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Behavioral Neroscien
First lecture set in PS2001
| Term | Definition |
|---|---|
| How does the brain facilitate cognition and behavior? | Monitor brain activity during behavior and cognition as well as casual experiments that manipulate brain systems to examine effects -use electric or genetic manipulation |
| Franz Joseph Gall (1758-1828) | First attempt to bring together biological and psychological concepts in study of behavior |
| Phrenology | Psychological functions can be localized to different areas of the cortex -bumps on skull relate to different parts of the brain |
| Aggregate field hypothesis | Popular theory as it goes against the reductionist idea that the human mind has a biological basis |
| Jean Pierre Flourens (1794 – 1867) | systemically removed Gall’s phrenological centres and concluded that any part of the cerebral hemisphere could perform any higher function |
| Distributed process | Individual areas of the brain perform specific functions but complex cognitive function involves interactions of many brain areas |
| Pierre Paul Broca (1824 -1880) | Described 8 patients with similar brain lesions who could not produce speech |
| Karl Wernicke (1848 – 1905) | Described patients with an inability to comprehend language |
| The Neuron Doctrine | Cellular connectionism, neurons are organized into functional groups which are interconnected by specific neural pathways -neuron is the signaling unit of the brain (Camille Golgi & Santiago Ramon y Cajal) |
| The aim of our research is to understand | how nerurons operate in organized systems and how the operation of these systems relate to behavior and psychological states |
| Multipolar neuron | the most common type |
| Bipolar neurons | usually found in sensory systems |
| Unipolar | somatosensory system |
| How do neurons communicate with each other | Action Potential |
| Resting potential of a neuron | -70 mV -due to difference in concentration of positively charged ions inside and outside -intracellular, more neg -extracellular, more pos |
| where is action potentials generated | Cell body |
| Action potential | Propagated down axon without changing size -reason for this is continually regenerated by ion channel along the axon-depolarization cases action potential to ensue -saltatory action |
| Glia | the connective tissue of the nervous system, consisting of several different types of cell associated with neurons -three types: oligodendrocytes, astrocytes, microglia |
| Oligodendrocytes | provides support for neurons and produces myelin |
| Astrocytes | housekeeping duties, support and insulation |
| Microglia | inflammatory response to infection and removal of dead tissue |
| 3 main types of glia | Oligodendrocytes, astrocytes, microglia |
| Functions of astrocytes | Provide energy in the form of lactate small quantity of energy stored in the form of glycogen remove dead tissue through phagocytosis support for neurons insulation |
| How is communication measured between neurons | Electrically and chemically |
| Neurophysiology | branch of physiology that deals with the flow of ions in brain tissue and the measure of that flow |
| Microdialysis | Allows measurement of levels of chemicals (including glucose and neurotransmitters) in the brain |
| Four Different types of neurophysiological recording | - Electroencephalogram (EEG) - Multi-cell recording - Single cell recording - Intracellular |
| Electroencephalogram (EEG) Advantages and disadvantages | Advantages Non-invasive (use with humans) High temporal resolution Disadvantages Low spatial resolution Only record from cortex |
| What are EEG's used for | -EEG can be used medically to study sleep and pinpoint the focus of seizure activity in epilepsy -Can be used to study cognitive processes ---sometimes placed electrodes on shoulders |
| What is multi cell recording used for | -Used to record from groups of neurons -Record brain rhythms (local field potential -LFP) |
| Connection between memory and attention | The hippocampus processes memory the prefrontal cortex processes attention |
| Advantages and disadvantages of multi-cell recording | Advantages OK spatial resolution (groups of neurons) OK temporal resolution (brain rhythms) Disadvantages Only record groups of neurons Invasive |
| Advantages and disadvantages of single cell recording | Advantages Very high spatial resolution (multiple single neurons) High temporal resolution (action potentials) Disadvantages Extracellular recording (no knowledge of intracellular events) Invasive |
| Advantages and disadvantages of intracellular recording | Advantages Very high spatial resolution (specific neuron) Examine sub-cellular processes Disadvantages Only one cell at a time Only in anaesthesised animals? |
| intracellular recording allows us to understand how ______ _________ work | Action potentials |
| _________ is important, not size | Frequency |
| Neurons communicate across _______ | Synapses |
| Neurotransmitters act on post-synaptic receptors on ________ | Dendrites |
| What are the two main types of receptors | Ionotropic and Metabotropic |
| Ionotropic | Transmit information relatively quickly and are also a simple mechanism |
| Metabotropic | Slow acting and long lasting and a complex mechanism |
| What are the two types of neurotransmitters | Excitatory and inhibitory |
| Excitatory neurotransmitter | causes depolarization - produces action potential also known as excitatory post-synaptic potential (EPSP) example: glutamate |
| Inhibitory neurotransmitter | Causes hyperpolarisation - stops action potentials being generated also known as inhibitory post synaptic potential (ISPS) Example: GABA |
| What are the four types of ion channels | Sodium, potassium, chlorine, and calcium |
| How do neurons communicate with each other | Action potentials |
| Computational power of the brain | 100,000,000,000 Neurons and 1,000,000,000,000,000 synapses |
| Point neuron hypothesis | 5,000 to 40,000 synapses on each neuron each synapse has an equal weighting in ability to make neuron fire only fires if the excitatory input is greater than the inhibitory input |
| two compartment hypothesis | Neurons split into two functional compartments - soma, basal dendrites, axon -apical dendritic tree |
| what are the functional compartments in neurons | Dendritic region, branchlet, spine cluster, and spine |
| Psychopharmacology | The study of the effects of drugs on the nervous system and behavior |
| What are the uses of psychopharmacology | Medicine - treatment for neurodivergent disorders, affective disorders, pain, sedation, and more Illegal drugs trade cognitive enhancers tool to study the mechanisms by which the brain controls psychological function |
| Agonist | a drug that facilitates the effects of a particular neurotransmitter on the postsynaptic cell |
| Antagonist | a drug that inhibits the effects of a particular neurotransmitter on the postsynaptic cell |
| What are the most common neurotransmitters in the brain | Glutamate and Gamma-Aminobutyric acid (GABA) |
| Nearly all neurons receive excitatory inputs from ______ releasing terminals and inhibitory inputs from _____ releasing terminals | Glutamate, GABA |
| What are the 4 types of glutamate receptors | NMDA, kainate, AMPA and metabotropic |
| What are the two types of GABA receptors | GABA(a) (Ionotrpoic) and GABA(b) (metabotropic) |
| Neural integration | The combination of excitatory and inhibitory signals |
| Acetylcholine (ACh) | Neurotransmitter within the nervous system |
| Two types of acetylcholine receptor | Nicotine(inotropic) - found in brain and muscles Muscarinic (metabotropic) - only found in brain |
| What are the tree main systems in Acetylcholine | Dorsolateral pons Basal forebrain Medial Septum |
| Dorsolateral pons | traditionally associated with sleep recently shown to play a role in higher cognitive functions like learning |
| Basal forebrain | Provides large input to the cortex and has a role in learning and attention historically studied as the area degrades in Alzheimers diseases |
| Medial Septum | Involved in learning and memory controls rhythms in the FLP in the forebrain |
| How many receptors are in the dopamine system | 5, D1-D5 |
| What are the 3 major dopaminergic systems in the brain | Nigrostriatal, Mesolimbic, Mesocortical |
| Nigrostriatal | Substantia nigra-> caudate nucleus/putamen - controls action selection and coordinated movement |
| Mesolimbic | Ventral tegmental area -> nucleus accumbens (also hippocampus and amygdala) - processing of reward |
| Mesocordical | ventral tegmental area ->prefrontal cortex - short-term memory, planning |
| What types of task are used to examine role of mesolimbic dopamine system in behavioral signals | non cued and cued |
| Noradrenergic system | catecholamine 4 types of receptor α1, α2, β1 and β2 (all metabotropic) Most important noradrenergic system originates in the locus coeruleus – involved in vigilance and attentiveness |
| Serotinergic system | Indolamine At least 9 receptor subtypes – most are metabotropic Most important serotinergic system originate in the raphe nuclei of the midbrain and pons Functions are complex; regulation of mood, eating, sleep and pain |
| neuromodulation | Acetylcholine, dopamine, noradrenalin and serotonin systems all originate in relatively small nuclei in the brainstem and midbrain All send projections to areas all over the forebrain Activation of these small areas of the brain have large impacts |
| synchronous firing | -produces measurable waves of activity in LFP -neurons firing together produces waves of activity that is detected in other areas of the brain, this coordinates different areas |
| sleep | -seen throughout animal kingdom -variation in sleep patters (bats for 18, giraffes for 2) -even some that don't stop swimming sleep for 4-60 second naps -some can rest one hemisphere of brain at a time |
| sleep in humans | -amount varies with age (16 hr infants, 9 hr teenagers, 7-8 hr adults -no adaptation to sleep deprivation -very different than unconsciousness |
| Rapid eye movement (REM) sleep | -characterized by EEG desychrony, lack of muscle tone (paralysis) and rapid eye movement |
| slow wave sleep (SWS) | -eeg synchrony, moderate muscle tone, absence of eye movement |
| measurements of sleeo | -EOG - electrooculogram -EEG - electroencephalogram - EMG - electromyogram |
| insomnia | -25% of population -treatment: pharmacology -sleep apnea: cease to breath during sleep -treated surgically or by wearing pressurized apparatus -can cause permanent damage |
| narcolepsy | -primary symptom is sleep attack -cataplexy -sleep paralysis -hypnoagogic hallucinations -genetic component causes loss of hypocretin/ orexin neurons -treated with modafinil |
| REM sleep disorder | -paralysis that normally appears during rem sleep is not present, act out genes -genetic disorder with alpha synuclein in neurons accumulating -treated with benzodiazepine |
| disorders of slow wave sleep | -sleep walking -bed wetting -night terrors --usually associated with childhood |
| sleep eating disorder | -thought to be induced by medications |
| arousal | -levels controlled by a variety of neurotransmitters including --acetylcholine, noradrenalin, serotonin, histamine, orexin |
| noradrenalin neurons | active during waking and not active during sleep |
| orexinergic neurons | -active during waking |
| Constantine von Ecinomo | -determined damage ti pre optic area of hypothalamus caused insomnia in rats -stimulation induces sleep -key area is ventrolateral preoptic area (vIPA) |
| what is key to wakefulness | orexiogeric / hypocretinergic neurons in lateral hypothalamus |
| neurons influenced by | -levels of adenosine (caffine blocks this) -influenced also by hunger and satiety levels |
| why do we sleep | -irresistible urge --reasons not to os to maximize foraging time and avoid predation |
| sleep deprivation | -affects cognitive abilities -do not make up lost sleep -after some stages predominate over others -sws and rem most important |
| Rechtschaffen & Bergmann (1995) | -rats control vs yoked 91% to 28% sleep -metabolic rate increases 210-270% -weight loss besides increase in food intake -inhability to thermoregulate (excessive heat loss) |
| functions of SWS | -reduced metabolic rate and blood flow -most active regions during wake show high delta wave activity (low metabolic activity) -cortex "shuts down": groggy -protect from free radicals and oxidative stress |
| what is a rare genetic sleep disorder in SWS | fatal familial insomnia |
| how does sleep protect the brain | -drives metabolic clearance from adult brain -measured the flow of CSF during wake and sleep -csf further into brain during sleep -toxic chemicals (amyloid beta) removed quicker in sleep |
| functions of REM sleep | -more active phase of brain development -more prevalent in new borns with less developed brains -differential roles for SWS and REM in declarative and non-declarative memory |
| declarative memory | -memory that can be consciously recalled (facts, events) |
| non-declarative memory | -automatic learning not under conscious control (riding. a bike) -improved by REM |
| declarative memory test | -paired associate test |
| neurodegenerative disorders | -covers range of conditions primarily affecting neurons -symptoms: psychological to motor symptoms like seizures -some are largely psychological Alzheimers) others not psychological (motor neuron disease) |
| different disorders | -parkinsons -alzheimers -huntingtons -amyotrophic lateral sclerosis -multiple sclerosis -neurological disorders |
| parkinsons | -loss of dopamine neurons from midbrain -2-3% pop over 65,3-4% over 85 |
| symptoms of parkinsons | -muscle rigidity -akinesia -bradykinesia -resting tremor |
| akinesia | -inhability to initiate movement |
| bradykinesia | -slowness of movement |
| pathology of Parkinson's disease | -loss of substance nigra pars compacta -more loss from putamen than from caudate nucleus -presence of lewy bodies in cytoplasm of neurons |
| what does the presence of lewy bodies mean | -index of neurodgeneration |
| what are symptoms caused by | excessive inhibitory activity in the basal ganglia |
| different treatments for parkinsons | -drug therapy: l-dopa (dopamine precursor, dopamine agonists (increase dopaminergic activity -side effects: tardive dyskinesia (uncontrolled movements) -less effective over time as dopamine. neurons still lost |
| there treatments for parkinsons | -replace lost dopamine cells: surgical implantation of fetal dopamine tissue, stem cells -gene therapy possibly -varying pos and neg results --- NO LONGER USED -surgery: lesions (internal globes pallidus), deep brain stimulation (release inhibition) |
| deep brain. stimulation | -not lesion but high frequency electrical stimulation delivered via surgically implanted electrode -symptomatic relief but has side effects |
| genetic case for parkinson | 5% have genetic cause on alpha synuclien, Parkin, and PINK1 |
| Alzheimer's disease (AD) | -10% pop over 65, 50% pop over 85-characterized by general cog. decline including memory, attention, language, and spacial orientation -degeneration begins entorhinal cortex, spreads through hippocampus, neocortex into modulatory system of midbrain/pons |
| biological markers of Alzheimers | -extracellular plaque made from accumulated 40/42 amino acid beta-amyloid peptide -intracellular accumulation of neurofibrillary tangles made of hyperphosphorylated Tau |
| treatments for Alzheimers disease | -drug therapy (acetylcholinesterase inhibitors, NMDA receptor antagonist memantine) -do not treat cause -some forms of AD genetic -vaccination against alpha beta protein |
| decrease in ____ correlates with slowing of ______ | alpha-beta, dementia |
| beta-amyloid | -can be reduced by immunization -not correlated with slowing of dementia -role unclear |
| huntingtons disease | -approx 5,000 in uk -hereditary -single gene on chrromosone 4 causes protein Huntington (htt) to be produced -crit feature section of repeated glutamine In protein -affect basal ganglia -sympt: cog deficits and chorea |
| chorea | uncontrollable movements |
| key features of huntingtons | -inclusion bodies (accumulation of htt -role of bodies debated -could be neuroprpotective |
| amyotrophic lateral sclerosis | -progressive disorder that attacks spinal and cranial nerve motor neurons -no cog decline -death 5-10 yr after onset due to respiratory muscle failure |
| treatments for amyotrophic lateral sclerosis | -no effective treatments --riluzole used to reduce glutamate neurotoxicity but only extends life by a few months |
| multiple sclerosis | -autoimmune demyelination disease 0-damage occurs in white matter and spinal cord -may suffer discrete attacks or progressive decline -life expectancy reduced by 5-10 yr |
| tumors | -many types, gliomas, meningiomas, angiomas -caused bu uncontrolled and non-functional cell division -damage: compression and infiltration -treated with surgery and focused radiation -metasesises |
| cerebrovascular accidents (stroke) | -hemorrhagic stroke - burst blood vessel -obstructive stroke - blood vessel blocked |
| what damage is done in stroke | -depetion of oxygen and glucose -ion transports disrupted -glutamate produced and cells die through excess sodium and calcium -damaged mitochondria produces free radicals that are toxic -drugs used dissolve blockages |
| short term memory | -working memory, gateway for information to enter long term memory |
| priming | improvement in identifying or processing a stimulus as a result of having observed it previously |
| perceptual priming | words presented quickly and ask subject to identify -some time later present with word stems and asked to complete -priming is increase prob of choosing previously presented words |
| procedural memory (knowing how) | learning a procedure, includes motor memory |
| classical conditioning | Previously neutral stimulus (conditioned stimulus - CS) paired with a positive (or negative) stimulus (unconditioned stimulus -US) that produces response (unconditioned response UR) -CS can illicit conditioned response, similar UR in absence of the US |
| non-associative learning | -learning that doesn't involve association of two stimuli to illicit behavioral response |
| habituation | -decrease in level of response through repeated exposure to stimulus |
| sensitation | increase in level of response through repeated exposure to a stimulus |
| semantic memory | memory for facts |
| episodic memory | memory for events |
| why is it important to study episodic memory | -first symptom of mild cognitive impairment (MCI) -recently described in Huntingtons disease -studies show episodic memory is dependent on hippocampus |
| what memory is impaired in patients with hippocampus damage | episodic memory |
| episodic memory recall | predicted by single cells in human hippocampus |
| importance of studying hippocampus for episodic memory | -if model in animal can test treatment for early stages of AD -treat early symptoms may be possible to stop before significant damage |
| what are the two questions for animals | -is hippocampus responsible for episodic memory in animals -are animals capable of episodic memory |
| what is tulving (1972) definition of episodic memory | receives and stores information about temporally dated episodes or events and the temporal–spatial relations among these events |
| episodic like memory in animals | Birds prefer wax worms If birds remember what, where and when they will retrieve the wax worms when they were cached recently but not when they were cached a long time ago -not good model |
| synaptic plasticity | cellular mechanisms for memory consolidation |
| what does long lasting long term potential (LTP) require | -proteins to stabilise the short term changes already produced -captured by tags set at relevant synapse |
| for long lasting memory we need long lasting LTP, this includes | -Short term LTP (insertion of AMPA receptors into postsynaptic membrane) -A chemical tag at the synapse to attract proteins -Proteins to stabilise the changes induced in short term LTP |
| Hebb's law | When an axon of cell ‘A’ is near enough to excite cell ‘B’, and persistently takes part in firing it, growth process or metabolic change takes place in one or both cells, such that ‘A’s efficiency in causing ‘B’ to fire is increased, associate |
| spatial memory | map-like cognitive representation of familiar spacial locations -one component of episodic memory -can also have semantic spacial memory |
| navigation | -mechanism to enable us to find our way around familiar and unfamiliar enviornments |
| Tolman 1984 - cognitive maps in rats and men | -first to suggest that rodent and humans have cog map of familiar environments - |
| neural system that support spatial memory and navigation | activation in right hippocampus increases |
| does structure of hippocampus change with navigational experience (Maguire et al., 2006) | -posterior hippocampus size is larger in London taxi drivers -posterior hippocampus volume correlates with years of taxi driving experience -incresee NOT seen in bis drivers |
| Morris watermaze | -hidden platform which rats learner time where the platform is |
| placed cells | -recieve two different inputs, one conveying information about a large number of environmental stimuli and other from a navigational system |
| inputs to hippocampus (place cells) | medial entorhinal cortex (MEC) lateral entorhinal cortex (LEC) |
| schizophrenia | -1% of pop will face 1 major episode in life -pos, neg, and cog symptoms -men and women equally effected, onset later for women -heritabiloty |
| early onset disorder | large implication for individuals and society |
| twin study | -show genetic component of schizophrenia, more likely to both have if identical but less if fraternal -DISC1- controls neuronal migration in development |
| rate of schizophrenia in twins | -fraternal 10%, identical 60% -early developmental environment important interaction of genes and environment |
| early schizophrenia info | -kraeplon (1887): dementia praecox -Bleuler first to use term and find pos and neg symptoms -before drug therapies used insulin coma, frontal lobotomy, or shock therapy |
| what was first schizophrenia drug therapy discovered | 1952, chlorpromazine, dopamine antagonist -side effects include tartive dyskinesia |
| dopamine hypothesis | -d2 and d3 receptor antagonist reduce pos symptoms -dopamine antagonists (cocaine, amphetamine, L-DOPA) can produce pos symptoms of schizophrenia |
| schizophrenic brains | -enlarged ventricles -reduced cerebral gray matter -dramatic loss of cortical gray matter in adolescence -hypofrontality |
| dopamine hypothesis explained | -inc activity in prefrontal cortex inhibits mesolimbic dopamine system-hypofrontality has opposite effect, increases dopamine |
| problems for drug therapy | -dopamine decreased in prefrontal cortex -dopamine increase in midbrain |
| affective disorders | -3% male 7%. female -bipolar -unipolar -28.8x more likely suicide -some genetic base, not a single gene implicated -likely serotonin transporter |
| genetic base | -short alleles for serotonin transporter gene increase risk of depression. only in individuals who have suffered from stressful life events |
| brain abnormalities in depression | -decreased activity in subgenus prefrontal cortex |
| amygdala in depression | -process fear and anger producing stimuli -activity reset after fearful stimuli by inhibition from anterior cingulate cortex -less prominent in depressed patients |
| affective disorders | -monamine hypothesis --decreased monaminergic activity causes depression |
| what drugs help alleviate depression | -monamone oxidase inhibitors -tricyclic antidepressants -specific serotonin reuptake inhibitors -seretonin and noradrenalin reupake inhibitors -lithium |
| how long dpi depression alleviate medicine take to have affect | 2 weeks |
| other depressive therapies | electroconvulsive therapy (ECT) -deep brain stimulation --subgenual anterior cingulate cortex and vagal nerve |
| sleep in depression | -sleep is affected -sleep deprivation can be used as a treatment |
| why do we study fear | -adaptive mechanism -long lasting -underlies disorders -easy ton study |
| fear responses | -behavioral: movement appropriate to situation -autonomic: blood vessels constrict or diet, heart rate change -hormonal: hormone produced to reinforce autonomic response (adrenaline) |
| fear and role of amygdala | -lesions of the central and lateral nuclei of amygdala produce deficits in fear conditioning -increase their firing rate to conditioned stimuli following training |
| LA | lateral nucleus |
| CE | central nucleus |
| CG | central grey |
| LH | lateral hypothalamus |
| PVN | paraventricular hypothalamus |
| fear conditioning in humans | -humans show increase skin conductance response to CS+ relative to CS- -pavlovian fear conditioning |
| humans are | social learners |
| amygdala activation in fear response to stimuli | -left amygdala is activated in response to CS+ following instruction that CS+ will be paired with shock -due to language being involved in instruction |
| normal conditioned fear induces | bilateral activation |
| extinction of conditioned fear | -conditioned fear arises through the pairing of a cue with an aversive stimuli -if cue presented many times in absence of stimuli conditioned response (CR) decreases) |
| within extinction | -association between US and CS is not forgotten -new association between CS and lack of shock/fear -if new learning is blocked in amygdala then rats do not show extinction |
| if original memory is not erased why do we stop being fraid | -activation in amygdala is high during learning of conditioned fear but low during extinction -during extinction amygdala is inhibited --this comes from ventromedial prefrontal cortex (vmPFC) |
| vmPFC during inhibition | -neurons become active during extinction -inhibits fear response produced by amygdala -electrical stimulation of vm PFC can speed up extinction |
| mechanisms of reducing fear | -extinction -cognitive regulation -reconsolidation |
| cognitive regulation | -reduces conditioned fear by decreasing activation in amygdala -inhibited by increase activation in prefrontal cortex (vmPFC and dorsolateral prefrontal cortex (dlPFC)) -same mechanisms that control extinction |
| reconsolidation | -if memories are recalled they become sensitive to change and must be reconsolidated -previously consolidated memory remembered -becomes sensitive to change -requires proteins to be reconsolidated |
| memories can be erased by | stopping reconsolitation |
| motor control and action selection | -capable of: complex sequences of actions, performing multiple behaviors simultaneously |
| penfield and boldrey 1937 | -stimulation studies identified the topographical organization of primary motor cortex --penfield stimulated primary motor cortex to examine parts of body controlled by motor cortex |
| cerebellum | -also controls motor function along with primary motor cortex -50 billion neurons in cerebellum (22 billion in cerebral cortex, 85 billion in the whole brain) -computes contributions of muscles to preform movements-projects ventrolateral thalamus |
| damage to different areas of cerebellum produces different effects | -flocculondular or vermis damage: [postural and balance problems -intermediate zone damage: limb rigidity -lateral some damage: weakness and decomposition of movement |
| premotor cortex and supplementary motor area (SMA) involved in | motor planning, also critical for learned sequences |
| neurons in SMA | -respond to specific parts of a learned sequence -inactivation does not disrupt single movement -stimulation of SMA provides involuntary movement |
| mirror neurons | -neurons in ventral premotor cortex and the inferior temporal lobe that respond to particular movement or sight of someone else preforming it -hard to study humans -increased activity during execution and observation of actions -inferior frontal gyrus |
| function of mirror neurons | -imitation -understanding actions of others |
| mirror neurons are less active in autistic chuldren | -lower activity in ventral premotor cortex when imitating facial expressions -level of activity correlated with the symptom severity -suggests mirror neurons enable process and understand actions and intentions of others -ability underlies imitation |
| lack of mirror neuron activity could lead to | autism |
| disorders of movement | -cerebellar damage -neurodegenerative disorders -damage to cortical motor areas: apraxia, relates to deficits of skilled learned movements |
| limb apraxia | -inappropriate limb movement especially to verbal commands -caused by damage to the left frontal/parietal cortex |
| patients with limb apraxia often have | -lesions in the left ventricle premotor cortex -also produce deficits in patients ability to comprehend others gestures -consistent with mirror neurons processing action/intention information |
| constructional apraxia | -inhability to perceive and imagine geometric relations -caused by damage to the right parietal cortex |
| what is consciousness | number of different definitions -internal knowledge -awareness, feeling, violation -sense of self |
| do we consciously process everything in our environment | -access overflow theory |
| what is the access overflow theory | -perceptual consciousness has a higher capacity than cog access -when cued we can remember all, shows consciousness to all -there is a limited capacity to remember if not cued to look at all |
| two forms of consciousness | -phenomenal -access |
| phenomenal consciousness | creates a rich detailed perception of everything we experience |
| access consciousness | refers to the information we can access through cognitive process |
| inattentional blindness | -not all info from visual experience is perceived -argues against phenomenal consciousness |
| change blindness | -suggests that obviously different items are consciously processed but subtly different items are not -details not in attentional focus are not consciously perceived -again not consistent with phenomenal consciousness |
| studying consciousness | mapped onto two problems: easy and hard |
| easy problem | -understanding the mechanisms supporting cog function such as language, attention, and working memory |
| hard problem | -what is it like to be conscious? -how does phenomenal experience arise from physical events in the brain? |
| conscious separate from brain? | -yes: mind vs brain, dualism, religion -no: reductionism -maybe: emergent properties |
| neurobiological basis of consciousness | -blind sight -split brain patients --need left hemisphere to consciously report experience --possible to treat epilepsy by severing corpus collosum -prevents seizure activity from speeding to other hemisphere |
| split brain patients | -can often identify stimulus that they have previously encountered even though they have no conscious recollection of experiencing it |
| recurrent processing-victor lamme | what rather than where is consciousness and do neural mechanisms support -visual information is processed very quickly by the visual cortex but this is sub-conscious -combined with recurrent processing in frontal parietal region result conscious Perc. |
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