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Biological Flashcards

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1
Q

How do we study what is inside the brain?

A
  • Phrenology bumps on skull reflected functions/traits
  • clinical cases
  • animal lesions
  • looking at living brain
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2
Q

What happened to Phineas Gage?

A
  • 1848 accident of 25yr old
  • personality before= pleasant, reliable, responsible
  • after= undependable, foul-mouthed and angry
  • his intelligence remained
  • left frontal lobe damaged
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3
Q

What is prosopagnosia?

A
  • inability to recognise faces
  • bilateral damaged to fusiform gyrus
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4
Q

how can we see the effect of direct brain stimulation?

A
  • stimulation using implanted electrodes
  • probe brain of person undergoing brain surgery
  • single cell recording
  • optogenetics: activate targeted neurons by device that shines laser
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5
Q

Why are there animal research studies?

A
  • important source of info
  • underlying mechanisms of behaviour + easier to study non human species
  • experiments can’t use humans
  • ethical debate- controversial
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6
Q

What is transcranial magnetic stimulation (TMS)?

A
  • applies intense magnetic field= temp (de)activates neurons
  • study brain area active> then inactive & active again
  • finds causal role
  • allows researchers to study brain-behaviour relationships in a more systematic way and in larger samples
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7
Q

what are different lesion studies?

A
  • knife cut= cut subcortical tract> fine metal tube is positioned next to it > once in position, the knife blade pivots out of the needle, cutting tract
  • electrolytic lesion: a subcortical structure can be destroyed by positioning an electrode tip in it and passing sufficient current across the tip to destroy the tissue
  • aspiration lesion: parts of the surface of the brain can be removed by sucking them away through a fine hand-held glass pipette connected to a vacuum pump
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8
Q

What is computerised axial tomography CT/CAT?

A
  • injection of dye
  • passes x rays through head> scanner rotates through head til measurements taken at each angle
  • computer constructs image> medium res images> looks at damage e.g. strokes
  • cheap
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9
Q

What is an MRI?

A
  • 3D view of brain> creates an image of the brain based on release of electromagnetic energy from atomic nuclei
  • images based on signal protons> hydrogen atom
  • noisy, shielded room
    + non-invasive & - ionising, safer& less expensive, excellent spatial res
  • time consuming
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10
Q

What is an electroencephalogram (EEG)?

A
  • EEG> records electrical brain activity via surface electrodes.
  • produce evoked potentials that self-reports sometimes don’t reveal.
    + cheap, mobile equipment, tolerant to movement, non-invasive & temporal resolution
  • lower brain areas weak signal, spatial resolution
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11
Q

what is a Magnetoencephalograph (MEG)?

A
  • non-invasive imaging technique> measure magnetic fields generated by electrical activity of neurons in brain.
  • currents in neurons dendrites in synaptic transmission> detectable signal= 50,000 active neurons
  • need shielding magnets
    + good temporal resolution
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12
Q

A PET (Positron Emission Tomography) scan?

A

-radioactive marker records emissions/gamma rays
-visualise brains blood flow
-Brain regions involved in specific tasks.
- invasive, Tracer needed

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13
Q

what is an fMRI scan?

A
  • strong magnetic field.
  • picks up blood oxygenation levels
  • excellent special resolution, safer & less expensive than PET non-invasive non-ionising radiation
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14
Q

what are the two types of cells in the nervous system?

A
  • neurons> receive & transmit info in electrochemical form
  • Glial cells> support neurons in function e.g. provide structure, nutrition etc
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15
Q

what are the main components of a neuron?

A
  • cell body> metabolic brain of cell+ nucleus
  • dendrites (tree-like branches)> receive info from other neurons> some contain dendritic spine= increase surface area= more info received
  • axon (thin fibre)> info sending pole, transmits nerve impulses towards other neurons, organs etc> covered w/ myelin sheath
  • axon terminal> end points of axon, release chemicals to communicate w/ next neuron
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16
Q

what is the structure of neuron cell body?

A
  • membrane: 2 layers of phospholipid molecules, uncharged molecules can pass through
  • protein channels: charged ions pass through
  • nucleus: contains DNA
  • mitochondrion: provides energy, fuel & oxygen
  • ribosomes: synthesise new proteins
  • endoplasmic reticulum: transport proteins to other cells
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17
Q

what are the different classifications of neurons by shape?

A
  • multipolar neuron> many dendrites + single axon
  • bipolar neuron> single dendrite at one end + single axon on other end
  • monopolar neuron: single branch extending in 2 directions
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18
Q

what are the different classifications of neurons by connections?

A
  • afferent: receiver info comes into a structure> receptor or sensory neurons (skin-CNS), sensory transduction= receive sensory input & convert to electrical impulse to other cells> highly sensitive
  • efferent (exit): sends info away from a structure> motor neurons (CNS-muscle), motor transduction: send impulses to muscles or glands
  • interneurons/ intrinsic neurons> dendrites and axons are contained within single structure e.g. spine> connection between motor + sensory neurons
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19
Q

what are the different types of Glial cells?

A
  • Astrocytes: largest glial cells> wrap around blood vessels + cell bodies, synchronise activity of neuron> remove waste material created when neuron dies
  • Microglia: smallest glial cell> remove waste material, viruses & fungi> part of immune system + protect brain from invading micro-organisms
  • Oligodendrocytes> myelinate multiple axons in CNS
  • Schwann cells: myelinate single axons in peripheral NS
  • Radial glia> guide migration of neruons & growth of their axons+ dendrites during embryonic development
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20
Q

What are nerve impulses?

A
  • electrical message transmitted down axon> speed=1 m/s-100
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21
Q

what is membrane potential?

A
  • diff in electrical charge between the inside and outside of the cell
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22
Q

What is resting potential & how does it work?

A
  • neuron is at rest= higher concentration of +ve charged ions outside than inside which has -ve charged ions> state of neuron prior to sending a nerve impulse
  • resting potential is not 0> (-70mV)
  • neuron membranes potential maintain electrical gradient (polarisation)
  • all parts of neuron covered by thin membrane> protein ion channels are selectively permeable= some chemicals pass more freely than others & when protein ion is at rest they are closed
  • negative protein molecules account for more of negative resting potential
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23
Q

what gradients drive ions in and out of neuron?

A
  • happens only when membrane channels are open but they are closed
  • concentration gradient= diffuses ions when there is high concentration in particular area> Na+ = pulls sodium ions into cell,, K+ = push it out
  • electrostatic gradient: opposites attract> -ve ion attract +ve> Na+ = -Ve charge= pulls in,, K+ = pulls into cell cos +ve charge as inside cell is -ve charge
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24
Q

what is the sodium-potassium pump?

A
  • active protein channel> uses energy to pump ions in & out> transports 3 Na+ out & 2K+ into cell
  • corrects leakage
  • more +ve out than in
  • works against concentration gradient&electrostatic gradient
  • uses lots of energy
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25
Q

what is the action potential?

A
  • electrical impulse that travels along the axon> surrounded by semipermeable membrane = only allowing certain ions to pass through
  • once threshold reached> membrane goes +ve when voltage gated (Na+) channels open= Na+ to go into cell= depolarisation (increase of +ve charge)> once reached peak=inhibition gate closes Na+ channel
  • repolarisation> K+ voltage gate opens & K+ diffuses out of cell= voltage inside cell becomes more -ve= -ve membrane potential (goes back to normal)
  • below threshold=both gates closed= hyperpolarised> relative refractory period before membrane returns to resting potential (-70mv)
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26
Q

what is the difference between absolute refractory period & relative refractory period?

A
  • relative refractory period= less likely for cell to be stimulated & undergo action potential right away cos its more negative than at normal resting period
  • absolute= action potential must go positive & must go negative before another action potential> whilst one action potential is happening can not have another one at same time
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27
Q

what is the presynaptic membrane?

A
  • on presynaptic terminal of axon
  • contains vesicles w/ neurotransmitters
  • membrane has high concentration of Ca++ channels> more concentrated outside
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28
Q

what is the structure of the synaptic cleft?

A
  • 20-40nm gap
  • separates pre-&post synaptic membranes
  • contained extracellular fluid
  • neurotransmitters diffuse here
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29
Q

what is the structure of the postsynaptic membrane?

A
  • on postsynaptic spine of dendrite or cell body
  • contained specialised proteins for neurotransmitters
    -neurotransmitter receptors function varies> often control ion channel+ cause hyper-polarisation
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30
Q

what is temporal and spatial summation?

A
  • temporal: several impulses from one neuron over time > if 2 or more excitatory stimuli close together= EPSP added together=action potential
  • spatial: impulses from several neurons at same time> can lead to EPSP added together= action potential> if inhibitory= cancel each other out
  • Only spatial summation can produce an action potential
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31
Q

what are graded potentials?

A
  • neural response varies in strength, depending on the intensity of the stimulus that triggers it> influence likelihood of action potential= graded potential> diff to action potential which follows all or none law when threshold is reached
  • occurs in dendrites or soma
  • Inhibitory postsynaptic potential (IPSP)> hyperpolarised postsynaptic membrane = more -ve> k+ ions leave= less likely for action potential to fire> decays over time & space
  • Excitatory postsynaptic potential (EPSP)> depolarises postsynaptic membrane (less -ve)> Na+ ions enter cell= more likely for action potental to fire> if the stimulus is not big enough to reach threshold =decays over time& space
  • action potential only generated if graded potential depolarises axon hillock enough to reach threshold
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32
Q

what is chemical transmission at synapse?

A
  • action potential arrives at presynaptic axon terminal
  • voltage-gated calcium channels open: Ca++ enters axon terminal
  • Ca++ causes vesicles to bind to presynaptic membrane & burst releasing NT into synaptic cleft (exocytosis)
  • NT diffuses across cleft> binds to reports in postsynaptic membrane
    ^ if receptor opens Na+ channels postsynaptic neuron depolarises (EPSP) > if receptor opens K+ or Cl- channels= IPSP
  • NTs separate from receptors & taken back to presynaptic neuron> diffuse away
  • postsynaptic cell sends -ve feedback to presynaptic autoreceptors= slow release of NT
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33
Q

what are the 2 main types of receptors at postsynaptic cell?

A
  • Ionotropic: ligand-gated ion channels> directly alters membrane potential> very fast
  • Metabotropic: slower but have greater effects
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34
Q

what is Neurotransmitters: Acetylcholine (ACH)?

A
  • first NT discovered> released by cholinergic synapses> project widely throughout CNS
  • 2 types of receptors> nicotinic (Ionotropic) & Muscarinic (Metabotropic)
  • important for muscle movement, processes during REM sleep, learning & memory> widespread loss of cholinergic neurons in Alzheimer’s
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35
Q

what are Cholinergic Pathways in the Brain?

A
  • The cholinergic system plays role in memory by maintaining neuron excitability+ active in waking up electroencephalographic pattern of cortex> death of cholinergic neurons & decrease in ACH = Alzheimers
  • found in basal forebrain cholinergic system, frontal cortex, corpus callosum
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36
Q

what are the different Monoamine neurotransmitters?

A
  • Catecholamines: play role in regulation of mood, emotion& cardiovascular function etc
    ^ dopamine: crucial in motor control> loss in Parkinsons, overactivity linked w/ schiz + regulates emotion
    ^ Norepinephrine: wide projection paths in brain, modulates behavioural & physiological processes + active in maintaining emotional tone i.e. decrease in NE = depression
  • Indoleamines: refers to serotonin & melatonin >play a role in mood regulation, sleep etc> low lvls= bipolar, anxiety etc
    ^ Serotonin (5-HT)> at least 15 types of 5-H T receptors
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37
Q

what are Serotonergic pathways in brain?

A
  • control sleep states, mood, anxiety, appetite etc
  • changes in serotonin activity related to OCD& schiz
  • decrease in serotonin = depression
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38
Q

What are the different types of drugs?

A
  • stimulants: Increase excitement, alertness, motor activity and elevate mood.
    ^ Amphetamine & Cocaine> blocks catecholamine reuptake> short term= heightened alertness & euphoria, no need for sleep// negative-paranoia & mental detoration
    ^ nicotine> increase heart rate, blood pressure + motor activity in bowel
  • Hallucinogens: LSD, peyote, mushrooms> distort sensory perception, affects NT systems + anti-psychotic block DA& 5-HT receptors
  • opiates: morphine, codeine &heroin> decrease sensitivity to pain, bind endorphin receptors + increase DA release
  • Marijuana: Cannabinoids> THC active ingredient> attaches to cannabinoid receptors
39
Q

What is the structure of the nervous sytem?

A
  • central nervous sytem> brain & spinal cord
  • Peripheral NS> connects brain/spinal cord to rest of body
    ^ somatic NS > axons send msgs from sense organs to CNS & from CNS to muscles
    ^ autonomic NS > controls heart, intestines + other organs> regulates involuntary (automatic) behaviours&raquo_space; made up of parasympathetic & sympathetic NS
40
Q

what is the difference between parasympathetic and sympathetic nervous systems?

A
  • sympathetic: prepares organs for rigorous activity- expends energy (excitatory effects) + heart rate, blood pressure etc > flight or fight > Chains of ganglia left and right of spinal cord + Postganglionic axons release mainly norepinephrine
  • Parasympathetic: non emergency responses> conserves energy, calming effects, decreases functions increases by sympathetic NS> Long preganglionic axons extending from brain & spinal cord + short postganglionic fibers attach to organs
41
Q

what is the role of the spinal cord in CNS?

A
  • communicates w/ sense organs & muscles below head- entering dorsal roots> sensory info - exiting ventral> motor info
  • white matter: myelinated axons carry info from grey matter( cell bodies/dendrites) to brain or other areas of spinal cord
  • brain + spinal cord wrapped in protective membranes> meninges
42
Q

what are the regions of the Hindbrain?

A
  • located posterior (back) part of brain> control of sleep & arousal, movement + vital reflexes e.g. breathing
  • Medulla: base of the brain> controls automatic functions- e.g. breathing & heart rate+ relaying info between spinal cord & the rest of brain> suppressed by opiates
  • Pons: above the medulla> regulating sleep & arousal+ serves as relay station for info between diff parts of brain.
  • Reticular formation: Network of interconnected nuclei> alerting or blocking msgs to higher brain areas> control attention, sleep, waking etc
  • Cerebellum: back of brain> coordinating movement and balance.
43
Q

what is the Midbrain (mesencephalon)?

A
  • located between hindbrain & forebrain> regulation of movement, vision, hearing, & arousal
  • Tectum: processing auditory (inferior Colliculi) & visual info (Superior Colliculi) & has “visual reflex” in animals, the optokinetic response
  • Tegmentum: regulation of movement & posture + contains substantia nigra & red nucleus
  • substantia nigra & red nucleus: muscle tone & is affected in Parkinson’s disease
44
Q

what is the forebrain?

A
  • most anterior
  • two hemispheres connected via corpus callosum & white matter
  • outer cerebral cortex & subcortical regions
  • receives sensory info> controls motor movement from opposite body side
  • regions: Thalamus, Hypothalamus, Basal ganglia, Cerebral cortex and limbic system
45
Q

what is the diencephalon region of the brain?

A
  • located in the forebrain> between- brain
  • Thalamus: relay station from sensory organs> all sensory info passes through> main source of input to cortex
  • Hypothalamus: small area near base of thalamus> contains several distinct nuclei> conveys msg to pituitary gland> alters hormone release, behaviours relating to survival e.g. flight/flight
46
Q

what is the Telencephalon region of the brain?

A
  • located in forebrain> cognitive functions e.g. perception, memory, language, & consciousness.
  • cerebral cortex: 6 layers, Parallel to cortex surface, cells divided into columns
  • basal ganglia: involved in regulation of movement + other functions e.g. learning & memory> structures lateral to thalamus> putamen, caudate nucleus & globus pallidus
  • limbic system: motivations + emotions e.g. eating, anxiety, aggression etc > Interlinked structures > Olfactory bulb, Hypothalamus, Hippocampus, Amygdala, Cingulate gyrus
47
Q

what is the cerebral cortex?

A
  • composed of folded grey matter& responsible for processing info from senses, controlling movement etc
  • parietal lobe: behind frontal lobe> Contains postcentral gyrus> recieves sensory cortex> touch sensations + processes & intergrates info
  • occipital lobe: posterior end of cortex> visual processing, damage= cortical blindness
  • temporal lobe: near temples> auditory info + processing spoken language & some vision e.g. movement
  • frontal lobe: front brain> Contains prefrontal cortex and precentral gyrus > Integration of sensory information + higher cognitive functions e.g. thinking planning, memory, regulates impulsive behaviours + voluntary body movement (motor cortex)
48
Q

what is Fluid exchange?

A
  • way nutrients get into brain w/o toxins
  • blood-brain barrier: blood vessles surrounding brain block most chemicals from entering> provides oxygen & disposes co2 from cellular respiration
  • ventricular system: Filled with cerebrospinal fluid (CSF) > 4 ventricles> CFS formed inside ventricles, released into subarachnoid space> Provides “cushioning” for brain (swims) during head movements + Reservoir of hormones & nutrition for brain & spinal cord
49
Q

What happens during early brain development?

A
  • within week of conception> mass of 150 cells (blastocyst) attaches to uterine wall> inner cell mass begins to form embryonic disk= 3 types of germ> endoderm(organs), mesoderm(muscles&bones), ectoderm( NS, skin)
  • week 2&3= part of ectoderm beign to fold & form neural tube (forebrain, midbrain& hindbrain)
50
Q

How does the brain mature?

A
  • growth & development of neurons:
  • cells of neural tube proliferate (production of new cells > cell lining in ventricles divide & stem or remain) & migrate (movement of primitive neurons & glia towards final destination guided by chemicals) outwards
  • during migration neurons, differentiate (develop axon& dendrites> axon grows while neuron migrates) to take final form
  • axons of neurons then myelinated (allow for rapid transmission) & synapses formed (process occurs throughout life> (neurons constantly forming new connections)
51
Q

How do neurons connect?

A
  • pathfinding axons> travel over long distances to precise locations
  • Sperry’s experiment> Discovered severed optic nerve axons will grow back to original gradients in tectum> process dependent on chemical gradients in target cell
  • chemo-attractants & repellents guide growing axons> growing axon follow oath of cell surface molecules> attracted/repelled by some> postsynaptic cell strengthen synapses of some & weaken for others
52
Q

What is neuronal survival/slection?

A
  • Levi montalcini 1987> discovered muscles do not determine how many axons form but how many survive> nerve growth factor= neurotrophin released by muscles promoting survival of axons> brains overproducing neurons & applying apoptosis system allows this
  • after maturity> apoptotic process becomes dormant> Neurotrophins used in adult brain to increase branching of axons & dendrites= neuronal sculpting> Huang & Reichardt, 2001
53
Q

Why is brain development vulnerable especially in early phases?

A
  • Intrinsic factor> brain development is largely determined by your genes e.g. twins having similar brains (almost identical EEG, Stassen et al; 1988)
  • extrinsic factors> malnutrition, toxic chemicals& infections or Drugs and toxins e.g. Alcohol > Fetal alcohol syndrome (FAS)= decreased alertness, motor problems etc > The dendrites of children born with fetal alcohol syndrome are short with few branches
54
Q

what is Cortical Plasticity?

A
  • Fine-tuning by experience
  • ability of brain’s cerebral cortex to change in response to experience or injury> changes in the structure & connections of neurons
  • Experience in form of stimulating environment has effect on dendritic branching + no. of synapses in brain (extrinsic)
    -PET recordings while blind &/ sighted ppt perform tactile task= blind ppl increased activation of extra-striate and primary visual areas= Reorganisation of cortical function in the blind
  • Phantom Sensations> Phantom limb > amputation= cortex reorganises itself after amputation of body part by becoming responsive to other parts of body= Original axons degenerate leaving vacant synapses into which other axons/neurons sprout> pain can be relieved if teach patient to use artificial limb
55
Q

What is the circadian rhythm?

A
  • daily rhythms e.g. sleep, secretion of hormones & body temp
  • Carpenter & Grossberg’s (1984) studies the sleep/wake pattern of flying squirrels in isolation= found 24h cycle > animals most active at earlier times in day
    -the approx. cycle= free running rhythm= not exact
  • external stimuli act as zeitgeber (time giver) > reset biological clock
56
Q

is it possible to adjust circadian rhythms?

A
  • easy to reset circadian rhythm into other 24h rhythm that’s in line with Zeitgeber
  • more difficult when Zeitgeber out of synchrony w/ our rhythms e.g. working at night w/ bright light
  • v difficult to readjust circadian rhythm to circles deviating from 24h (Kelly et al 1999)
57
Q

What is the role of Suprachiasmatic nucleus (SCN) in circadian rhythms?

A
  • part of hypothalamus> located above optic chiasm
  • SCN recieves input from ganglion cells in eyes via retinohypothalamic pathway
  • SCN alters circadian rhythm through:
    a) production of proteins> PER & TIM protein= promote sleep & inactivity
    ^ light activates chemical= breaks down TIM> increasing wakefulness & synchronising SCN w/ external world
    b) controlling activity lvls in brain areas> regulates pineal gland (secretes melatonin)> increases sleepiness> melatonin secretion begins 2-3hrs before sleep & feedbacks to reset biological clock through effect of SCN
58
Q

what is sleep?

A
  • state that the brain actively produces> moderate decrease in brain activity and decreased response to stimuli
  • differs from coma (steady low brain activity+ little response to stimuli), veg state (alternate between sleep & moderate arousal but no awareness of surroundings), minimally conscious (limited speech& comprehension) & brain dead (no brain activity or response to stimuli)
59
Q

How are the different sleep stages measured?

A

_ EEG> records gross electrical potentials in area of brain through electrodes attached to scalp
- allows researchers to compare brain activity at diff times during sleep
-EEG waveforms> classified by frequency, amplitude &location > measured in HZ= 1HZ> one cycle per second

60
Q

What do the staged collected by EEG show?

A
  • relaxation> alpha waves
  • stage 1> alpha& beta activity= EEG dominated by irregular jagged low V waves= brain begin to decline
  • stage 2> sleep spindles & K-complexes
  • stages 3-4> slow wave sleep (SWS)> increasing amt of slow large amplitude wave> synchronised neuronal activity& slowing heart, breathing rate
  • REM> rapid eye movement> EEG similar to stage 1 but muscles paralysed> associated w/ dreaming
61
Q

what are the different brain structures involved in arousal?

A
  • Reticular formation: part of midbrain> responsible for arousal> damaged to it decreases arousal=coma
  • Pontomesencephalon: part of reticular> stimulation of it awakens sleeping individual or increases alertness in alr awake person
  • Locus coeruleus: found in Pons> inactive most times but emits impulses= releasing norepinephrine> responding to meaningful events> role in memory
  • Hypothalamus: has neurons that release histamine= widespread excitatory effects in brain + neuron that release NT orexin= needed for staying awake
  • Basal forebrain: release inhibitory NT GABA> needed for sleep or acetylcholine= excitatory> increases arousal
62
Q

What are the brain structures of REM sleep?

A
  • Increased activity in Pons= trigger onset REM
  • during REM while activity in primary sensory & motor cortex decreases while increased activity in parietal & temporal cortex
  • PGO waves present during REM> pattern of high amplitude electrical activity
  • REM NT> Acetylcholine increases REM state & Norpinephrine & serotonin interrupt REM sleep
63
Q

How can sleep be localised in brain?

A
  • Sleepwalkers: awake in one part of brain & asleep in others> mostly occurs in children in stages 3/4> not dreaming
  • Lucid dreaming: dreaming but aware of being asleep & dreaming
  • Night terrors: intense anxiety> person awakens in terror > occurs in NREM sleep
64
Q

what are different sleep disorders?

A
  • insomnia: caused by> diet, street, pain etc or Parkinsons, epilepsy + dependence on sleeping pills of alcohol & shifts in circadian rhythms
  • Narcolepsy> frequent & unexpected periods of sleepiness> cataplexy, sleep paralysis or hallucinations> runs in families caused by lack of hypothalamic cells- stimulant drug helps
  • sleep apnea> inability to breathe while sleeping> impaired attention & heart problems> caused by old age, hormones, genetics etc> may lead to cognitive impairment
65
Q

why do we need sleep?

A
  • energy conservation> decreased body temp 1-2 degrees in mammals + decreased muscle activity
  • restoring body & brain> During SWS brain metabolism decreases to 75% (Maquet, 1995), sleep dev= dizziness & hallucinations etc
  • memory consolidation> performance on newly learned tasks better next day w/ adequate sleep, brain strengthens synapses & weakens others during sleep Liu et al., 2010; Maret et al., 2011)
  • Behaviourists> sleep is response to environmental cues> e.g. slight/dark
66
Q

What is the anatomy of the cerebral cortex?

A
  • two hemispheres> not mirror images of each other
  • division of labour between the two hemispheres known as lateralisation
  • most ppl left side is specialised for languages
67
Q

what is the anatomy of the corpus callosum?

A
  • fibre bundle that connects areas within two hemispheres
  • allows each hemisphere of the brain to access info from both sides
  • gradually grows and thickens as myelin increases around axon during childhood & adolescence> young children have difficulty comparing left & right hands
  • matures between ages of 3-5 to facilitate comparison of stimuli between two hands
68
Q

what is the anatomy of the Anterior & Hippocampal Commissures?

A
  • left & right hemisphere exchange info primarily through set of axons called corpus callosum
  • other areas that exchange info: the anterior commissure, the hippocampal commissure> info crossed the other hemisphere w/ only brief delay
69
Q

what is the anatomy of visual connections?

A
  • each hemisphere of brain gets input from opposite half of visual world> left half of each retina connects to left hemisphere= sees right visual field> vice versa
  • half of the axons from each eye cross to the opposite side of the brain at the optic chiasm
70
Q

what is the anatomy of the somatosensory & motor connections?

A

lateralisation> left primary somatosensory cortex receives info from the right body side- vice versa + right motor cortex controls the left side- vice versa
- somatosensory cortex located in the parietal lobe behind the central sulcus & each motor cortex is located in frontal lobe of the central sulcus> have complete but distorted presentation of the body

71
Q

what is lateralisation of function- neuropsychology of language?

A
  • left hemisphere damage to BA 44& 45>broca’s aphasia (poor language) & part of BA 39&40> wernickes aphasia also known as fluent aphasia (impaired comprehension)
  • handedness & lang> left hemisphere dominant for speech in 95% right-handed ppl// left-handers have left hemisphere dominance & may have right hemisphere or mixed dominance for speech
    ^ planum temporale> critical for speech comprehension> area of temporal cortex> larger in left hemisphere for 65% ppl
72
Q

what is lateralisation of function- attention?

A
  • ability to select current relevant info from stream of sensory info
  • diff forms of selective attention shown> reflexive attention (exogenous), voluntary attention (endogenous), spatial attention & temporal attention
  • right hemisphere damage can lead to spatial neglect> tendency to ignore left side of the body & its surrounding of left side of object> exact location of damage can affect what person neglects> e.g. damage to inferior part of right parietal cortex= neglect if everything left of body// damage t superior temporal cortex= neglect of left side of objects
    ^ procedures can increase attention to neglected side e.g. pay attention to left side, look left while feeling object w/ left hand & crossing hands in front of body
73
Q

what is split brain research?

A
  • 1960’s Roger Sperry & Michael Gazzaniga carried out numerous studies in patients who undergone commissurotomy (severing of callosal fibres) to contain spread of epileptic seizures> allows for assessment of how 2 hemispheres operate in isolation
  • split brain ppl maintain normal intellect & motivation but use hands independently & respond to stimuli presented to only one side of body
74
Q

what is the Anatomical and functional basis for evolution of language?

A
  • lang is form of communication> high productivity (improvise new combinations of signals to represent new ideas)
    -chimpanzees use lang but differs from humans> use of symbols lacks productivity & primarily used ti request not describe.
  • human brain has stronger connections between auditory prefrontal cortex compared to other species
  • lang evolves from gestures> sound+ mouth gesture may have been precursor to spoken lang
  • no correlation w/ brain size & overall intelligence i.e. full brain size can show severe lang deficits
  • Chomsky & pinker> acquisition device= built in mechanism for acquiring lang> evidence from children ease of developing lang
75
Q

what is consciousness?

A
  • mind-brain relationship> Rene Descartes proposed mind/brain interact at single point= pineal gland
  • today’s hypothesis> experience/brain activities are inseparable & mental activity needs brain activity
  • consciousness can’t be observed
76
Q

what are experimental paradigms- conciousness?

A
  • attention> fate of unattended> Stroop task> brain is unconscious & can influence behaviour + attends to some things even if you’re not conscious of stimuli
  • masking> consciousness of stimuli depends on amt & spread of brain activity>. conscious stimuli produce more consistent responses from one trial to another
  • binocular rivalry> stimulus seen by each eye evokes pattern of brain responses measured by fMRI
  • phi phenomenon> occurs when we see a sot in one position alternating w/ a similar dot nearby= perceptions after an even can alter changes in event already occurred
77
Q

what do these experimental paradigms of consciousness show?

A
  • unattended info influences perception> role of attention
  • consciousness can be fleeing (binocular rivalry)
  • consciousness lags in time
  • brain imaging allows study of neural basis of how consciousness is formed
78
Q

what is Williams syndrome?

A
  • rare condition in which people are retarded in many ways, but yet are remarkably skilled in their use of language
79
Q

what are hormones?

A
  • chemical messengers> act as signals in body
  • secreted by specialised cells or endocrine glands
  • act on specific reports
  • usually transported by bloodstream
  • distributed, slow, analog, involuntary
80
Q

what are the differences between hormonal vs neuronal communication?

A
  • both use chemical substances to communicate
  • neurons & endocrine glands produce & store chemicals
  • many neurotransmitters 7 hormones
  • both involve secretory receptors
  • both use second msngr
  • hormonal> distributed, slow, analog & involuntary but neuronal> specific, fast, digital, voluntary
81
Q

what is neuroendocrine communication?

A
  • integration between NS & endocrine system
  • main endocrine glands> pineal gland, pituitary gland, thyroid, adrenal glands, pancreas, gonads
82
Q

what are sex hormones?

A
  • steroid hormones: derived from cholesterol> bind membrane to receptors like NT, enter cell & activate certain proteins in cytoplasm, binding chromosome where they activate or inactivate certain genes
83
Q

what are the 2 categories of sex hormones?

A
  • steroid hormones: males + females:
  • estrogens: group of primarily female hormones> e.g. estradiol> women have higher lvls than men
  • androgens: primarily male hormones> e.g. testoserone> higher in males
84
Q

what are the effects of sex hormones?

A
  • promote development of gendered features> estrogen activates breast growth, androgen activates gene for facial hair growth in men
  • organising effects> occur at sensitive stages of development > determine of brain & body will develop male or female characteristics
  • activating effects> occur at any time of life and temporarily activate particular responses e.g menstruation
85
Q

what are advantages of sexual reproduction?

A
  • increases variation in gene pool
  • benefits of variation in gene pool species> quick evolutionary adaptations to changes in environment, corrects genetic errors & disadvantageous mutations
86
Q

what are atypical sex chromosomes?

A
  • turner syndrome: XO> female w/ only one X chromosome 23> external female appearance but ovaries fail to develop, webbed neck, higher than avg verbal but poor math skills
  • Klinefelter’s syndrome: XXY> male w/ additional X chromosome> less body hair & underdeveloped genitals, poor lang skill & passive temperament
87
Q

what is meant by gender identity?

A
  • how we identify sexually + what we call ourselves
  • gender= ppls thoughts abt themselevs> female/male
  • sex= biologically defines
88
Q

what is congenital hyperplasia CAH?

A
  • xx chromosomes
  • overdevelopment of adrenal glands from birth by genetic defect> increased cortisol production> overstimulation of adrenal gland = extra testosterone production
  • female fetus= partly masculinised> higher testosterone during prenatal & postnatal life
  • CAH girls show greater preference to boy typical toy than other girls + adolescence> have masculinised interests e.g. rough sports
89
Q

what is androgen insensitivity/ testicular feminisation?

A
  • XY
  • completely insensitive to androgen
  • internal testis but external feminine appearance
  • normal female gender orientation
90
Q

what are the organising effects of sex hormones on the differentiation of human genitals?

A
  • within 6 weeks after conception> undifferentiated gonad in fetus
  • gonads become either> ovary or testis depending on chromosomes
  • wolffian duct> male internal sex organs
  • Mullerian system> female internal sex organs
  • if XY present (male)= SRY gene by week 7= SRY protein= gonads>testis= testosterone & anti Mullerian hormone secretion
    if XX present (female)= No SRY= gonad>ovary= little hormone secretion
91
Q

what do animal studies show about organising effects of sex hormones on differentiation of human genitals?

A
  • female rats exposed to testosterone during sensitive periods= masculinised in anatomy & behaviour> clitoris grows larger than normal, sexual behaviour becomes masculinised
  • if male rat lacks androgen receptors> develop female-like anatomy & behaviour
92
Q

what are the differences in the hypothalumus depending on sex hormones?

A
  • amygdala + other brain areas: produce anatomical & physiological differences
  • sexually dimorphic nucleus> area in anterior hypothalamus that is larger in male> contribute to male sexual behaviour
  • parts of female hypothalamus generate cyclical pattern of hormone release> male one cannot
93
Q

what are activating effects of sex hormones in the female monthly cycle?

A
  • in females> hypothalamus + pituitary interact w/ ovaries to produce menstrual cycle
  • menstrual cycle is the periodic variation in hormones & fertility over course of 28 days
  • periovulatory period> time of max fertility & high estrogen lvls when ovulation occurs> women become more sexually responsive in this time

PSYCHOLOGY BCS (2 decks)

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