Biological Flashcards
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
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
3
Q
What is prosopagnosia?
A
- inability to recognise faces
- bilateral damaged to fusiform gyrus
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
20
Q
What are nerve impulses?
A
- electrical message transmitted down axon> speed=1 m/s-100
21
Q
what is membrane potential?
A
- diff in electrical charge between the inside and outside of the cell
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
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
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
25
what is the action potential?
- 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)
26
what is the difference between absolute refractory period & relative refractory period?
- 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
27
what is the presynaptic membrane?
- on presynaptic terminal of axon
- contains vesicles w/ neurotransmitters
- membrane has high concentration of Ca++ channels> more concentrated outside
28
what is the structure of the synaptic cleft?
- 20-40nm gap
- separates pre-&post synaptic membranes
- contained extracellular fluid
- neurotransmitters diffuse here
29
what is the structure of the postsynaptic membrane?
- on postsynaptic spine of dendrite or cell body
- contained specialised proteins for neurotransmitters
-neurotransmitter receptors function varies> often control ion channel+ cause hyper-polarisation
30
what is temporal and spatial summation?
- 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
31
what are graded potentials?
- 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
32
what is chemical transmission at synapse?
- 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
33
what are the 2 main types of receptors at postsynaptic cell?
- Ionotropic: ligand-gated ion channels> directly alters membrane potential> very fast
- Metabotropic: slower but have greater effects
34
what is Neurotransmitters: Acetylcholine (ACH)?
- 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
35
what are Cholinergic Pathways in the Brain?
- 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
36
what are the different Monoamine neurotransmitters?
- 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
37
what are Serotonergic pathways in brain?
- control sleep states, mood, anxiety, appetite etc
- changes in serotonin activity related to OCD& schiz
- decrease in serotonin = depression
38
What are the different types of drugs?
- 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
What is the structure of the nervous sytem?
- 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 >> made up of parasympathetic & sympathetic NS
40
what is the difference between parasympathetic and sympathetic nervous systems?
- 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
what is the role of the spinal cord in CNS?
- 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
what are the regions of the Hindbrain?
- 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
what is the Midbrain (mesencephalon)?
- 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
what is the forebrain?
- 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
what is the diencephalon region of the brain?
- 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
what is the Telencephalon region of the brain?
- 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
what is the cerebral cortex?
- 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
what is Fluid exchange?
- 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
What happens during early brain development?
- 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
How does the brain mature?
- 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
How do neurons connect?
- 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
What is neuronal survival/slection?
- 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
Why is brain development vulnerable especially in early phases?
- 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
what is Cortical Plasticity?
- 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
What is the circadian rhythm?
- 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
is it possible to adjust circadian rhythms?
- 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
What is the role of Suprachiasmatic nucleus (SCN) in circadian rhythms?
- 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
what is sleep?
- 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
How are the different sleep stages measured?
_ 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
What do the staged collected by EEG show?
- 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
what are the different brain structures involved in arousal?
- 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
What are the brain structures of REM sleep?
- 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
How can sleep be localised in brain?
- 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
what are different sleep disorders?
- 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
why do we need sleep?
- 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
What is the anatomy of the cerebral cortex?
- 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
what is the anatomy of the corpus callosum?
- 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
what is the anatomy of the Anterior & Hippocampal Commissures?
- 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
what is the anatomy of visual connections?
- 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
what is the anatomy of the somatosensory & motor connections?
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
what is lateralisation of function- neuropsychology of language?
- 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
what is lateralisation of function- attention?
- 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
what is split brain research?
- 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
what is the Anatomical and functional basis for evolution of language?
- 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
what is consciousness?
- 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
what are experimental paradigms- conciousness?
- 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
what do these experimental paradigms of consciousness show?
- 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
what is Williams syndrome?
- rare condition in which people are retarded in many ways, but yet are remarkably skilled in their use of language
79
what are hormones?
- 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
what are the differences between hormonal vs neuronal communication?
- 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
what is neuroendocrine communication?
- integration between NS & endocrine system
- main endocrine glands> pineal gland, pituitary gland, thyroid, adrenal glands, pancreas, gonads
82
what are sex hormones?
- 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
what are the 2 categories of sex hormones?
- 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
what are the effects of sex hormones?
- 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
what are advantages of sexual reproduction?
- 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
what are atypical sex chromosomes?
- 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
what is meant by gender identity?
- how we identify sexually + what we call ourselves
- gender= ppls thoughts abt themselevs> female/male
- sex= biologically defines
88
what is congenital hyperplasia CAH?
- 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
what is androgen insensitivity/ testicular feminisation?
- XY
- completely insensitive to androgen
- internal testis but external feminine appearance
- normal female gender orientation
90
what are the organising effects of sex hormones on the differentiation of human genitals?
- 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
what do animal studies show about organising effects of sex hormones on differentiation of human genitals?
- 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
what are the differences in the hypothalumus depending on sex hormones?
- 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
what are activating effects of sex hormones in the female monthly cycle?
- 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
