Uni-year 1 & 2 > Brain and Behaviour > Flashcards

Brain and Behaviour Flashcards

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1
Q

Basic brain facts

A

350g at birth, 1300g at adulthood
85 billion neurons, trillion of synapses
brain development and maturation not linear

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2
Q

what happens in germinal stage development

A
  • zygote formed - fusion of egg and sperm
  • through process of cleavage forms a cluster of homogeneous cells called morula
  • morula continues to divide-forms blastocyst
  • blastocyst implants in uterus
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3
Q

embryonic stage: gastrulation

A
  • embryonic disc
  • three distinct layers: ectoderm, mesoderm and endoderm
  • ectoderm folds within itself to form neural tube
  • neural tube becomes CNS
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4
Q

stages of brain development

A 
cell birth/proliferation
cell migration
cell differentiation and maturation
synaptogenesis and synaptic pruning
cell death
myelination
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5
Q

what happens at cell birth/proliferation

A
  • neurogenesis and gliogenesis
  • stem cells form progenitor cells
  • each progenitor cell can be neuroblast or glioblast
  • once formed, migrate out of ventricular zone
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6
Q

what is neurogenesis and gliogenesis

A

formation of new neurons

formation of non-neural glia

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7
Q

what is neuroblast and glioblast

A

cell that will form a neuron

cell that can form oligodendrocytes or astrocytes

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8
Q

what’s the alternative name for a progenitor cell

A

precursor cell

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9
Q

what happens in cell migration

A
  • cell movement to final destination
  • subventricular zone contains primitive map of cortex
  • predisposes cells born in specific regions to migrate to certain cortical zones
  • chemical signals and physical support aide cell migration
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10
Q

what are the chemical signals and physical support in cell migration

A

immunoglobins and cytokines

radial glia

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11
Q

what happens in differentiation and maturation stage of brain development

A
  • at destination, primitive neurons express particular genes
  • form axons and dendrites; give distinctive shape
  • differentiation dependent on destination
  • immature cells can acquire characteristics of location but once mature, lose that property
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12
Q

what occurs during dendritic development

A 
dendritic aborization (branching)
growth of dendritic spines
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13
Q

what happens during synaptogenesis and synaptic pruning stage

A
  • growth cone at end of axon develops extensions called filopodia
  • target sights release cell adhesion molecules and tropic molecules; attract growth cones
  • synaptic pruning: synapses activated maintained and strengthened, those not are eliminated
  • plasticity: ability to form and eliminate synapses
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14
Q

what happens at stage cell death

A
  • inactive synapses eliminated = neural darwinism
  • apoptosis= programmed cell death
  • survival signals are proteins secreted by target cells to promote survival and growth
  • neurotrophins and active communication prevents apoptosis
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15
Q

what happens in myelination stage

A
  • glia form fatty sheath surrounding axons
  • speeds transmission
  • first occurs in spinal cord, moves up towards forebrain
  • slow process
  • Schwann cells in PNS - singular cell surrounds singular axon
  • oligodendrocytes in CNS - singular cell surrounds multiple axons
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16
Q

research impact neurons

A
  • originally believed no new neurons form in adulthood
  • songbirds have steady replacement of neurons in ‘‘singing” region
  • olfactory bulb receptors continually replace dying ones
  • hippocampus neurogenesis to facilitate learning
  • cerebral cortex is controversial, following strokes or injury
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17
Q

regrowth of axons

A
  • better in younger brains or the periphery
  • destroyed body cells not regrow, but damaged axons can
  • collateral sprouting: new branches formed by non-damaged axons that attach to vacant spots on dendrites and cell bodies
  • secretion of neurotrophins allow collateral sprouting to occur
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18
Q

examples of brain adaptation

A
  • blind have enhanced tactile and auditory ability
  • burton 2002: braille letters, PET and fMRI showed activity of occipital cortex and increased response in visual areas of cortex due to auditory stimuli
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19
Q

critical periods of brain development

A
  • when brain most sensitive to experience
  • absence of visual stimuli lead to blindness or lack of exposure to language leads to ability to use it (blakemore and cooper-cats)
  • immature brain is vulnerable
  • chemical distortions in early development can cause sig impairment
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20
Q

neural tube defects

A
  • spina bifida: failure of closure of neural fold at level of spinal cord
  • anecephaly: brain fail to develop
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21
Q

impact of neglect and trauma on brain development

A
  • poor modulation of impulsivity - ‘primitive’ emotional and behavioural functioning
  • trauma environment lead to excessive active and reactive stress-response
  • overdevelopment of specific areas result in predisposition to aggression, impulsive and reactive behaviour
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22
Q

epigenetics

A

tracing disorders to development

environmental factors interact with genes

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23
Q

human dna facts

A

23 pairs chromosomes

share 99.9% dna wih eachother

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24
Q

dna structre

A

deoxyribonucleic acid
double helix of phosphate and deoxyribose
adenine, cytosine, guanine, thymine

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25
what is the name for natural variations in DNA
single nucleotide polymorphisms (SNPs)
26
cell division
mitosis: somatic cells (genetically identical) meiosis: gametes, homologous recombination (genetically different)
27
process of genes to proteins
- transcription: transcription factor activated in development or intracellular signalling, gene DNA sequence copied to form mRNA - translation: ribosome attach to mRNA, reads triplet codons, tRNA forms amine acid chain - amino acid chain folds to form protein
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Mendel's law
- inheritance through 'transmissible units' | - Peas: height was dichotomous, small characteristic only visible in second gen
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what are alleles
variants of gene dominant or recessive if identical called homozygous if different called heterozygous
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what is a genotype
genetic information
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what is phenotype
physical appearance of genetic information
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what is huntington's chorea
- single gene; autosomal dominant inheritance - degeneration of brain leads to progressive deterioration of movement, temperament and cognition - chromosome 4, excessive repeat of CAG bases - onset 35-55 years
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what is phenylketonuria
- single gene recessive inheritance - mutation in PAH gene (phenylalanine hydroxlase) - enzyme breaks down dietary phenylalanine - build in brain is toxic: epilepsy/learning disabilities
34
chromosomal abnormalities
monosomy: singel copy of chromosome trisomy: three copies of chromosome most are lethal
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example of trisomy
downs syndrome three copies of chromosome 21 smaller brain size, mild to mod intellectual ability and high risk of early Alzheimer onset
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X-linked conditions
- wrong number of chromosomes impact normal development - importance of gene dosage - Y chromsome mostly male sexual function genes - in activiation in females switches off one copy of X chromosome in embryogenesis
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Rettsyndrome
- progressive neurodevelopment disorder - almost exclusivet o females - profoudn mental impairment - mutation to gene MePC2 - X in activation means not all cells express the mutated MePC2 gene
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fragile X
- most common inherited from of mental retardation - predominantly in male - mutation of FMR1 gene - amplification of CGG repeat - encodes for FMR protein
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epigenetics
- inherited change in phenotype - not due to change in genotype - environmentally activated
40
example of epigenetics
maternal care switches on seratonin, action through 5-HT7 receptor to activate transcription factor NGFIA whihc switches on gene for glucocorticoid receptor absence of maternal licking: promoter methylated, low levels GR, increased stress hormones and anxiety/depression
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gene association studies
sort SNPs in candidate gene genome wide asosociation studies look for what SNPs associate with disease state functional SNPs vs genetic tags
42
Alzheimer's disease
mutation in genes amyloid precurosor protien risk genes identified using GWAS studies one SNP difference between APOE3 and APOE4
43
polygenetic factors: twin studies
concordance rates | see how biological the inheritance is
44
genetics of schizphrenia
largely genetic but not purely | genes to do with synpatic transmission, glutamate and dopamine
45
what is voltage
difference in charge between two points
46
what is current
rate at which charge is flowing
47
structure of a neuron
dendrites soma axon terminal boutons
48
resting potential
- 65/-70mV - diffusion and electrostatic pressure of ions leads to equilibrium potential - sodium potassium pump ensures this it not met
49
what is equilibrium potential
force of diffusion = force of electrostatic pressure | initial conc important: high conc = large eq. pot.
50
Nernst equation
E = 61 x log(ion outside/ion inside)
51
where is action potential generated
axon hillock by summation of converging inputs from dendrites or electrical stimulation
52
what is hyperpolarisation
when membrane potential becomes more negative than resting pot.
53
what is depolarisation
when membrane pot. becomes more positive than resting pot.
54
what is the all or nothing principle
depolarisation must reach threshold for action potential to be generated, if it doesn't there it not an action potential
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stages of action potential ``` d = diffusion ep = electrostatic pressure ```
- resting pot. majority channels closed - small depolarisation opens a few sodium channels, d & ep into neuron - reach threshold, majority na channels open - as neuron depolarises, k channels open and k diffuses out - na channels refractory as positive potential reached, remaining k channels open - repolarisation - k diffuses out, membrane pot decreases - hyperpolarisation - some k channels close, na channels return to normal state - final k channels shut, membrane returns to resting pot due to na/k pump
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propagation of action potential
unmyelinated: depolarisation along whole length of axon myelinated: depolarisation only at nodes of ranvier
57
multiple sclerosis
damage to myelin sheath | results in loss of sensitivity, muscle weakness, difficulty with coordination and balance
58
types of synapse
electrical: rare in adult mammalian neurones, gap spanned by proteins which communicate between neurons chemical: neurotransmitters
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types of synapse location
axodendritic: dendrite to dendrite axosomatic: dendrite to cell body axoaxonic: dendrite to dendrite of another neuron to the cell body of another neuron
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why is location of synapse important?
- activation of excitatory synapse = local and small depolarisation (EPSP) - decays over length of dendrite - closer to soma the greater influence on production of action potential in axon
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process at a chemical synapse
- action pot arrive at terminal button - depolarisation opens voltage gated calcium channels - calcium diffuses in - vesicles containing neurotransmitter fuse with membrane and release into gap - binds to receptors on postsynaptic cell - depolarisation or hyperpolarisation
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classes of neurotransmitter
``` amino acids monoamines soluble gases acetylcholine neuropeptide ```
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ionotropic receptors
ion channels | excitatory or inhibitory
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metabotropic receptor
g protein coupled receptor - neurotransmitter bind to receptor and activate g protein - g protein splits and activates otehr enzymes - break down of GTP turns off g protein activity - series of chemical reactions lead to amplification of signal (secondary messenger)
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what is glutamate
excitatory neurotransmitter in CNS | activates different types of receptors eg AMPA receptors
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what is GABA
inhibitory neurotransmitter activates ionotropic receptor which opens chloride channels -involved in anxiety -certain hormones or drugs enhance its activity
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autoreceptors
located on presynaptic terminal regulate internal process controlling synthesis and release of neurotransmitter neg feedback system
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categories of neurotransmitter
classical: amino acids, monoamines, acetylcholine neuropeptides
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synthesis, storage and break down of glutamate
- synthesised in nerve terminal from glucose or glutamine - stored in vesicles by vesicular glutamate transporters - released by exocytosis - reuptake by excitatory amino acid transporters
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what happens if amino acid transmitter release is not regulated
hyperexcitability - epilepsy | excitotoxicity
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action of neurotransmitters at receptors
agonist: produces a cellular reaction antagonist: blocks activity or agonist or ligand
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what is kinetics, selectivity and conductance
rate of transmitter binding and channel gating determine duration of effects what ions are fluxed rate in flux
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glutamate receptor diversity
three ionotropic receptors - NMDA - AMPA - Kainate
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what are the agonist and antagonist of NMDA receptor
agonsit: NDMA/glutamate antagonist: APV
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what are the agonist and antagonist of AMPA receptor
agonist: AMPA/glutamate antagonist: CNQX
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what are the agonist and antagonist of kainate receptor
agonist: kainic acid/glutamate antagonist: CNQX
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how does NMDA receptor work
at resting: binding of glutamate opens the channel but nothing passes through as mg2+ s blocking the pore depolarised membrane pushes out the mg2+, so the channel is open and ions can move
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selectivity and conductance of AMPA/kainate and NMDA receptors
AMPA: fast opening channels and permeable to na/k NMDA: slow opening, permeable to ca, na, k and requires glycine
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dysregulation of NMDA receptors
- receptor blocked by phencyclidine and MK801, produces symptoms that resemble hallucinations associated with schizo - glutamate excitotoxicity caused by excessive ca influx, activates calcium dependent proteases and phosholipases that damage cell
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GABA synthesis, storage, reuptake
- synthesised from glutamate - stored in vesicles by vesicular GABA transporter - released by exocytosis - reuptake by transporters on glia and neurons including non-GABAergic neurons
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what happens if amount of GABA isnt regulated
too much = coma/sedation -GHB gamma hydroxybutyrate is a GABA metabolite that cna be converted to GABA, moderate dose gives effects of alcohol, too much leads to unconsciousness
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GABA receptor diversity
GABA iontopic receptors: ligand gated channels with fast IPSP GABA metabotropic receptors: G protein coupled, indrectly coupled with K or Ca through 2nd messenger, slow IPSP
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GABA a receptor
heteropentameric structure - 2 alpha, 3 subunits - Cl channel gated by binding of GABA - complex receptor with multiple binding sites - agonist: muscimol - non competitive: benzo, barbs
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evidence of GABAergic dysfunction in anxiety disorders
- PET radiolabelled flumazenil - panic disorder patients fewer benzo bindign sites - lack sufficient inhibitory control in cortical and limbic regions to suppress inappropriate fear responses
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problems with barbiturates
general depression of neuronal activity: including vital functions poor therapeutic ratio dependency and withdrawal only for severe insomnia
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advantage and disadvantage of benzodiazepine
- fast acting anxiolytic - large therapeutic window - may cause dependence - effects potentiated by alcohol
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diffuse modulatory systems
specific populations of neurons that project diffusely and modulate activity of glutamate and GABA neurons in target areas
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what is neuromodulation
altering of presynaptics cells ability to release more transmitter or postsynpatic cells ability to respond
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what systems is dopamine involved in
midbrain projects to forebrain - nigrostriatal : movement - mesolimbic: reinforcement and reward - mesocortical: memory and planning
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synthesis, storage and reuptake of dopamine
- synthesised from tyrosine by tyrosine hydroxylase to form L-DOPA which is synthesised by dopa decarboxylase to form dopamine - loaded into vesicles - reuptake by transporters powered by electrochemical gradient, enzymatically regarded by monoamine oxidases
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regulation of tyrosine hydroxylase activity
feedback inhibition by end products: dopamine competes for binding with essential factor - presynaptic activity lead to phosphorylation of TH which increases its activity - prolonged activity in presynaptic neuron leads to increase in transcription of TH gene leading to more enzyme synthesised
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drugs affecting dopamine synthesis and storage
reserpine impairs storage of monoamines AMPT inactivates TH psychostimulants like cocaine block reuptake of monoamines
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noradrenergic system
role in arousal and attention | dysfunction: anxiety, depression, heroin withdrawal
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seratonergic system
raphe nuclei with diffuse projections descending projections to cerebellum and spinal cord function in: mood, sleep, pain, emotion, appetite
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serotonin synthesis, storage and reuptake
tryptophan synthesised by tryptophan hydroxylase, forms 5-HCT which is catalysed by aromatic amino acid decarboxylase - loaded into vesicels - reuptake by transporters and degraded by MAOs in cytoplasm
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drugs affecting serotonin release and reuptake
- fluoxetine blocks reuptake - fenfluramine causes release of serotonin and inhibits uptake - MDMA causes noradrenaline and serotonin transporters to run in reverse
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cholinergic system
acetylcholine | basal forebrain complex
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synthesis, storage and reuptake of acetylcholine
made from choline loaded in vesicles released dependent on calcium exocytosis rapidly degraded in synaptic cleft by acetylcholinesterase
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drugs affects acetylcholine release and reuptake
acetylcholinesterase inhibitors block breakdown of Ach | botulinum and tetanux toxins block docking of vesicles
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disorders related to cholinergic system dysfunction
peripheral: myasthenia gravis brain: alzheimer addition epilespy
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what is learning
response of brin to environmental events and involves adaptive changes in synaptic connectivity which results in behavioural changes strengthening and weakening of synapses
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what is long term potentiation
mechanism underlying synaptic strengthening | results in long lasting increased synaptic efficacy
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properties of long term potentiation
temporal: summation of inputs reaches threshold that leads to induction of LTP input specific: LTP at one synapse is not propagated to adjacent synapse associative: simultaneous stimulation of strong and weak pathway will induce LTP at both pathways
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molecular mechanism of LTP
glutamate released onto inactive cell AMPA receptor activated creating EPSP NMDA receptor blocked by mg depolarisation by MAPA not sufficient to unblock NMDA receptor Glutamate released onto active cell NMDA unblocked Ca entry activated calcium calmodulin dependent protein kinase II CaMKII phosphorylates AMPA receptors increasing effectiveness and stimulates insertion of new AMPA receptors into post synaptic membrane
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Ca calmodulin-dependent protein kinase
sustains activity after repolarisation autocatalytic activity: phosphorylates self, no longer requires Ca molecular switch maintains increased excitability of neuron
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presynaptic events in LTP
- post synaptic neuron feed back to presynaptic by retrograde neurotransmitter (Nitric oxide) - Ca diffuse through NMDA and activates nitric oxide synthase - NO diffuses from site of production and activates guanylyl cyclase in presynaptic - guanylyl cyclase produces secondary messenger cGMP - signal transduction cascade lead to increased glutamate release from presynaptic bouton
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late phase LTP
protein synthesis required protein synthesis inhibitors prevent consolidation of term term memories and LTP stages of memory formation: acquisition, consolidation and recall
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early vs late phase LTP
early: lasts minute to hour, explained by movement of Ca and enhancement of AMPA receptors late: hours, days months, requires Ca activated signal transduction cascade to activate new protein synthesis
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long term depressin
created in slice preparations by high frequency stimulation | AMPA receptors are dephosphorylated and removed from membrane
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Theta rhythms
hippocampal theta activity accompanies behaviours such as running, swimming and spatial orientated responses in rats seem play role in synchronising activity id different brain regions
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manipulating LTP
genetically: increased amounts of particular NMDA receptor enhances LTP age: as get older, decreased LTP as decreased expression NMDA receptors enrichment: more enrich environment, potentiate LTP
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fear and anxiety disorders
fear is useful and innate response | anxiety disorders are by-product of inappropriate fear responses
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amygdala and fear
- Kluver-Bucy syndrome: disorder when both right and left medial temporal lobes malfunction, little or no fear response - Feinstein 2011: women with bilateral amygdala lesions had little fear responses to films
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fear elicits the stress response, what are the steps that occur
- sensory info to amygdala - amygdala excites locus coeruleus and hypothalamus - hypothalamus releases CRH - Pituitary response releases ACTH - Adrenal cortex releases cortisol - Locus coeruleus releases noradrenaline
115
what does the sympathetic nervous system and CNS do when fight or flight response activated
sym: increases HR & BP, blood flow to muscles, fast breathing, perspiration and inhibited digestion CNS: behavioural arrest & arousal, narrowing of attention, augmented startle response, cortical activation and emotional response
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Role of GABAergic receptors in anxiety disorders
PET study with radiolabelled flumazenil panic disorder patients have fewer benzodiazepine binding sites frontal cortex hyperactive responsiveness during periods of anxiety
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effects of benzodiazepine
``` anxiolytic anticonvulsant sedative muscle relaxant amnestic -partial agonist best therapeutic ratio ```
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animal models for anxiety
elevated maze: anxiety is degree to which avoids open arms of maze, diazepam increases time spent in aversive open arms
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genetically turning of BZD binding site
- 5 subunits form doughnut structure around ion channel - BZD binding is dependent on histidine on N-terminal in extracellular domain - 'knock in' mice made with insensitive BZD subunit
120
BZD and amygdala
- high density of BZD bidning sites in amygdala - injection of soluble BZD into amygdala induces anxiolytic effect in rats - injection of BZD antagonist abolishes anxiolytic effect of BZD given systematically - even after amygdala destruction, BZD retains anxiolytic effect
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hippocampus and anxiety
- provides info about contextual stimuli important for fear conditioning - lesions have anxiolytic effect - BZD direct effect on GABAergic inhibition in hippo - chronic stress; chronic activation of glucocorticoid receptors in hippo, excitotoxic
122
locus coeruleus and anxiety
- events important for survival lead to firing of LC - noradrenergic projections to cerebellum, hippo, neocortex and thalamus - increased arousal and attention - BZD decreases noradrenergic release
123
raphe nucleus and BZD
* Serotonergic projections to striatum, nucleus accumbens, frontal cortex and hippocampus * Punishment stimuli -> activation of serotonergic system -> behavioural inhibition * BZD decrease serotonergic activity in RA
124
definition of schizophrenia
'break from reality' | split mind
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positive symptoms of schizophrenia
thought disorders: disorganised, irrational, rhyming delusions: persecution, grandeur, control hallucinations: auditory an olfactory
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negative symptoms of schizo
``` flattened emotional response poverty speech lack initiative persistence anhedonia social withdrawal ```
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cognitive symptoms of schizo
``` difficulty sustaining attention low psychomotor speed deficits in learning an dmemory poor abstract thinking poor problemsolving ```
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schizo performance on stroop and wisconsin card tests
schizo are slower and less accurate at stroop schizo don't show same increase in regional blood flow to dIPFC
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sensory-motor gating deficits in schizo
difficulty screening our irrelevant stimuli and focusing on salient one - p50 signal, schizo show no change in response to second auditory stimulus - pre pulse inhibition: schizo do not show startle response inhibition
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oculomotor functions of schizo
eye movement in tracking a moving stimulus is not smooth compared to control
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structural differences of schizo brain
size of lateral ventricles is twice as big as normal person | reduced brain volume in temporal, frontal lobes and hippocampus
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heritability of schizo
-adoption and twin studies show heritable trait but not due to one single gene mutation of DISC1 gene: increases chances of schizo paternal age: older fathers more likely schizo child -monochorionic MZ twins 60% concordance
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early neurodevelopmental model of schizo
events in early life casuedeviations from normal development -lie dormant until brain matures sufficiently enough to activate affected systems early events such as infections, obstetric complications, nutritional deficiencies
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evidence of early neurodevelopmental mdoel of schizo
walker 1994: hoem movies, children displaying more negative affect and abnormal behaviour had schizo schiffmann 2004: less sociability and deficient psychomotor functioning develop schizo
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late neurodevelopmental model of schizo
schizo results from abnormality or deviation in adolescence when synaptic pruning takes place
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two hit model of schizo
atypical development in early brain development and adolescence - early-dysfunction of specific neural networks that account for premorbid signs - adolescence-excessive synaptic pruning and loss of plasticity may account for emergence of symptoms
137
dopamine hypothesis of schizo
- abnormalities in DA functioning in brain - overactivity of DA in mesolimbic system result in positive symptoms - underactivity of DA in mesocortical results in neg and cog symptoms
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evidence of DA hypothesis of schizo
DA agonist induces psychosis | symptoms alleviated using antipsychotics which are antagonists
139
problems with DA hypothesis
only explains part of schizo
140
glutamate hypothesis
hypofunction of NMDA receptors
141
evidence of glutamate hypothesis
phencyclidine and ketamine cause positive negative and cog symptoms both are NMDA antagonists glutamate agonsit improves pos and neg symptoms
142
neuroinflammatroy hypothesis of schizo
microglial activation brains immune cells hyperactive in people at risk of schizo animal studies show link between pro-inflammatory agens and schizo symptoms symptoms reversed with antibiotic aimed at microglial
143
oestrogen hypothesis of schizo
estrogen plays protective role peak onset of schizo around menopause women less severe symptoms, later onset, better response to treatments
144
antipsychotics
2 major families: D1 and D2 both both D2 receptors 20-30% people not respond long term treatment leads to symptoms resembling parkinsons or tardive dyskinesia: unable stop moving
145
atypical antipsychotics
for those resilient to the others no parkinson effects improves both pos and neg symptoms clozapine: reduces suicide rates
146
definition of sleep
natural, periodic state involving reduced response to environmental stimuli and decreased mobility
147
what are the two processes that control sleep
homeostatic - accumulate sleep debt if not get enough | circadian - happens at particular time in 24hr cycle
148
what is actigraphy
use of special watches to record activity during day and night
149
what is polysomnography
recording of electrical activity from multiple sources EEG - brain/neurons EOG - eye movement EMG - muscles
150
what waves present when awake
beta - irregular, 13-30Hz | alpha - 8-12Hz, when resting
151
stages of sleep
1-theta activity (transition) 2-sleep begins, irregular activity, spindles and k complexes 3-high amp low freq delta activity, regular and synchronised, body functions slow REM - increased brain activity, asynchrony, facial twitches, erections etc
152
what is sleep cycle and how long last
when fall asleep progress through 1-3, then cycle back through 1-3 then enter REM each cycle lasts 90mins
153
contemporary views on dreaming
activation synthesis hypothesis: -brainstem activated during REM, send signal to cortex, creates images from memory, less activation of frontal cortex so no logic of timing coping hypothesis: -dream about events find threatening
154
neural basis of sleep
melatonin secreted by pineal glands during dark promotes sleepiness adenosine accumulates during day after prolonged wakefulness and promotes sleep
155
brain inhibition during sleep
constantine: patients with encephalitis have continuous sleep and only wake for food drink etc, damage to base of brain vIPOA: contains GABA, damage to vIPOA causes insomnia in rats, electrical stimulation causes sleepiness
156
brain mechanisms of wakefulness (moruzi and mogoun 1949)
when anesthetised cats brainstem was stimulated, brain waves changed from delta to beta waves, the cats then woke up
157
role of orexin/hypocretin
peptide released from lateral hypothalamus highly responsible for maintenance of wakefulness implicated in narcolepsy
158
what is a circadian rhythm
rhythms or regular patterns of activity associated with 24 hr cycle humans are diurnal
159
early discoveries of biorhythms
not unique to humans and animals mimosa plant continues rhythmic behaviour even when removed from light and temp humans in underground bunker with no cues, maintained daily rhythms but it shifted to 25hrs
160
setting and resetting the biological clock
zeitgebers are external cues, when resets biorhythm the rhythm is entrained most potent zeitgeber is light
161
jet lag and circadian rhythms
disruption of circadian rhythms due to crossing time zones stems from mismatch of internal cloc and external time phase delay - travelling west phase advance - travelling east
162
variability of circadian rhythms
-chronotypes - larks and owls rhythms have genetic basis but change as function of age children and elderly are larks, in adolescence tend to ward larks
163
experiment that detected biological clcok
richter electrical lesions of rat brain regions lost rhythmic behaviour when lesion hypothalamus
164
suprachiasmatic nucleus
in hypothalamus, lies above optic chasm if lesioned, still engage in rhythmic behaviours, just haphazardly single cell extracted continues rhythmic firing
165
how does light reach SCN
- receives info from retinohypothalamic tract | - made of photosensitive retinal ganglion cells with pigment called melanopsin which can respond directly to light
166
how does SCN work
hall and rosbach 1984 - PER protein builds up in cells overnight and is broken down during day young 94 - TIM protein meets PER, combine and shut down period gene
167
feedback loop of SCN
transcription from DNA to mRNA, to translation to proteins which form dimers dimers enter nucleus and inhibit transcription dimers decay cycle begins again
168
other effects of scn
breeding: control of pineal gland, increased melatonin inhibits gonads, in summer less melatonin, gonads enlarge, produce testosterone time of day affects performance on cog tasks
169
why do we sleep
sleep is ubiquitous - adaptive: conserve energy - restorative: feel refreshed, remove free radicals from brain - learning and memory: REM enhance non-declarative tasks, slow wave enhance declarative tasks - developmental: brain development in babies
170
sleep epidemic
modern societies getting busier compromise sleep for activities chronically sleep deprived if 6hr or less every night insufficient sleep -> mood disorders
171
what is a somatosensory system
a system al over the body that allows us to distinguish between what world does to us and what we do bodily sensations such as touch, temp, pain, position/movement
172
what are nocioreceptors
free nerve endings perception of pain and temperature damage to dendrite or surrounding cells releases chemicals that stimulate dendrite and produces action potential
173
what are haptic receptors
dendrite attached to hair, connective tissue distinguished touch, pull, vibration, indention, flutter mechanical stimulation produce action pot.
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what are proprioceptors
perception of location and body movement | movements stretch receptors to mechanically stimulate dendrite and produce action potential
175
sensory receptor adaptation
slow adapting : signals presence of long sustained stimulus rapid adapting: respond at beginning and end of stimulus
176
dorsal-root ganglion neurons
carry info from skin to CNS via spinal cord each spinal cord segment has one d-r gn each side in spinal cord, axons may synapse onto other neurons or continue up to brain
177
what is deafferentiation
loss of incoming sensory input due to damage of sensory fibres
178
what is the dorsal spinothalamic tract
carry haptic and proprioceptive info - axons from d-r gn enter spinal cord - ascend ipsilaterally until synapse in dorsal column nuclei - axons from column cross over to opposite side and brain and project up through brainstem as part of medial meniscus pathway - axons synapse with neurons in ventrolateral nucleus of thalamus, projects to somatosensory cortex and motor cortex
179
ventral spinothalamic tract
nocioreceptive info - axons from d-r gn enter spinal cord and cross over - synapse onto contralateral side - ascend to brain where join with other axons forming medial lemniscus - synapse with neurons located in ventrolateral nucleus of thalamus - project to somatosensory cortex
180
monosynaptic reflex
relfex requiring one synapse between sensory input and movement
181
what is the vestibular system
receptors in each inner ear that respond to body position and movement of head three semicircular canals and otolith organs
182
how does vestibular system work - semicircular canals
fluid in semicircular canals pushes against hair cells, causing bending of cilia, responds to angular acceleration, lead to potentials in cells -direction of cilia bent determines if hair cell is depolarised or hyperpolarised
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how does vestibular system work - utricle and saccule
gelatin and octonia push against hair cells, altering rate of action potentials of cells that form vestibular nerve respond to linear acceleration
184
hierarchal organisation of homunculus
areas 3a and b project to area 1, whihc projects to area 2 | each successive relay of info, increases size of receptive field
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forebrain role in movement
prefrontal cortex: planning of movement, specify goal premotor cortex: organise motor sequence primary motor cortex: produce specific skilled movements
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topographic organisation
neural spatial representation of body | parts of motor cortex that controls hands, fingers and lips and tongue are larger
187
corticospinal tracts
bundle of nerve fibres directly connecting cerebral cortex to spinal cord originates from layer V pyramidal neurons branches at brainstem lateral tract : opposite side of body, move digits and limbs ventral tract: same side body, moves muscles of midline body
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motor neurons
project to muscles of body laterally located neurons project to muscles that control fingers and hands intermedially project to shoulders and arms most medially project to msucles that control trunk
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extensor and flexor muscles
e-move limb away from trunk | f-move limb toward trunk
190
characteristics of motor cortex neurons
planning and initiating movements code force of movements simple coding of mvoement direction
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volume hypothesis
internal globus pallidus acts like volume dial and projects to thalamus which projects to motor cortex direct: inhibitory effect of GPi as too muhc activity lead to overactivity in thalamus, amplifies force of movement indrect: excitatory effect on GPi too muhc activity lead to underactivity in thalamus and reduced force movement
192
what is huntingtons chorea
muscle coordination affected abrupt, excessive spontaneous irregularly timed movements atrophy og caudate nucleus an dputamen antipsychotics or anxiolytic drugs
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what is hemiballism
caused by stroke to subthalamic nucleus results in involuntary fast movements dopamine blocker
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what is parkinsons disease
affects movement, muscel control and balance loss of sub nigra that sends dopamine projections to putamen L-dopa
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mouse model of PD
symptoms induced following dopamine projection lesions in striatum light sensitive D1R-expressing neurons in lesioned area optogenic activation of D1R-expressing striatal neurons by shining blue light onto striatum improvement in fine movement
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cerebellum and movement
acquiring motor skill flocculus: small and dense lobe involved in eye movement and balance lateral hemisphere: controls movement of limbs, hands, feet and digits medial hemispheres: controls movement of face and midline body
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what ae the main motor functions of cerebellum
- timing of movements - maintaining movement accuracy - motor associative learning
Uni-year 1 & 2
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