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PSYC2020 QUIZ 1

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QUIZ NUMBER ONE~
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Afferent nerves
Sensory and to the central nervous system (somatic nervous system)
Efferent nerves
Motor and from the central nervous system (somatic nervous system)
Autonomic nervous system
Afferent from internal organs
Efferent to internal organs
Sympathetic and Parasympathetic divisions- nerves are both efferent- TO internal organs
Meninges
Dura Mater- layer of membrane, tough and leathery- strong mechanical protection- surrounds and supports larger venous channels (dural sinuses) carrying blood to brain/heart

Arachnoid Meninx- net/lattics

Pia mater meninx- envelope that adheres firmly to surface fo the brain and spinal cord- pierced by blood vessels that travel to brain and spinal cord

- over the pia mater and separated from it by a space is subarachnoid space- thin, transparent membrane; cerebral spinal fluid is here which cushions the mechanisms of the brain
Cerebral Spinal Fluid
- sinus
- chloroid plexus- makes cerebral spine fluid; is replaced about 5 times per day
Ventricles
- empty spaces within the brain; lateral, third and fourth ventricles
cerebral aqueduct- connects third and fourth ventricles to ensure flow of CSF through these areas
Central nervous system in early development
Spinal Cord
- track of nerves which features H shapes; structure in middle which is the collection of all cell bodies of particular neurons- typical motor neuron
- off white matter are axons
- as nerve fibres approach cord, divide and split- afferent nerves into dorsal (closest to surface of back) and efferent like motor neuron axons into the ventral side which is inside side of spinal cord
Major divisions of the brain:5: Myelencephalon: hind brain- MEDULLA
- Composed of axonal traps/nerve fibres, reticular formation implicated in controlling your state of arousal
- Pons and cerebellum- mini cortex coordination of movement and sensory/ motor control
Metencephalon- hind
Consists of pons and cerebellum; arousal, balance, cardiac relfexes, circulation, fine muscle movement, sleep/breathing
Mesencephalon- midbrain
- Having 2 sections:
Top portion is TECTUM with colliculus- responsible for coordination of hearing/sound; superior colliculus plays a role
TEGMENTUM- CSF flows through hole; periaqueductal- management of bodies internal pain system- it sends pain blocking signals down spinal cord so pain signals is stopped from reaching brain
Substantia Nigra
- controls voluntary movement
- if this is diminished, may lead to symptoms pf Parkinson's
- these effects are mediated through STRIATUM- important for eye movement, motor planning, reward seeking, learning and addiction
Diencephalon (Forebrain)
- Thalamus; 3 major nuclei
LATERAL GENICULATE NEUCLEI- first synpase after the optic nerve leaves the eye- mainly rely for axons of eyes to visual cortex
MEDIAL GENICULATE NUECLI- auditory relay- inputs going through to temporal lobe
VENTRO POSTERIOR NUCLEUS- sensorimotor relay- just below optic chiasm (where axons leave 2 eyes, portion of the axons cross over to the other side of the brain)

HYPOTHALAMUS
- just below thalamus- controls pituary gland; four f's- feeding, fighting, fleeing and reproduction
Telencephalon (forebrain)
- cerebral cortex, basal ganglia, corpus striatum and olfactory bulb
- controls all voluntary actions of the body
- mainly; emotions, hearing, vision, personality
- primary motor cortex, primary sensory areas (somatosensory, gustatory, olfactory)
- olfaction- sense of smell
- language and communication
Gyrus and Sulcus/fissure
Gyrus- peak
Sulcus/ fissure- valley
Layers of neocortex
Two cells:
PYRAMIDAL- cognitive ability, normal motor control- long dendrites, thick layer in the motor cortex
STELLATE- cells primarily in visual cortex; star shaped, many shot dendrites
- so each layer differs in concentration of cells in relative size and concentration of cell bodies: vertical flow of information via long axons is basis of columnar organisation
Forebrain: Limbic system
- composed of cingulate cortex
- amaygdala- emotional responses (fear) and hippocampus in formation of new memories
Basal Ganglia
PUTAMEN AND TAIL OF CAUDATE= STRIATUM
- interest is focused on connections between striatum and substantia nigra in midbrain- Parkinson's is associated with degeneration of this pathway
MOTOR NEURON
EFFERENT- moving toward a central organ/point, relays messages form the brain or spinal cord to muscles and organs; short dendrites and long axons, dendrites and cell body are located in the spinal cord; axon is outside the spinal cord and conduct impulse to an effector (muscle/gland)
SENSORY NEURON
AFFERENT NEURON- moving away from a central organ/point, relays messages from receptors to the brain/spinal cord; long dendrites and short axon; cell body and dendrite outside of spinal cord, cell body in dorsal root ganglion; conduct impulses to spinal cord
INTERNEURON (RELAY)
- Relays message from sensory neuron to motor neuron- make up brain and spinal cord; short dendrites and short or long axons- entirely within the spinal cord/CNS, interconnect the sensory neuron with appropriate motor neuron
Resting membrane potential
5 FACTORS
1. Random motion- some bounce in and out of membrane by chance
2. Differential permeability of the membrane- permeable to sodium and potassium ions' some easy other difficult
3. Electrostatic pressure- like charges tend to repel one another and opposite charges tend to pull things together
4. Concentration gradients- things with high concentration in one area, they tend to diffuse and flow down concentration gradient and dissapate to areas of less or low concentration
5. Sodium Potassium pump- active and uses energy from within the cell
Absolute/ Relative refractory period
Absolute- when cell is so negatively polarized that no amount of stimuli will cause cell to have an action potential
Relative- membrane potential less than 70 but not so negative that it wont fire, will if given more stimulation
*ABSOLUTE ensures information only travels in one direction and RELATIVE allows us to know intensity of expression of the stimulus
COMMON TYPES OF SYNPASES
1. Axodendritic (axon terminal buttons on dendrotes)- prototypical
2. Axosomatic (axon terminal buttons on soma/cell body)
BUT ALSO
3. Dendritic spines- axon terminal button on sines of dendrites
4. Dendrodendritic- dendrite to dendite and often bidirectional transmission
5. Axoaxonic (can mediate presynaptic facilitation and inhibition of that button on post-synaptic neuron)

NOTE: small molecules produced and packaged in terminal buttons and neuropeptides are large; synthesized and packaged in cell bodies and transmitted down micro tubules SO neuropeptides are larger molecules
2 types of receptors
IONOTROPIC RECEPTORS
- associated with ligand activated ion channels (fast acting and gate receptors) open protein channel, ions (permeable) rush in
METABOTROPIC- associated with signal and G proteins; slower and where information transmits across membrane via signal protein; G protein effect could open/close channels r it could travel to nucleus and change expression of DNA in cell- non directional and slow acting
7 STEPS IN NEUROTRANSMITTER ACTION
1. NT molecules synthesized from precursor under influence of enzymes
2. NT molecules stored in vesicles
3. NT molecules that leak destroyed by enzymes
4. Action potential causes vesicles to fuse with presynaptic membrane and release neurotransmitter into the synapse
5. Released NT bind with autoreceptors and inhibit subsequent NT release
6. Released NT bind to postsynaptic receptors
7. Released NT deactivated by uptake, reuptake or enzyme degradation
Pharamacology: DRUGS
- alter NT activity by:
AGONISTS: increase or facilitate activity
ANTAGONISTS: decrease or inhibit activity
Can alter NT activity at any point in life cycle
- whilst in neruone (presynaptically); reduce production, inhibiting release
- at synapse/junction- promoting destruction, blocking up-take, blocking re-uptake
PULFRICH ILLUSION
- the speed of transduction of signals, from retina to the brain, correlates with luminescence intensity- by reducing intensity with a filter, you delay signals from the filtered eye relative to signals from unfiltered eye
Pendulum
Pendulum swining to the RIGHT WITH LEFT EYE FILTERED:
- at first, pendulum corresponding points in the two eyes
- as pendulum begins swing, ;left eye delay makes pendulum seem to lag behind the right eye image- as wining to right signals uncrossed disparity
- as the pendulum nears the bottom, accelerates so disparity signal increases
- as pendulum begins to move up, it slows, so disparity decreases until movement stops therefore pendulum at corresponding points again
BUT, IF WE FILTER THE RIGHT EYE
Backward/anticlockwise rotation
When right eye filtered, signal form right eye lags, so disparity signal increases with pendulum acceleration whereas left eye perceives ball as further to the left. As a result crossed disparity, then uncrossed.
MONOCULAR DEPTH CUES?
OCCLUSION- images hidden by one another; objects in front seem closer
LINEAR PERSPECTIVE- lines converge into distance
RETINAL SIZE- more distant objects seem smaller
TEXTURE GRADIENT- texture elements decrease with size
LIGTH SCATTER- distant objects hazier? bluer?
MOTION PARALLAX- head movements similar to getting input from multiple eyes
SHAPE FROM SHADING- can give rise to depth perception
Visualising and stimulating the brain: X-ray
- X-rays not effective
- Contrast x-rays- inject a contrast substance to accentuate the difference between the target tissue and the surrounding tissue
- X-ray computed tomography= CAT SCAN
- Computer assists in reconstructing 3-D structure of the brain from man individual "slices"
Positron Emission Tomography (PET)
- Inject a radioactive isotope (2 deoxyglucose)
- Inhale a radioactive isotope of CO2
- Isotope is taken up by active portions of the brain but not broken down
- Radioactivity is short lived- half-life of isotopes is less than three hours
Magnetic resonance imaging
- Detects the waves emitted form hydrogen atoms when in a magnetic field
- fMRI scanning- giant magnet0- lines all hydrogen atoms in neat row and it pulses; device detects what happens to waves of hydrogen atoms as they fall in and out of alignment
Functional Magnetic imaging: fMRI
- captures areas of increased oxygenated blood flow
- more active areas take up more oxygenated blood
- oxygenated blood has magnetic properties
- BOLD signal- blood oxygen level dependant signal
o Advantages: no injection required, structural and functional information in the same image, good detail (spatial resolution), 3D images of activity over the whole brain
o Disadvantages: poor temporal resolution (1-1/2 second lag)
Transcranial magnetic stimulation
- Single magnetic pulses are applied to specific locations on the scalp at specific times during a behavioural task; or repetitively prior to task performance (rTMS or "virtual lessoning)
- Magnetic activity disrupts activity in the targeted structures by inducing an electrical current
- Cognitive or behavioural consequences are then observed
- A nice adjunct to fMRI, PET because it permits causal inference about the necessity of a specific brain region for performing a given task
Magnetoencephalography (MEG)
- Measures changed in the magnetic fields on the surface of the scalp
- Very good temporal resolution
- Poorer spatial resolution
Electroencephalography- EEG
- Recording psychophysiological activity
- Records the sum total of all electrical brain activity occurring at a particular time- not as specific as MEG with magnetic fields; utility of this technique is not in localising specific points in time but you can take aggregate of all information and take average to find specific types of wave patterns emerging
Electromyography- EMG
- Recording from specific muscles- records the number of action potentials or spikes associated with a particular muscle action
Electrooculography
- Monitors the specific contractions of the ocular muscles; if record from lateral and medial rectus muscle, can tell whether moving eyes left or right
Skin conductance:
- Often changes in response to emotional stimuli
- SCL" the skin conductance level (baseline)
- SCR" the skin conductance response, the change in skin conductance in response to a stimulus
Cardiovascular activity
- Electrocardiogram (ECG)
- Blood pressure
Invasive research methods: stereotaxic surgery
- Involves he placement of a recording or stimulating device in a target region of the brain
- Need a stereotaxic atlas (each page refers to a thin slice of the rat brain) and device
Lesion Methods:
- Removing or disabling a portion of the brain and observing the resulting behaviour
o Aspiration lesion- sucks up some neural tissue- sucks up cell body and leaves axons in tact
o Radio frequency lesion- delivers a microwave pulse, destroys a patch of tissue in close proximity to the device
o Knife cuts- cutting connections between nuclei and brain; cut axons or nerve or neural fibres
o Cryogenic blockade- reversible probe with coolant that cycles though and it cools the tip of a probe; when you cool a neuron its activity reduces so you can observe behavioural consequences
Interpreting the effects of lesions:
- Lesions are seldom administered with 100% accuracy
- The target tissue is lesioned but so is some of the neighbouring tissue
- Functions are inadvertently attributed to the target structure that are actually carried out by the neighbouring tissue
- Sometimes the entire structure is not lesioned and a portion remains- as well as some function. That structure may be discounted as playing a role in the associated behaviour
Invasive electrophysiological recording methods
- Intracellular recording- super fine microelectrode into the cell body of a neuron; moment to moment fluctuations in the membrane potentials
- Extracellular- recording number of action potentials and the number of times a neuron fires in a particular area
Pharmacological methods
- The goal is to increase/decrease the effects of particular neurotransmitters
- Drugs are injected or fed to the subject but often do not pass through the blood brain barrier
- Use of a cannula (to inject drug directly to target tissue) to deliver the drug to the target tissue
Chemical Lesions
- Instead of mechanically removing target tissue, neurotoxic chemicals for which the target tissue has an affinity are injected
- Kainic acid destroys cell bodies close to the administration site but leaves axons unaffected
- 6- hydroxydopamine is taken up only by neurons that release norepinephrine or dopamine- other cells unaffected
Measuring chemical activity in the brain:
- 2- deoxyglucose technique
- 2-DG is similar to glucose but not rapidly metabolised by neurons.
- Is taken up by active neurons
- After the animal engages in the target behaviour, it is sacrificed and its brain is sliced and get fine resolution to which regions are involved in the target behaviour
- Regions with high concentrations of 2-DG are identified as responsible for the target behaviour
Genetic methods:
Twin studies:
- Monozygotic twins share 100% of their genotype
- Dizygotic twins share 50% of their genotype
- Concordance rates versus discordance rates
o Look at records for various disorders
o If the monozygotic sample has a higher concordance rate than the dizygotic sample, this is evidence for heritability
o Eg. Schizophrenia
Genetic Engineering
- Gene knockout techniques
- Genes govern the structural and behavioural development of the organism
- Knock out a specific gene and observe the consequence- infer a link
Problems:
- Behaviour is often the result of the actions and interactions of several genes
- Elimination of one gene often influences the expression of other genes
- Don't forget about environmental determinants
Behavioural research methods of biopsych:
Neuropsychological testing
- Generally involves two stages
- A battery of general tests
- A follow up of more specific tests guided by the first tests
General tests include:
- IQ tests
- Token test- language ability
- Language lateralisation: one hemisphere typically participates more than the other in language, identifying the language hemisphere is important when planning surgery, sodium amytal test- anaesthetic that shuts down the brain
Maintenance and reorganization of neural circuits
1. TIME DEPENDANCE:
- window of opportunity within which experience can influence development
Critical Period- when it is absolutely essential that an experience occurs within a given time limit- and then other mechanisms follow on
Sensitive period- when an experience can still have an influence outside the interval
2. EXPERIENCE/USE
Hebb: neurons that fire together wire together- if circuits are established, then not used, they do not survive- they need to be maintained: USE IT OR LOSE IT- nurture as well as nurture
DEPRIVATION, ENRICHMENT AND EXERCISE MAY IMPROVE REORGANIZATION AND GENERATION OF NEURAL CIRCUITS
Effects of experience on hippo campus
- In adult rats, increase in neurons in the dendate gyrus of the hippocampus and in olfactory bulbs
- enriched environments: 60% more hippocampal neurones
- associated with exercise and interaction with the enriched environment
IN HUMANS:
- post exercise, the volume of blood flow through the hippocampus is related to the first trial of learning- so after exercise, people tend to remember more words
Competition in neural development: evidence from VISION
Selective deprivation- e.g. monocular deprivation
- occular dominance columns (layer IV) in many species are developed at birth
- deprivation of input in one eye during sensitive period leads to reduced activation of layer IV of the corresponding visual cortex
- but the activation of the other cortex by the intact eye is increased
- not just a single process, but rather one of shifting and re balancing of inputs
Brain Plasticity and Guided Recovery
Cortical maps and modification by experience:
- cutting nerves, sewing together fingers of one hand (denervation=peripheral), altering demands on system by increased use
- changes somatosensory maps= cortical
- relevant part of the cortex no longer responds to the touch of that finger
- but that now defunct area soon starts to respond to stimulation of the ADJACENT finger, it fills in the silent area and takes over
- so the adult cortex is a dynamic area, where changes can still happen
Re organisation of sensory maps in primate cortex
- mapping of the somatosensory hand area in the normal monkey cortex- individual digit representations revealed by single unit recordings
- if the two fingers of one hand are sewn together, months later the cortical map change so that the sharp border once present between the two fingers is now blurred
Brain plasticity and Guided Recovery- (young) humans
- musicians
- stimulated thumbs and fingers, and showed that responses were higher in musicians- suggests that larger cortical area is dedicated to touch in musicians
- the size of the effect correlated with the age at which they had begun their musical training
Brian Plasticity and Guided Recovery
- but can these changes happen in adults?
- simple motor task (touch finger to thumb in particular sequence)
- performed task a few minutes each day- accuracy and speed improved with practice
- fMRI; trained and untrained sequences
- greater changes in corresponding motor cortex for trained than for untrained after a few weeks
SO IN NORMAL BRAIN, TRAINING CAN INDUCE RAPID CHANGES IN ORGANISATION THAT REFLECT PLASTICITY, SO THERE IS A DEGREE OF FUNCTIONAL PLASTICITY IN THE CORTEX
Effects of experience on topographic sensory cortex maps
- Knudsen and Brainard- raised barn owls with prisms over their eyes
- prisms displace visual field X degrees to the left or right
1. vision mapping shifted in the direction of the prism
2. auditory map also shifted in the tectum in the corresponding direction and by a corresponding extent
- this makes sense because objects need to be heard in the location in space they occupy
Phantom Limb Phenomena
- after amputation, patients can still feel as though they have the limb and can feel pain and other sensations in or on it
- after time elapses, they still feel as though it exists, it "reduced in size"/telescoped- if the amputated part is hurt, the limb can feel enlarged again
Neural degeneration after brain damage
ANTEROGRADE- form the point of disruption forwards to the synaptic terminals (the distal segment); happens fast because of separation from metabolic center
RETROGRADE- from the point of disruption backwards to the cell body (the proximal segment); slow, over days; reduction in size, then death; there may be an increase in production of proteins, but the regeneration is not guaranteed
TRANSNEURAL DEGENERATION
- damage spreads to neurones that are linked synaptically
Concussion
- blow to the head, extremely breif loss of consciousness, or may have no loss at all
- temporary confusion, behavioral, affective and cognitive problems
- no evidence of structural (neuronal) damage; break down of micro tubules then neurotransmitters don't have an easy pathway down the axons
CUMULATIVE EFFECT
- internal; bleeds
- linear and rotational forces can lead to cell death
NOW evidence that there is damage, a well as cognitive and behavioural consequences
Closed Head Injury
- the blow does not penetrate the skull BUT
- contusions- bruises; when the brain slams against the skull
"coup" and "contracoup"
BUT ALSO
Haematomas- bleeds due to the shearing of blood vessels; alcohol is anti-coagulant
AND ALSO:
Oedema- swelling due to fluid- actually protective mechanisms, but damage because of pressure
Loss of consciousness- downward pressure on brain stem but also when brain moves forward it tends to "twist" in the skull, disrupting brain stem functions including consciousness
Epilepsy- disrupted tissue can start to produce impaired neural activity
Penetrating Head Injury
- when the blow penetrates the skull
- as for closed HI plus infections, scarring and thus epilepsy
SKULL FRACTURES:
- linear or depressed
- depressed is more complicated because it impacts drives fragments into dura and brain- infection and focus for epileptic activity
POST TRAUMATIC EPILEPSY:
- due to presence of scar tissue (changes in membrane structure and function)
- patients typically receive anticonvulsants prophylactically
Biomechanics of TBI" the neuronal level
- with either anterograde or retrograde degeneration, the neurone is not activated by the post synaptic axon; domino effect of metabolic changes
- neurons that are not completely ruptured may re-sprout axonal projections- restoration
- BUT they may also form unwanted connections- behavioural disturbance
Cerebrovascular accidents (strokes)
- sudden disruptions to brain's blood circulation
- any abnormality of the brain resulting form pathology of the blood vessels:
- lesions of vessel wall
- occlusion of lumen due to thrombus/embolus
- increased viscosity or other change of the blood)- blood becoming too thick or thin
STROKES- HARMORRHAGE
- bleed into the brain when blood bessel ruptures
- may happen because of weakness in blood vessel wall or because of aneurysm
ISCHAEMIA
- disruption in blood supply; thrombus, embolus and arteriosclerosis
- the consequences of ischaemia typically take a few days to develop
Cerebrovascular accidents (Strokes)
- strokes cause INFARCTS" areas of dead tissue
- this is surrounded by the PENUMBRA which is 'alive' but dysfunctional, which may recocver depending on treatment
Mitochondria and cerebral hypoxia
- sites of aerobic metabolism and converts food energy into useful form
- cerebral hypoxia leads to mitochondrial dysfunction
- on reperfusion (give more oxygen to gain more function but more likely than that is it is going to relapse again) dysfunction is partially and transiently reversed
- secondary energy failure
- neurotransimtter dysfunction
- neurone death
Neural regeneration in adults
- in mammals including humans, this is not as simple as lower vertebrates
1. the capacity is high in early development but drops off with maturity
2. distinct between CNS and PNS regenration
- PNS more capable, schwan cells produce neurotophic factors to stimulate growth and cell adhesion molecules on their membranes provide paths for growth
Neural regenration in the PNS
Regenration from the proximal stump fo the nerve starts about 2 to 3 days after damage
1. If the Schwann cells are not damaged, the axon can re-grow through and get to its original target
2. If there is complete but small separation (including Schwann cells) the axons may re-grow into the wrong sheaths=wrong destination= poor coordination
3. If there is complete but large separation, there may be no regeneration, and the re-growing axons become a tangle, with no destination
4. When an axon degenerates, axons from neighboring intact neurones may grow to synapse at the vacated sites=collateral sprouting
Mechanisms of CNS reorganisation
1. Establishment of new connections by collateral sprouting- long term reorganization can be too great to be explained by changes to existing connections only
2. Strengthening of existing connection due to release from inhibition (by original connections)- reorganization can be so rapid but also restricted, it cant be explained by normal growth, rather a change in the balance of maintenance
Recovery of function after brain damage
- AGE;
if the cerebral cortex is damaged while neurogenesis is still ongoing, the brain is able to compensate by making neurons and there is a better functional outcome than if the injury is in adulthood
- if there is damage during the time of neural immigration, there is poor functional outcome
- injury during the peak time of synaptogenesis allows for compensatory synpatogenesis and correlated functional improvement- thus an injury during the 3rd trimester and birth will lead to poor functional outcome because this is the time of maximum migration
- in contrast, injury during the next 18 months will allow a better outcome because this is the peak time of synaptogenesis
- INTELLIGENCE;
- higher premorbid intelligence, better recovery
- possibly due to greater plasticity (more education, more synapses)
- generate more strategies to solve problems
Other factors to recovery of function after brain damage:
SEX;
- females have less functional lateralisation than males in imaging studies, hence may show more functional recovery
HANDEDNESS
- left handers, less lateralisation of function than right handers=advantage for recruiting undamaged regions after brain injury
PERSONALITY
- optimistic, extroverted and easygoing individuals tend to have a better prognosis following brain injury, possibly due to greater compliance with rehab program
Treatment of NS damage- reducing brain damage
Rehabilitative training:
- Reducing the extent of lesions
- rehabilitative training
*competition
- strokes in humans: neurones compete for synaptic sites and neurotrophins; this can be turned to advantage; increased training with affected limb or constraining intact limb and forcing use of affected one