane except for with channels Neuron at rest- most are closed But potassium can be open- they d not allow other ions- only few are open- the intercellular concentration is higher then outside- potassium is moving in and out of the cell- diffusion and electrical forces- when come in balance= potassium equilibrium= no movement Maintain resting potential and returning it- because of sodium potassium pump takes 3 Na out for every k moved in- ions pumped against their concentration gradients – r=needs energy All cell membranes are polarized Action potential (AP): a rapid change in membrane potential that is propagated down the length of the axon Threshold potential for AP firing = ~-50 mV -Voltage-gated Na+ channels open, Na+ flows in; generates rapid change in membrane potential to more +ve = depolarization Polarized- more negative inside AP- happen at myelin sheath- every once and a whole Rest, receptors bound, channels open- change into positive= AP Voltage gated channel is open- when cell gets more pos- sodium rushes in causing It to become pos- potasssium- leaves

Answer 14

Various stimuli can cause an AP and open ion channels: electrical change chemical (taste, drugs, smell, neurotransmitters) mechanical (touch, pressure, sound) light (vision, photodetection) temperature (hot and cold receptors) Small amounts of ion channels opening causes small, local changes in ion distribution and potential differences called local potentials-Depolarizations and hyperpolarizations Many stimuli can cause AP Small changes in the ions- graded potential- If Na+ channels open, Na+ enters cell and causes local depolarization excitatory post-synaptic potential (EPSP) If Cl– channels are stimulated to open, Cl– enters cell and results in hyperpolarization, which is inhibitory. inhibitory post-synaptic potential (IPSP) If gated K+ channels open, K+ leaves the cell which also results in hyperpolarization. Depolorazied- sodium channel open sodium flows in- EPSP- ion come in make it more pos CL- channels open- make it more negative- harder to generate AP-

Answer 15

Graded: larger stimulus  greater magnitude of hyperpolarization or depolarization Summation: several small depolarizations  big changes Bigger stimuli- lead to bigger responses= leads to AP Summation- adding the stimulations t reach potential Action potentials- only depolarize If summation of local potentials reaches the threshold, large numbers of Na+ channels open and Na+ rushes into the cell very quickly. -Causes rapid change in membrane potential from –50 mV to +40 mV = rising phase of AP Getting stimulation and inhibiting- reach temporal summation- fire an AP

Answer 16

Resting potentials Threshold Happening very quick 430 km/hr Have thought- say it= instant Different channels going on all the time Potassium= leaky channel- always open

Answer 17

Absolute refractory period - the time following an AP where a stimulus can't elicit a second AP due to closure of Na+ channels Relative refractory period - the time following an absolute refractory period when the threshold for initiation of a second action potential is increased: Na+ channels recover from inactivation and K+ channels close absolute- sodium channel closed- can relate to disorderds- constantly firing

Answer 18

In myelinated axons, regeneration of the action potential occurs only at nodes of Ranvier The conduction seems to jump along the axon = saltatory conduction. Less energy is needed because Na+-K+ pumps are only at the nodes. - AP moves along axon because Na+ ions spread passively to nearby regions, which changes the membrane potential to threshold, which opens more Na+ channels. AP- only generated at nodes of fancier- sodium ions spread across the myelin

Answer 19

Some drugs alter AP conduction by blocking the voltage-gated Na+ channels (e.g., Novocaine): These drugs are used for local anesthesia. Bacteria within the pufferfish generate a toxin called tetrodotoxin (TTX) TTX blocks Na+ channels, paralyzing its victim Cocaine- block sodium channel- touch info doesn get to brain TTX- block sodium channel get paralyzed but conciuos- sodium cant get I n

Answer 20

Graded- differ in size- more stimuli bigger response= signal lessens as it goes o rest of body AP- happens or doesn’t, not graded, same intensity through out spatially- how many across pace, temporal- time AP fires based on how many AP you see

Answer 21

Brain development depends upon: Maturation Learning We can refine this understanding by learning how: Neurons develop Their axons connect Experience modifies development (Plasticity!) Neural development- depends on maturation and learning-brain changes from learning Is it due to brain just maturing- growing in size- no learning plays a part- new synaptic connections Brain development needs both learning and maturation Start in fertilization- sperm fertilizes egg- cell division starts Day 15- considerend embryo At day 20- neural plate starts to form- a couple weeks after conception- brain starts to form- neural plate is first neural tissue- becomes a groove- forms a neural tube The neural tube closes

Answer 22

Human CNS begins to form when embryo is ~3 weeks old: Dorsal surface thickens, forming neural tube surrounding fluid filled cavity Anterior end enlarges, sinks under skin surface Hindbrain, midbrain, forebrain, spinal cord Our CNS- brain and spinal score form at 3 weeks- neural tube forms- completed at 4 weeks Cerebral hemispheres- side of brain formed Brain gets bigger and grows- gets bumps that become parts of brain Forebrain- covers midbrain and hindbrain- rest is spinal cord in CNS Fluid (CSF)-filled cavity becomes central canal & 4 ventricles (walls = neuron production) The rest of the neural tube becomes the spinal cord Has cerebral spinal fluid- neural cavity filled with CSF- becomes spinal cord and ventricles in brain(fluid filled space) where neurons are produced During brain development- the neurons start in walls of ventricle Neural tube folds on to itself Forebrain- gets bumpy- form gyro- covers midbrain and Hindbrain Changes happen during development- brain gets bigger but looks the sa,e

Answer 23

At birth, brain weighs ~350 g By the first year, brain weighs ~1000 g By 18 years old, (adult) brain weighs ~1400 g 18 years is adult- no finished (especially prefrontal cortex) until 30 brain develops front to back Brain develops in proportion with body- but connections change brain through life

Answer 24

The development of neurons in the brain involves the following processes: Neurogenesis Migration Differentiation Maturation Synaptogenesis Pruning & Cell Death Myelination Neurogenesis happens first- around 2 months- rest is out of order – once neurons formed- migrate Later processes- continue after birth Littleneurogenesis occurs through life

Answer 25

The production of new cells/neurons in the brain Early in devt, cells lining the ventricles (in the subventricular zone) divide Stem cells continue to divide Neurons (E42) or glia migrate to other locations >250,000/min! Almost all form within ~28 weeks of gestation Proliferation of new neurons Primarily in early life- but some areas do form neurons Cell lining ventricles(subventricular zone) dividing a lot and specializing- continue to divide and form cells- some become neurons or glial cells(migrate) Cell division at this time produces one stem cell and one neuron- have stem cell and neuron each division of ste, cell Sem cell stays there neuron leave and migrate Around 100 billion neurons Developing of neurons is happening very fast- if anything happens during this development that causes abnormal development Born before 28 weeks- brain not fully developed- more vulnerable to abnormalities Environment changes and neuron production is inhibited Stem cells in pancreas, hippocampus, can develop new stem cells- turn into neurons Nerve cells in hippocampus in adult brain- need these them cells of new neurons to learn new info In general new neurons do not form in other areas

Answer 26

The movement of the newly formed primitive neurons and glia to their eventual locations Some don’t reach their destinations until adulthood Occurs in a variety of directions throughout the brain Chemicals known as immunoglobulins and chemokines guide neuron migration After become neuron or glial cell- migrate to new location Some don’t reach destination to adulthood Damage to brain- can damage migration Moves in different directions- some slide along glial cells(help neuron migrate)- radial glia Tips of migrating neurons form growth cone- has feelerssensing environment- guiding neuron Chemicals- help neuron find way- act as guide- Migration requires precise chemical environment

Answer 27

Local environmental signals (ie. chemicals produced by other cells) influence the way cells develop & form layers in the cortex Intercellular signals progressively restrict the choice of traits a cell can express G X E Local environmental signals(neuron reached destination) has signals and chemicals that influence development of cell and layers it forms in cortex Differentiation forms these layers Cells release different neurotransmitters,otters- because of neuron itself- restricts development of certain genes All have same gene- environment activates certain genes

Answer 28

Formation of axon & dendrites The axon grows first: either during migration or once it has reached its target-followed by the development of the dendrites Maturation and ifferation go hand in hand Forms axon and dendrites- give neuron shape As neuron mature- form structures- axon grows first After migrating- dendrites start to form- happens before birth continues forever- as experiencing- dendrites change Axon grow 1000 time faster Newborn- broccas area- don’t have many dendritic formation Have same cell body across time- by 2 years old have many more dendrites- as forms synaptic connections

Answer 29

In lab animals- the formation of dendritic spine and branches- influenced by environment and environment simulation (friends vs no friends) Autisms- partly due to abnormal neural maturation- have different dendrites Have less dendritic spines,, size is different Environment- chemical and social- lead to growth and maturation o neuron

Answer 30

Axons must travel great distances,form correct connections Sperry’s (1954) research on newts shows axons follow a chemical trail to reach appropriate targets Growing tips of axons also respond to cues from: Cell adhesion molecules (CAMs) Tropic molecules Netrins Axon and dendrites need to find way- what to synapse with Axon travels great distanced to connect Not easy for axons to find way In 1920- graphed extra leg on salamander axons grew into it causing them to move together 1954- cut the optic neurve and rotated it- found the axons grew back to original target- had to travel different difference but went to were they should \ The chemical environment is important to signal correct axonal growt CAMS- growth cone and growing axon, stick to it or repealed high causes guidance and tropic molecules- attracts or repels neurons Netrins

Answer 31

Protein got rid of certain axon Emx2- in normal- more posterior- causes normal development Mutate emx2- pax6 tries to shift it- causing change in development Mutaepax6- causes change in development Proteins and correct level- important for normal development

Answer 32

A growing axon follows a oath of molecules attracted by chemicals and repelled by others. Eventually axons sort themselves over the surface of their target by following this molecular trail Axon follow molecular trail- certain proteins guiding axon along causing proper development

Answer 33

Formation of synapses Begins before birth, occurs throughout life: neurons are constantly forming new connections (& discarding old ones!) Slows significantly later in life Each neuron may synapse with >1000 others  adult brain estimated to have > a quadrillionsynapses! Formation of synapse- connect neurons Synapses change all the time- slows down in later life Synapses dependent on genetic info and experiences

Answer 34

When axons initially reach their targets, they form synapses with several cells (in approximately the correct location). Postsynaptic cells strengthen connection with the most appropriate cells and eliminate connections with others. Elimination = synaptic pruning -depends on the pattern of input from incoming axons Chemical gradient is not perfect don’t use it you lose it Cells may die as we;;- depends on environment and input from axon- selection process- neural darwinism- only most stimulated survive Huge synaptic pruning in puberty bug decrease in amount of synapses As solidifying personality- selective pruning Influenced by a lot of factors

Answer 35

Different cells have different life spans: -Skin cells are the newest; most under a year old -Heart cells tend to be as old as the person Mammalian cerebral cortices form few new neurons after birth Some cells survive longer than other- neurons not often replaced

Answer 36

Neuronal targets determine who survives Nerve growth factor (NGF): protein released by neuronal targets, promotes survival & axonal growth The brain’s system of overproducing neurons, then applying apoptosis (cell death) if they don’t get NGF, enables the exact matching of the number of incoming axons to the number of receiving cells Sympathetic ganglian- muscles that synapse with axon that come from ganglia- ganglia- don’t determine how many neurons- target of the synapse- decides what synapse stays Muscles creates NGF- any neurons without enough ngf- experience apoptosis Brain is overproducing neurons- expecting some to die Only neurons that make sig connections survive U to 50% of neurons produced may die off

Answer 37

Chemicals that promote the survival and activity of neurons (i.e., NGF, brain-derived neurotrophic factor (BDNF)) Increase dendritic branching & axonal growth Neurons that are not exposed to NGF after making connections undergo apoptosis NGF- neurotrophin NGF- during development BDNF takes over in adult hood- important for learning- need it for synaptic remodeling After maturation don’t need ngf Healthy adult system- has not neurons that failed to make connections Don’t have enough- cortical shrininking

Answer 38

The massive elimination of nerve cells is part of normal development and maturation Depends on appropriate environmental stimulation Ex. The visual cortex is actually thicker in blind people due to a lack of visual stimuli It cannot prune out ineffective neurons Happens to about 50% Big elimination- depends on environment stimulation- need appropriate enviroment y Don’t have visual stimuli- brain doesn’t now which neurons to prune- within appropriate simulation- don’t prune synapses that should

Answer 39

Glia (oligodendrocytes) Speeds up transmission of neural impulses in many vertebrate axons First occurs in spinal cord and then in the hindbrain, midbrain and forebrain Occurs gradually for decades Slower stage Happening across time Myelin sheath gets put over axons-c overs most neurons Astrostyces and oligodendrocytes( produce myelin in CNS) after Happens after neurogeneiss Happens in spinal cord first Schwann cells- create myelin in PNS Myeliation- tends to occur with developemental milestones- more neurons myelinated- able to learn more words Some et ions myelanted earlier Myelination vulnerable to environement

Answer 40

Early stages of brain development are critical for normal development later in life & are remarkably similar across species. Ex. FASD The dendrites of FASD children are short with few branches Decreased Glu andincreased GABA Lower neurotrophins Toxic chemicals, infections, malnutrition- doesn’t hae same impact in adulthood as it does n development FASD- repeated exposure to alchol- suppresses glutumate(excitatory transmitter) and releases GABA- causes too much inhibition - causing shorter dendrites with fewer branches, lower exposure to neurotrophins- not as much growth factor, causes neronal death Not just alchol- pesticide, led FASD- affects child different based on time and quantity of alchol Many have behavioural problems Hard to diagnose- assess exposure during pregnancy, neurodevelopmental impaired ent, physical features typical of FASD- many don’t have this

Answer 41

Hard and soft neurologic signs (including sensory-motor signs). Brain structure (occipitofrontal circumference- indirect measure of brain size, magnetic resonance imaging, etc.). Cognition (IQ). Communication: receptive and expressive.- receive instructions, communicate with others Academic achievement. Memory- Executive functioning and abstract reasoning. Switch tasks, inhibit functions Attention deficit/hyperactivity. Adaptive behaviour, social skills, social communication. Degree of severity for FASD Considered impaired – if on a measure- 2 std below average More than 2 std away- outside of nom Have a mean- see the scores for Ind and compare to average Hard signs- impaired in basic motor and sensory skills- reflexes Soft signs- Any neurological abnormality- not defined by any specific abnormality- cant pinpoint what the issue is All these can be affected Look at to find severity of FASD

Answer 42

Newborn brain is fully functional, but lacking. Dramatic growth of synapse. Greatest growth in cortex Brain looks like adult brain After birth- growth of synapse By 3 years old number of synapse- has increased drastically- Lots of development Neuronal development activity- peak at age 3, forming social connections, cognitive skills Pet scans show activity Most active areas emit radioactive activity PET scans give a fuzzy idea of the tremendous amount of development taking place in a brain.

Answer 43

Maturation does not always reflect growth; but rather, refinement! Maturation is also refinemen- not growing in size but synapses get refined Brain becomes more detailed- develops stringer connection Pruning is refining synapses

Answer 44

By the end of the 1st year, there are ~100 billion neurons, but even more connections 50-80% overgrowth of connections. Only the best and most efficient will survive (Edelman, 1987) Brain overproduces synapses- doesn’t have lots of functionality- needs to be reduced bases on experience- lots of competition between synapse- most efficient synapses survive- establish themselves in neural circuitry

Answer 45

Progressive Changes in Cortical Thickness Trajectory of cortical gray-matter density in children scanned longitudinally every 2 years for 8 years. The reduction in gray- matter density begins in primary areas and spreads to secondary and teritiary regions. Looked at gray matter density and matter loss and reduction Scanning child every 2 years- reduction in grey matter reduction of synapses and dendritic- starts in primary regions- where Brain first matures- control basic functions Other areas- mature later- not needed to survive projectors of maturation- keeps going to age 30 or beyond

Answer 46

Cortical regions where change in cortical thickness was associated with change in IQ. B. Scatter plot for the relation between IQ changes and CTh changes at the peak vertex inferior pre-central gyrus; C. Changes in cortical thickness at the same peak vertex represented in panel B. Loose synapses- inc white matter- these changes coincide with behavioural changes Relationship between iq and cortical thickness- iq seems to stay constant In some people- inc or Dec in iq- when look at change in cortical thickness- thickness is bigger, iq is higher Individual differences in rate of change in cortical thickness, related to changes in iq Grow bigger brain, increase in iq score

Answer 47

If there is more activity in one eye, the connections from the deprived eye to visual cortex shrink , while the connections from the good eye expand. Neural plasticity- brains ability to change Developing neural connections from eyes- compete for space Suture cat eye closed- deprive eye of stimulation- connections fail to develop, not stimulation visual cortex Shows there is a mechanism of neuron that allows it to detect aqvtivity, most activated- form strongest connections, least likely to die off

Answer 48

This change due to simulation After closure, deprived eye has no dendritic spines- no activity- leads to skinny neuron

Answer 49

Rats were trained to reach into a tube to retrieve a food reward with their preferred paw (rats, like humans, are right- or left-handed). The rats were then trained to use their non-preferred paw to grasp the food. After training to use the non-preferred paw, examined changes in branches from pyramidal neurons. Providing more stimulating environment Putting toys in rats environment, giving them friends Rats right or left handed- in this, give rat extra practice, does it change brain activity- rat has to use non dominate paw The peramital neurons in the cortex- had difference in neuronal structure, difference in dendritic brans Dendritic morphology of pyramidal neurons in layer III of the somatosensory cortex in a rat housed in standard (left) and enriched (right) environments, as viewed in confocal imaging B – the trained neurons, inc branching- assume inc in synapse Rats were trained to reach into a tube to retrieve a food reward with their preferred paw (rats, like humans, are right- or left-handed). The rats were then trained to use their nonpreferred paw to grasp the food. After training to use the nonpreferred paw, examined changes in branches from pyramidal neurons. The number o branches- not a big difference But it is significant

Answer 50

Rats raised in an enriched environment develop a thicker cortex and increased dendritic branching. Measurable expansion of neurons has also been shown in humans as a function of physical activity. Research looking at fish- raised in isolation- have neurons with fewer branches With friends- have more branches In humans- physical activity- adding physical stimulation= more dendrites and dendritic spine An enriched environment is ‘enriched’ in relation to standard laboratory housing conditions. A combination of complex inanimate and social stimulation Effects of elements of enrichment, such as learning and exercise, on cell proliferation (one day post BrdU exposure) and neurogenesis (four weeks post BrdU exposure) in the dentate gyrus. Enrichment is leading to new neurons being formed and new dendrites BRDU- incorporated into newly synthesized dna Put brdu on environment- gets substited for another molecule, use it as marker for neurogensis Control- no enrichment, have new neurons but not a lot In any of enrichment- more neurogenesis happening in hippocampus Detect small changes, can do this with developed organisms Any enrichment can lead to neurogenesis Extensive practice of a skill changes the brain in a way that improves the ability for that skill. Areas marked in red showed thicker grey matter among professional keyboard players Practicing a skill- enriched their environment, brain has changed, inc grey matter(synapses) in certain areas Enriching own life= can lead to brain changes

Answer 51

Prevalence: 3-5% of school-age children 5-10% of the entire population 3x to 6x more prevalent in males than females Typical changes as children mature If synaptic development impacts behaviour- disorder can occur from abnormal synapse development \ ADHD core symptom- not able to inhibit behaviour- executive functioning Most prevealent developmental disorder Many factors influence onset of adhd- hormones, enviroment Core symptoms change with age Development disorder-changes as mature

Answer 52

= the best studied, and one of the most common, of the childhood disorders In DSM-5, ADHD is listed as a neurodevelopmental disorder: Viewed as brain-based. Children with ADHD are motorically and often verbally hyperactive; have problems maintaining focus; show impulsive or erratic behaviours. Often create problems in schools and families 1/3 retain diagnosis A third of those diagnosed in childhood have it in adult hood

Answer 53

Inattention Does not pay attention, loses things frequently, is easily distracted, is forgetful, has problems with organization, does not seem to listen or to follow instructions. Hyperactivity Fidgets with hands or feet and squirms in seat, leaves seat when inappropriate, runs around or climbs excessively, often talks excessively to self and others, has difficulty engaging in quiet activities, frequently gets in trouble. Impulsivity Blurts out responses while others are talking, has difficulty waiting his or her turn, often interrupts or intrudes on others. Inattention- linked to academic problems Functional impairment – causing issues Symptoms must be present during childhood Symptoms present before age 7 Clinically significant impairment in social or academic/occupational functioning Some symptoms that cause impairment are present in 2 or more settings (e.g., school/work, home, recreational settings) Not due to another disorder (e.g., Autism, Mood Disorder, Anxiety Disorder)

Answer 54

2 Subtypes: hyperactivity/impulsivity, and inattention  the primary symptoms of ADHD. Main type of symptom the child presents with will determine the specifier: inattentive type adhd i- more common in girls(may be ignored) hyperactive/impulsive type- adhd h hyperactive-inattentive or combined type adhd hi

Answer 55

Comorbidity: 50% Prevalence: ~2% in preschool-aged children, 6% among children and adolescents, 4% among adults. Developmental Trajectory. Most require chronic approach to management through adolescence and adulthood. -most important long-term issue is increased risk for developing another psychiatric disorder. Nearly half of adults with ADHD also have a mood or anxiety disorder. 50% have another disorder- most common is conduct or oppositional defiant, anxiety isorders In later years- ma experiences depression or substance use Most diagnosed need long term approach

Answer 56

Exact cause is unknown -biological cause expected: multiple risk factors interact Generally reduced brain size- reduction in gray matter, abnormalities in the metabolism of DA & NE- noradrenaline MRI studies linked ADHD with brain abnormalities:-prefrontal cortex, associated with executive functioning-basal ganglia, associated with higher motor control, learning, memory, and emotion regulation Abnormalities in pfc, basal ganglia Recent studies have found delay in reaching thickness of cerebellum- slower developed- symptoms in child but not adult

Answer 57

No obvious brain differences The amount of energy the brain is using is less Less activity in PFC Overacticity in basal ganglia Delayed Frontal lobe development and ADHD Delayed frontal lobe development At age 6- less developed than normal Normal pattern of development is delayed by 3 years Most difference in pfc Leads to smaller Brain size Differences in brain maturation, structure, and function: Frontostriatal circuitry Prefrontal cortex Basal ganglia Major implications for attention and response inhibition Fronstostrial region and its connections- most important in the dysfunction f those with adhd Less activity Cant hold memory, cant pay attention, cant inhibit behaviour

Answer 58

Prefrontal cortex- connected with other areas These areas connected through neurostransmiter pathways If one part not functioning- mess up loop Parkinson’s- damage substantia nigra Under activity in PFC- in adhd

Answer 59

Reduced fronto-straital activation Neurotransmitter differences, particularly in levels of Dopamine Norepinepherine Serotonin Things in frontal cortex- not enough dopamine, dopamine system not working Reduced striata Different pathways involved in adhd Dopamine transporter- Dopamine created- gets packed in vesicles- goes to receptor, dopamine transporter recycles dopamine- may be abnormality in transported= dopamine dysfunction

Answer 60

Fronto-striatal circuitry is disrupted, both functionally- connection with other areas and structurally- look different. frontal cortex is responsible for inhibition of attention and behavioural responses to salient but off task events basal ganglia is responsible for the motor response to these interfering events. Disruption of dopamine regulation in fronto-striatal circuit leads to decreased dopamine release & blunted response of receptors, resulting in behavioral presentation seen in ADHD Less dopamine released, receptor not being stimulated properly= behavioural presentation in adhd

Answer 61

Heritability may be 77% No gene linked directly Gestational factors: -pregnancy and delivery complications-prenatal toxin exposure: poor diet, antidepressant use, exposure to mercury, lead, alcohol, caffeine, cigarettes, illicit drug use, etc. Psychosocial factors: low socio-economic status, large family size, paternal criminality, poor maternal mental health, child maltreatment, foster care placement, family dysfunction Very genetic- genetic component Genes involving dopamine- have no found adhd gene Hard to find one link of adhd- often occur together

Answer 62

Gene-environment interactions (G X E) -ADHD results from an interaction between genes and the environment -similar to diathesis-stress perspective Ex. ADHD & ODD more common when children with certain type of dopamine receptor gene also had inconsistent parenting. Ex. ADHD symptoms present in children with a certain dopamine transporter gene only when mother smoked during pregnancy. G X E- any phenotypic event that resulted from both gene and environment Have genetic vulnerability- experience adverse event- causes activation of gene Gene and environment interact to make disorder more likely to present

Answer 63

Pharmacotherapy: stimulant medications -Ritalin (methylphenidate), Dexedrine (D-amphetamine).  Increase DA & NE release, and block reuptake Most likely symptoms to respond to medication are hyperactive, restless, impulsive, disruptive, aggressive, and socially inappropriate behaviours. Academic, social, and emotional difficulties generally do not improve Side effects commonly observed.- headaches, cant fall asleep, inc BP Usually pharmacotherapy Inc dopamine and norepinephrine and block transported that reuptake Hyperactive presentation- drugs work best for it

Answer 64

Psychoeducational interventions Parent training helps parents develop skills to manage their child’s behaviour: Contingency management- rewarding certain behavior most effective. Family therapy, CBT, individual psychotherapy, social skills training seem to be less effective. Teach parent and teacher techniques

Answer 65

Grey matter continues to decline up to 60 years of age. White matter peaks ~50 years of age Total Brain matter levels- Grey matter- declines up to 60, slow decline then levels off, may dip again at death White matter- peaks at 50 then decreases Grey matter- associate w inc in white matter(myelination of axon) CSF- inc across life- more space in Brain Development progressing- still can Learn

Answer 66

Associated with a gradually progressive loss of memory, mostly occurring in old age Affects 50% of people over 85, and 5% of people between 65-74 years old. Early onset seems to be influenced by genes 99% of cases late onset No drug treatment is currently (very) effective End of life Brain atrophy in Alzheimer’s Big spaces were ventricles were, neuronal loss

Answer 67

Alzheimer’s disease is associated with abnormal genes that lead to an accumulation and clumping of the following brain proteins: Amyloid beta protein Abnormal form of the tau protein clumps, producing tangles Amyloid beta deposit in brain cause neuronal degeneration Tau protein- cause take tangles- clumps of degenerated neurons Breaks down an neurons degenerate

Answer 68

Cell in prefrontal cortex, neuronal deteration Plaque- all old stuuf and tangle has formed- cells alll tangled

Answer 69

As it is being made, amyloid precursor protein (APP) sticks through the neuronal membrane Enzymes cleave beta-amyloid protein, releasing it into the space outside the neuron Clumps of beta-amyloid collect and begin to form a plaque Betamyloid get formed form app Small piece is logged in neuron rest is outside, enzymes clip off the beta amyloid- in normal it gets turned off and flushed with outer membrane In alzeiimer- get snipped at wrong place- each beta- amyloid causing plaque and neuronal death

Answer 70

Profusion of neurofibrillary tangles (Tau protein) Caspase theory: Beta-amyloid stimulates caspase formation  apoptosis Both plaques & NFTs occur early in AD Hippocampus & entorhinal cortex Memory and retention of learned information Tau protein maintains stability of microtubule In Alzheimer’s tau changes- cant support microtubules- get wound around each other, cause tangles, nerve cant communicate- die Happens ealr in the process- progress substantially before see issue- progressing for years

Answer 71

http://www.iflscience.com/health-and-medicine/slowdown-brain-s-waste-removal-system-could-drive-alzheimer-s/ BBB tight in young, healthy ppl Gatekeeper, but also waste removal β-amyloid movement slower in older people, builds up  damages brain and BBB more β-amyloid. Also other toxins enter! BBB ‘leakier’ in older people with MCI vs cognitively normal old people Could be issue with blood brain barrier- keeps stuff out of brain and takes bad stuff out of brain beta amyloid- movement slower n older people- bbb should get it out, if damages bbb, cause it to be leaky, toxins get into brain Memory problems- have leaky bbb

Answer 72

Number of ACh cells declines with age The final step in ACh synthesis catalyzed by the enzyme choline acetyltransferase (ChAT) In AD, ChAT is less active = The cholinergic hypothesis of AD Anti-AD medications: Preserve ACh by inhibiting acetylcholinesterase (AChE)  less enzymatic degradation Nuclei in areas are main source of ach- get loss in alzeiherms \ In presynaptic area- Chat- regulation ach, in Alzheimer’s- chat is less active= less ach= less activity in brain Begins as deficiency in ach

Answer 73

Synapse: describes the specialized gap that exists between neurons Neurotransmitter binds to receptor- causes change- open channel, lead to secondary effects When a drug binds to receptor may activate or inhibit it- have different effects n receptors Some will bind to them but not activate Bind to receptor= ligand(no matter what) Natural ligand- neurotransmitter Not alll act the same- don’t lead to same behaviour Can you control Brain functioning Neurons communicate via neurotransmitter transmission at the synapse(tiny gap) Synapse exist between neurons(not touching) and neurons are interacting at synapse- have neurotransmitter release and receptor

Answer 74

Over active amygdala- causes specific reactions such as freezing Control amygdala- control anxiety In anxiety- overactive amygdala and underactive GABA- over activating some areas under activating other areas- case symptoms o anxiety Anti anxiety- hack stress cycle- inhibit amygdala Gaba agonist- increases gaba activity- inc gaba function, inc inhibition- decrease activity in other area Rats with more musicinol gaba- did not learn fear response

Answer 75

Presynaptic neuron: neuron that delivers the synaptic transmission Postsynaptic neuron: neuron that receives the message- has receptors

Answer 76

German physiologist Otto Loewi The first to convincingly demonstrate that communication across the synapse occurs via chemical means The great majority of synapses rely on chemical processes Led to the development of psychiatric drugs .nerves- axons stimulate muscles by releasing neurotransmitter(chemical) Synaptic transmission can be both- most is chemical Revoloutionized drug research- can give chemicals to alter brain functioning

Answer 77

1 vagus nerve of frog heart stimulates 2 fluid transferred to second container 3 both frogs heart rates decrease after stimulation Stimulated vagus nerve of heart- decrease in heart beat Transferred fluid of heart to another frog- observed decrease in heartbeat (has to be chemical

Answer 78

Otto Loewi’s (next) findings: Stimulating the vagus nerve released something that inhibited HR; stimulating a different (accelerator) nerve released something that increased HR Realized that he was collecting and transferring chemicals, not loose electricity Neurotransmitters (NTs): chemicals that travel across the synapse and allow communication between neurons Stimulate different nerve- accelerate heart- inc heart rate Inhibition and excitation happening Has to be chemical

Answer 79

Transmitter must be synthesized or present in neuron. 2 When released, transmitter must produce a response in target cell Transmitter' 3 Same receptor action must be obtained when 4 There must be a transmitter is experimentally mechanism for removal after placed on the receptor. the transmitter's work is done. To be neurotransmitter- made in neuron Removed- diffuse, reuptake, diolved

Answer 80

Vesicles: tiny spherical packets located in the presynaptic terminal where typical NTs are held for release Exocytosis: bursts of release of NT from the presynaptic terminal into the synaptic cleft Triggered by an AP Most synthesize in presynaptic terminal- packed in vesicles- stay there until AP- Vesicles- release neurotransmitter upon AP AP reaches terminal- neurotransmitter releases

Answer 81

Transmission across the synaptic cleft by a NT takes fewer than 0.01 microseconds Transmission floats across synaptic cleft Attach to receptor most common synapse- at theaxon to dendrite

Answer 82

Step 2: The Importance of Calcium 1 When an action potential reaches the voltage-sensitive terminal, it opens calcium channels. 2 Incoming calcium ions bind to proteins, forming a complex. 3 This complex binds to vesicles, releasing some from filaments and inducing others to bind to the presynaptic membrane and to empty their contents by exocytosis. AP Combes- voltage activated channel open- forms complex with binding proteins of neurons lead to vesicle release Calcium causes complex to form- vesicle release NT Attaches to receptor and has effect on postsynaptic cell Can have second messenger affects

Answer 83

The effect of a neurotransmitter depends on its receptor on the postsynaptic cell Transmitter-gated or ligand-gated channels are controlled by a neurotransmitter: These are ionotropic. Ionotopic – ligan bind to receptor- ion Chanel open- ions flow through

Answer 84

Occur when a NT attaches to receptors and immediately opens an ion channel to allow ions to move across the membrane Most effects: Occur very quickly (sometimes less than a millisecond after attaching) & are very short lasting Happens immediately within Ms Happening all the tike Ion channel open and closes quickly

Answer 85

Occur when NTs attach to a receptor and initiate a sequence of slower & longer-lasting metabolic reactions Metabotroppic- slower- metabolic reaction NT initiate sequence of reactions ] NT binds to receptor, has intraceelur effect- G protein acticated( energy storing molecule) Opens ion channels but is much slower Or couples to ion- has many effect and can last longer- destroy dna When neurotransmitters attach to a metabotropic receptor, it bends the receptor protein that goes through the membrane of the cell Bending allows a portion of the protein inside the neuron (the G protein) to react with other molecules NT attach- G protein receptor- bends protein- G protein can detach- go and has effect

Answer 86

G-protein activation: coupled to guanosine triphosphate (GTP), an energy storing molecule Increases the concentration of a “second-messenger” = chemical that carries a message to different areas in the cell The second messenger communicates to areas within the cell May open or close ion channels, alter production of activating proteins, or activate chromosomes Proteins coupled to energy storing molecule gtp Can go and have second messenger effect- activate protein or enzyme

Answer 87

Negative feedback in the brain is accomplished in two ways: Autoreceptors: receptors that detect the amount of transmitter released and inhibit further synthesis and release Postsynaptic neurons: respond to stimulation by releasing chemicals that travel back to the presynaptic terminal where they inhibit further release-retrograde neurotransmitter One transmission has happened – don’t want it to happen forever- negative feedback- tells it to stop Autoreceptor- on presynaptic terminal- sense own neurotransmitter Auto receptor activated- inhibit transmission release Ppostsynaptic- respond to simulation of self- releases neurotransmitter- travels back to cell and inhibits activity at presynaptic terminal Can be happening at anytime

Answer 88

Many have both ionotropic and metabotropic receptors Gaba- open sodium- decreases membrane potential of cel Typical neurotransmitter molecules

Answer 89

Metabotropic effects utilize a number of different neurotransmitters Neuropeptides are often called neuromodulators Release requires repeated stimulation Released peptides trigger other neurons to release same neuropeptide Diffuse widely and affect many neurons via metabotropic receptors Use metabotropic receptors Neuron synthesizes these in cell body and dendrites Transported top other areas of cell Released at dendrites, cell body, side of axon- anywhere Modulate activity of nearby cells Release needs multiple stimulation Has cascade effect- activates other neurons triggering them to release same neuropeptide Released- every thing around is effected

Answer 90

Neuropeptides Neurotransmitters Place Cell body Presynaptic terminal synthesized Place released Mostly from dendrites, Axon terminal also cell body and sides of axon Released by Repeated depolarization Single action potential Effect on They release the No effect on neighbors neighboring cells neuropeptide too Spread of effects Diffuse to wide area Duration of effects Many minutes Effect mostly on receptors of the adjacent postsynaptic cell Less than a second to a few seconds Neurotransmitter- contain to synapses

Answer 91

Chemicals secreted by a gland or other cells that is transported to other organs by the blood where it alters activity Produced by endocrine glands Important for triggering long-lasting changes in multiple parts of the body Hormones are chemicals secreted by glands or neurons Conveyed in blood stream- released in blood stream and travel throug it, influencing organ behaviour Hormones convey message to any organ with receptors for it testosterone- in development- causes long term effect Hypothamalams releases to posterior Adrenal gland on top of kidney produce cortisol

Answer 92

Composed of chains of amino acids Attaches to membrane receptors where they activate second messenger systems Bind to membrane receptor- causes second messenger responses- metabolic

Answer 93

Medical Student in 1925 (17 yrs old) Noted similarities in symptoms of sick patients. “Since these were my first patients, I was still capable of looking at them without being biased by current medical thought. Had I known more I would never have asked myself questions, because everything was handled just the way it should be.” All suffering from different conditions but had similarities Had sore muscles, increased tonsils Why would they have similarities Forward to the 1930’s -working with ovarian extracts from cows. Seemed to produce a sickness syndrome (Stress) Injected rats with ovarian extracts Made the rats sick Developed symptoms from injections Enlarged adrenal gland, loosing hair More shots= more symptoms Regardless of what they were injected with, they got sick Took kidney extract- same thing happened Sickness syndrome Not the extract, injecting them repeatedly makes them stressed, causing them to experience sickness- non specific bodily response of stress demands

Answer 94

Alarm Body mobilizes to confront the threat Resistance Body copes with the threat by fighting or fleeing Exhaustion Physiological resources are depleted trying to cope with the threat Some mechanism in body whos respinse to external stressors- general Stress response- responds to anything that upsets homeostasis- severe enough= adapt to it Alarm- body responds to stressor, get stressor If it doesn’t go away- resistance- adapt to stressor If it still doesn’t go waway- exhaustion= cant fight threat, no more resources- get sick He thought only absence of stress- in death- have constant stressors

Answer 95

The endocrine system The autonomic nervous system The immune system Other body systems respond to stress All 3 interacting with each other and the brain initiate stress- feel physical stress Fight or flight response activated- primitive stress response- fight or run away- biological response to acute stress

Answer 96

Acute stress response Sam Respond quick fight or flight Chronic stress response Hpa Long term High alert Fight or flight response activated- primitive stress response- fight or run away- biological response to acute stress Onset of stress- associated with physical responses- fight or flight response Part of an axis- many systems working together SAM- Acute not chronic Respond quic, readies body fo fight vid flight HPA- Complex pathway interacting systems, help respond to constant stressor Interaction of orans- influence many processes, digestion, immune system, Mood and emotions affected by it Energy depletes 2 main stress responses

Answer 97

Automatic Amygdala- processes emotional significance of stimulus- mostly eye as negative Limbic system- adds emotion, feel fear or stress or anxiety Stress response- involves feeling not just physical Amygdala sends signals to hypothalamus- control centre between brain and endocrine system- connected to Pituitary gland Beginning of stress response- starts with perceptual response- what you think is stressful Amygdala- gives meaning to event Hypothalamus- has many nuclei and important connections to hormones galnds

Answer 98

Body threatened by immediate danger Physical response is immediate- followed by hr increase, sweating- cause by sympathetic nerves-stimulate nerves- release norepinephrine The adrenal gland relaseing- adrenaline and cortisol Sympathetic is faster Hormone release is slower Nervous system response faster than endocrine response Happens within seconds Adrenaline and cortisol- help with fight v flight

Answer 99

Stressful events that persist Perceived by hypothalamus- releases crh acts on pituitary to release acth Travels to adrenal glands- causes them to release cortisol Hypothalamus- CRH to pituitary- releases ACTH- goes to adrenal- releases cortisol Cortisol has negative feedback- continue stress- keep releasing cortisol

Answer 100

Adrenal gland cortex- releases cortisol Medulla- releases adrenaline or epinephrine

Answer 101

Stress response allows for wide range of adaptive circumstances. This is 'allostasis': achieving stability through change. It occurs via the 'stress response'.

Answer 102

HPA activates in morning Baseline-6 Afte eating goes up Rises and falls of cortisol Go back to baseline

Answer 103

How crisis changes during stressor Studies recruits for military looked at stress response while jumping out of plane Each days looked at cortisol anterior pituitary releasing hormones, cortisol eleveated before jump Do more jump- get used to it- reduce cortisol secretion Less activation of stress After becoming less stressed to it- have less response Testosterone and cortisol- antagonistic effect

Answer 104

Less-dramatic real-life situations also evoke clear endocrine responses Riding in train Normal not crowded- a title inc in epinephrine Crowded= more stressful= greater stress response- longer= more epinephrine

Answer 105

Determine the influence of psychological and physiological variables in determining the eating response to stress Stress respinse release energy store- chronic level of cortisol- influence eating behaviour If we depleteenrgy storage in stress- do we tun to higher calories Stress respinse release energy store- chronic level of cortisol- influence eating behaviour If we depleteenrgy storage in stress- do we tun to higher calories During 3 stress session- exposed to cognitive challenges - designed to be stressful- not enough time Speeches, puzzled, math puzzels On the stress day- had increased stress activity Wasn’t instant- lots of cortisol release after test Mood reactivity- had more negative mood and anxiety On control day had Dec in negative mood After stress and on rest day- given basket of snacks- left in room for 30 min- not pressured to eat, invited to Ate more calories on stress days- relationship between cortisol release and more eating Total calories consumed on the stress day was significantly related to change in cortisol Stress response uses energy- need to inc intake

Answer 106

Harry Harlow’s experiments on the effects of extended maternal separation. Examined maternal separation effect, mother infant reaction is important to developing normal stress response The ones who did not have access to mother- caged with other animals at time- when got to play with other animals- would not play- would sit together cautiously, seemed stressed

Answer 107

Neonatal handling impacts development. Environmental manipulation occurring early in life resulted in changes in the adrenocortical axis that persist through the entire life of an animal. High levels of stress hormones early in life manifest in many ways Changes in adrenal cortex axis- higher levels of stresss hormones Stress them by- holding them, seperate mother If held- still had warmth Used water maxe to test adults spatial memory- defects emerged as they were older- didn’t have good memory In handled rats- didn’t show any difference- touch and warmth In swim maze- hidden platform associate cues- remember where platform is Differences in cortisol release in response to stress test Not handled- released more cortisol- effects were delayed Look at offspring stress hormone receptor Had more glucocorticoid receptors in hippocampus- more effient negative response- lower levels of cortisol Affects hippocampus size Handled rats- don’t loose neurons or cell density Not handled rats- Dec in hippocampus size- not enough feedback- kills cells in hippocampus

Answer 108

Parental separation- inc stress response Depends on the care given University students described their parents Those wit could/ unloving parents- more likely to develop illness, higher level of substance abuse and MDD Experinestress in development has lasting impact on brain developement

Answer 109

Government of Romanian- forced to pay dents of old government- stopped sending money to orphanages Kids not taken care off- cold, grey dark spaces, many kids in bed Interacted with kids but not caregivers Showed us how it impacts the kids Many of them adopte Highest cortisol levels- had lowes scores later in motor and cognitive development Less glucocorticoid receptors- causes changes in kids Orphaned kids- had decrease rate of glucose metablixation Had less brain activity overall- less neurons The timing of deprecation- when it began and how long it lasted- linked to severity of problems Lived in orphanage for 9 months at least Compared to Canadian children and early adopted kids from Roman orphanage In orphanage for long time- more problems One girl- stayed 8 months then adopted- early child experiences led to abnormal adult behaviour- killed cats, fantasizes abt killing ppl Diagnosed w conduct disorder then institutionalize

Answer 110

Cope with stress Try to get chronic stress responses balanced- return to baseline- stress doesn’t go away reach exhaustion Cortisol necessary for normal functioning- immune response, metabolic Low cortisol can cause fatigue, dehydration Actuate stress response not stopped- cause chronic stress repsone Stress can’t be turned of cause secondary symptoms- ulcers, sickness Antacids- help ulcer pain Chronic stress- reduces gastric activity- acid secretion unbalanced-damages tissue Cant turn stress off- not good for body, acute stress is okay- not prolonged In humans- ruminate

Answer 111

Researchers looked at stres– lots of stress inc risk of dying by 43%- only if they thought they couldn’t handle stress Negative view of stress and chronic stress- kills many Change perspective on stress- Chronic stress- restrict blood vessels When told stress is helpful response to threat- had less restricted blood vesssel

Answer 112

Stress= pituitary activated- releases oxytocin(social upport and bonding) Compels you to seek support Part of stress response- stimulated to bond. Released into blood stream to act on target- released by hypothalamus activity- axon terminals release oxytocin from anterior pituitary- releases into blood stream Human connection- mechanism to regulate stress Oxytocin anti inflammatory- maintains blood cells(help recover from damage) Stress and SoCal interaction How much stress- ho much have you helped others in community, friends Every major stress- inc risk of death but ppl who spent time with helping activities- showed no stress related. Inc In dying- being socially bonded creates resistance ] harmful effect of stress— can be mediated by oxytocin

Answer 113

Additional support for the notion that more active responding leads to a diminished stress response Serotonin neurons ost active with repetitive movement Measured serotonin in cats No firing when not moving Walking on treadmill- can it stimulate serotonin release and mimic anti anxiety Serotonin release reduceing stress respone Sustained running exercise and HIT Looked at hippocampus generation Runners- had more new hippocampus neurons Different types of exercise- had same effect

Answer 114

Stress can be controlled by exercise, connection and perception of stress F we think we can control and manage it- less stressed Happy make T cells Uncontrollable- low T cells Controllable- if push button may be able to stop shock sometimes- if they believe they had control- inc in T cells Mindset of controlling stress- changes brain functioning Belief that you will do things to achieve your goal Self efficacy Is thei a relationship between stress and depression- was it managed ny self efficacy ]those with higher self efficacy- believe in themselves- decreased depression.

Answer 115

PFC damaged- executive function impaired- cannot assign specific roles to pfc subregions- probably due to interaction of these regions and the communication via the rest of the body

Answer 116

Prefrontal cortex- frontal lobe anterior to motor cortex- universally decided have subregions-dorsolateral pfc, ventrolateral pfc, ventromedial pfc, dorsomedial pfc Makes up a lot of the brain- linked to executive functions- process that function on short sided behaviour to acheieve a goal- self control, goal monitoring, problem solving- probably many areas of brain as it is very complex- distributed networks

Answer 117

processes hearing, dedicated to language, has memory storage, many functions, hippocampus located here

Answer 118

Parietal- interpret touch and somatic sensory info, touch sensations create movement and identify movement

Answer 119

If have PTSD- have deficits in DLPFC- cognitive and memory problems, can cause lack of emotion, attention deficit problems

Answer 120

Lots of evidence links executive function to PFc Cognitive flexibility- think of multiple things at once, strop task- hard for most people Cog flexibility- crucial aspect of frontal lobe processing those with frontal lobe damage- mentally rigid Wisconsin task- solution is constantly changing- have to not stick to what you think is role- have to be able to change thinking Those with frontal lobe injury- cant change mental state or approach to problem Associated to DLPFC

Answer 121

Right VLPFC- updates actions plans, controls attention Left VLPFC- more important for attentional control, resisting temptations Makes decisions based on connections from other areas, amygdala, hippocampus, temporal lobe, thalamus VLPFC- connected to rest of brain VMPFC- helps VLPFC in social decisions, social nctioningm suppressing negative emotions CRT- measure tendenc to override problem solving processes that are incorrect- predicts how they can overcome cog biases

Answer 122

Schwann cells: form myelin sheaths in peripheral nervous system (PNS); wrap only one axon; release growth factors and promote regeneration of damaged axons

Answer 123

Oligodendroglia: form myelin sheaths in central nervous system (CNS); wrap many axons

Answer 124

provide structural support for neurons and help maintain ionic balance in the extracellular environment; take up excess NTs- maintain homeostasis- take up excess transmitters

Answer 125

Microglia: remove dying cells by phagocytosis at sites of nerve damage; responsible for immune response- waste removal, immune response All glial cells important May contribute to disorders

Answer 126

cytoskeleton: network of microtubules and neurofilaments that provide shape and structure to the cell. Microtubules form a track that proteins travel along by the action of motor proteins.

Answer 127

Most ion channels are gated, but some K+ channels are not (=leaky); K+ moves freely K+ moves into the cell because it is attracted to the negatively charged particles (electrostatic pressure)

Answer 128

K+ moves back out of cell when its concentrationrises (down its concentration gradient)

2 Flashcards

(152 cards)