NEURO Flashcards
White matter
Axonal structure
Connects different part of the cortex together and connects cortical matter to the deep grey matter
How does magnetic resonance imaging work
Body has tiny magnets - brain is 75% water
Hydrogens have protons - causes it to have magnetic moment
What does the image intensity depend on in T2 weighted images
T2 - more fluid = brighter signalling.
Water content, tissue structure, blood flow, perfusion, diffusion and paramagnetic
What is T1 weighted images related to
Time it takes for the magnetisation to realign with the magnetic field
Why do white and grey matter have different relaxation time?
Approx. 50% of tissue volume in white matter is from myelin structures - relaxation of 1H in lipid structures is very short.
Therefore white matter shows very bright
What does diffusion MRI measure
Measures how freely water diffuses in a variety of directions - what is the max and min diffusion.
How does functional magnetic resonance work
Venous side is paramagnetic - variation in magnetic field so decrease in MR signal
How does positron emission tomography work
Emit beta particles - annihilation occurs and 2 gamma ray released in opposite direction.
Scanner detects rays and joins lines together to where annihilation occurs.
Relating to metabolism of cellular functions
Microtubules
Polymer of the protein tubulin – located in axons and dendrites and important in axoplasmic transport
Microfilaments
Polymer of the protein actin – found throughout the neuron but particularly abundant in axons and dendrites
Neurofilaments
A type of intermediate filament – particularly abundant in axons and important in regulating axonal shape
Glial cells
‘Support cells’ within the nervous system and can be classified into 4 categories based on structure and function.
Can myelinate axons
Astrocytes
Most numerous type of glial cell within the human brain.
Regulate extracellular environment in the brain
Microglia
Accounts 5-15% of total CNS cell number - broadly distributed in brain and spinal cord
Function of microglia
Phagocytosis of neuronal and glial debris
Synaptic connection remodelling
Directing neuronal migration during brain development.
Ependymal cells
Lines the ventricular system and acts as a physical barrier separating brain tissue from CSF
Oligodendrocytes and schwann cells
Function to provide myelin - a membranous sheath around axons to neurons in the nervous system
Oligodendrocytes
Situated in CNS - myelinate many axons
Schwann cells
Situated in the peripheral NS - myelinate only single axon
Glutamate synthesis
Glutamine into glutamate
By enzyme glutaminase - phosphate activated.
Transported into vesicles by VGLUT - counter transport with H+
Degradation of glutamate
Glutamate reabsorbed from synaptic cleft into glial cell via EAAT
Glutamate into glutamine by glutamine synthetase
Then move through SN1 and SAT2 into neuron.
Consequences of glutamate signalling in the brain
Excitatory neurotransmitters will lead to neuronal membrane depolarisation - membrane becomes more + value.
ESPC - flow of ions, change in current across post synaptic membrane
EPSPs - increase the chances of action potential
Excitotoxicity
Pathological process by which excessive excitatory stimulation leads to neuronal damage and death
Mechanism of long term potentiation (LTP)
Glutamate activates AMPA receptors – Na+ flowing leading to post synaptic neuron and cause depolarisation
NMDA receptors open. Removing the voltage gated Mg2+ ion block
Ca2+ ions enter the cell activate post-synaptic protein kinases such as calmodulin kinase II (CaMKII) and protein kinase C
CaMKII and PKC trigger a series of reactions leading to insertion of new AMPA receptors into post synaptic membrane
AMPA receptors increase sensitivity to glutamate and increase ion channel conductance
This underlies the initial phase of LTP
Memantine
Low affinity NMDA receptor antagonist that blocks the NMDA receptor ion channel to reduce glutamate mediated neurotoxicity
Glutamate
Major excitatory neurotransmitter in CNS
GABA
Major inhibitory neurotransmitter in CNS
Synthesis of GABA
Glutamate converted in GABA by GLUTAMATE DECARBOXYLASE
Has a co-factor - PYRIDOXAL PHOSPHATE.
Degradation of GABA
GABA converted into Succinic semialdehyde by GABA transaminase
Then becomes succinic acid by SUCCINIC SEMIALDEHYDE DEHYDROGENASE
GABA A receptors
Ionotropic
Ligand gated Cl- channel
GABA B receptors
Metabotropic
G protein coupled receptors - lead to efflux of K+ and prevent entrance of Ca2+
Cerebellum
Does not initiate movement but detects differences in ‘motor error’ between intended movement and actual movement.
Aids motor cortex to produce precise and co-ordinated movement
Purkinje cells
Class of GABAergic neurons - send projections deep to cerebellar neurons.
Epilepsy
Brain disorder characterised by periodic and unpredictable seizures mediated by the rhythmic firing of of large groups of neurons.
GABA A receptor enhancers
Barbiturates
Benzodiazepines
GAT blockers
Tiagabine
GABA transaminase inhibitor
Vigabatrine
GAD modulators
Gabapentin Valproate
Glycine
2nd major inhibitory neurotransmitter in CNS
Synthesis of Glycine
3-phosphoglycerate converted into serine converted into Glycine
By SERINE HYDROXYMETHYL TRANSFERASE
Degradation of glycine
Various enzymes responsible for the breakdown of glycine.
Glycine into serine = SERINE HYDROXYMETHYL-TRANSFERASE
Glycine receptor
Ligand gated Cl- channel
Hyperekplexia
Rare disorder characterised by hypertonia (increased muscle tone) and an exaggerated startle response.
Gene mutations - can disrupt normal glycinergic neurotransmission
Can lead to neuronal hyperexcitability
List the 4 main systems in Monoamine system
Noradrenergic locus coeruleus
Serotonergic Raphe Nuclei
Dopaminergic substantia Nigra and ventral tegmental area
Cholinergic basal forebrain and brain stem complexes
List the 4 systems with common principles in monoamine system
Small set of neurons at core
Arise from brain stem
1 neuron influences many others
Synapses release transmitter molecules into extracellular fluid
Synthesis of Noradrenaline
Tyrosine into DOPA by TYROSINE HYDROXYLASE
DOPA into Dopamine by DOPA DECARBOXYLASE
Dopamine into noradrenaline by DOPAMINE BETA HYDROXYLASE
Noradrenaline into Adrenaline by PHENYLETHANOLAMINE N METHYL TRANSFERASE
Regulation of noradrenaline
Reserpine depletes NA stores by inhibiting vascular uptake.
Amphetamine enter vesicles displacing NA into cytoplasm, increasing NA leakage out of neuron.
Cocaine blocks NA re-uptake
What is dopamine involved with
Movement
Inhibition of prolactin release
Memory consolidation
Where are D1 and D2 receptors found
Striatum, limbic system, thalamus, and hypothalamus
Where are D3 receptors found
Limbic system
Where are D4 receptors found
Cortex and limbic system
Main pathways of Dopamine
Substantia nigra to basal ganglia
Midbrain to limbic cortex
Termination of Noradrenaline
Neuronal uptake and MAO
Termination of Dopamine
MAO, neuronal uptake
Serotonin function
Mood. Psychosis (5HT antagonism antipsychotic)
Sleep/wake (5-HT linked to sleep, 5-HT2 antagonist inhibit REM sleep)
Feeding behaviours (5HT2A antagonist increase appetite)
Pain, migraine (5HT inhibit pain pathway)
Vomiting
5-HT1 receptors
inhibitory, limbic system – mood, migraine
5-HT2 receptors
excitatory, hallucinogenic, limbic system & cortex
5-HT3
excitatory, medulla – vomiting
5-HT4
Presynaptic facilitation (ACh) - cognitive enhancement
5-HT6 and 5-HT7
Novel targets, cognition, sleep
Synthesis of serotonin
Tryptophan into 5 hydroxytryptophan by TRYPTOPHAN HYDROXYLASE
hydroxytrptophan into serotonin by DOPA DECARBOXYLASE
Pharmacological effects of amphetamine like drugs
Increase alertness and locomotion stimulation.
Euphoria/excitement
Anorexia
Decrease physical and mental fatigue
Cocaine pharmacological effects
Euphoria
Locomotor stimulation
Heightened pleasure
Effects of MDMA
Inhibits monoamine transporters (mainly 5-HT)
Large increase in 5-HT (followed by depletion)
• Increase 5-HT linked to psychotomimetic effects
• Increased DA linked to euphoria (followed by rebound dysphoria)
Where does the pituitary lie
In the bony cavity (sell turcica or pituitary fossa) in the sphenoid bone
Connected to hypothalamus by a stalk
What are the key nuclei where neuroendocrine secretory cells are in the hypothalamus
Medial
pre-optic
arcuate
paraventricular
Function of TRH/TSH
TRH from the hypothalamus stimulates the anterior pituitary to release TSH
TSH acts on thyroid to increase T4/T3 secretion – T3 is most potent thyroid hormone and target tissues contain a deiodinase enzyme (DI) to convert T4 to T3
Pituitary also express DI to convert T4 into T3 for negative feedback
Where is vasopressin and oxytocin synthesised
Supraoptic and paraventricular nuclei
Mechanism of Tyrosine kinase
Binding of insulin or growth hormone to its cell surface receptor leads to dimerisation of the receptors
Recruit tyrosine kinases and phosphorylate target protein to induce biological responses.
Laron syndrome
Mutation in GH receptor
Defective hormone binding or decrease efficiency of receptor dimerization leading to GH resistance.
What happens when oxytocin and GnRH bind to GPCRs
Stimulate phospholipase C
Phospholipase C converts PIP2 into IP3 and DAG
IP3 stimulates Ca2+ release from intracellular stores.
DAG activates PKC - stimulates phosphorylation of proteins and alter enzyme activities to initiate biological response
Cytoplasmic/nuclear receptors
Steroid and thyroid hormones - diffuse across the plasma membrane of target cells and bind to intracellular receptors in the cytoplasm or nucleus.
Receptors function as hormone regulated transcription factors, controlling gene expression
Nuclear receptors, commonly share transcriptional domain
Disorders of neuro-hormone production
Pituitary adenoma Hypothyroidism Hyperthyroidism Addison's disease Cushing's syndrome
Pituitary adenoma
Too much GH – gigantism & acromegaly Too much ACTH excess cortisol secretion (Cushing syndrome) Hypogonadism & infertility Hypopituitarism Too much PRL (hyperprolactinaemia)
Hypothyroidism
COMMON CAUSE = Hashimoto’s disease - immune system makes antibodies against thyroid
If untreated can lead to mental retardation, slow growth, cold hands and feet and lack of energy
Hyperthyroidism - Grave’s disease
Autoimmune disease - antibodies attack thyroid gland and mimic TSH to thyroids make too much thyroid hormone
Goitre
Complications = heart failure, osteoperosis
Goitre
Enlarged thyroid gland
Difficulty breathing, anxiety, irritability, difficulty sleeping, weight loss
Addison’s disease
Adrenals do not secrete enough steroids - most common cause = autoimmune
fatigue, muscle weakness, decrease appetite, low BP, nausea
Cushing’s syndrome
Excess cortisol
Weight gan, rounded face, diabetes, hypertension, osteoperosis, muscle loss.
Can also occur due to pituitary tumours - produce too much ACTH (Cushing’s disease)
Primary visual pathway
Retina Optic nerve Optic chiasm Optic tract Lateral geniculate nucleus Optic radiation Primary visual cortex (area 17)
Cones
Day vision
Does not fire action potentials - no voltage gated channels
Synaptic terminal secretes glutamate - release depends on level of depolarisation
Cones response to increased light
Hyperpolarises - more negative
Na+ close and synaptic transmission stops - no release of glutamate
Cones response to decrease light
Depolarise
More Na+ open and glutamate opens
Initiation of light response
CONES
cGMP keeps Na+ channels open
Photopigment - opsin and retinal (11 cis retinaldehyde)
Retinal is unstable - when light strikes it will become trans retinaldehyde
Causing photopigment to be activated
Amplifying biochemical cascade
CONES
Active photopigment activate G-protein, activating enzyme and the enzyme destroys cGMP.
Leading to decrease in cGMP and Na+ channels to close so decrease in Na+
Termination of response
CONES
G proteins inactivate automatically
Stop photopigment from activating more G proteins - cascade biochemical events remove the activated retinal.
Allow 2nd enzyme to rebuild cGMP
Peripheral vision
Visual image is optically blurred
Cone photoreceptors are large and widely spaced (separated by large number of rods)
Signals from many cones converge onto single ganglion cells
Central vision
Fovea specialised for high resolution
Only cone photoreceptors, primarily red and green.
Which are narrow and closely packed
Fovea centralis
Foveal pit - where photoreceptors are uncovered - no retina sitting between them and the light path
No image blurs
Excellent sampling - no rods. Cones packed close together
No convergence - only input from 1 cone each
How do photoreceptors adapt to changes in illumination
When light strikes a photoreceptor there is a strong response.
Same position = receptor adapts and resets - go back to resting potential
Retina function and adaptation
Set up to look at relative brightness
Adaptation = retina responding changes in brightness over time
Retina circuitry
Pull out changes in brightness from 1 place to neighbouring place - does that with lateral inhibitions
Central photoreceptor response to decreased illumination
Depolarised
Bipolar and ganglion cells depolarised by excitatory synapses
Central photoreceptor response to increased illumination
Hyperpolarised
Bipolar cell depolarised by inverting synapse, excites ganglion cell
Classes of retinal ganglion cells
Parvocellular
Magnocellular
Parvocellular features/function
Small field with strong surround. Fine resolution
Accurately follows changes in light
Needs stable image
Magnocellular features/function
More convergence
Large field with weak surround, Coarse resolution
Transient response to change
Responds well to fast movements
Parietal visual areas encode…
Encode information about location and movement
Cortical area processes…
Processes colour
Inderotemporal visual areas encode….
Encode information about object identity
Saltiness mechanism of taste transduction
Na+ passes through Na+ selective channels and decrease conc. gradient.
Depolarising the taste cell and activating Voltage gated Ca2+ channels
Vesicular release of neurotransmitter and gustatory afferent axons are activated
Sourness mechanism of taste transduction
H+ pass through proton channels and bind to and block K+ selective channels.
Depolarising the taste cell and activating VGCC and voltage gated sodium channels
Vesicular release of neurotransmitter and gustatory afferent axon activated
What mechanism does bitterness, sweetness and umami use
GPCR mechanisms via T1 and T2 taste receptors
T1Rs and T2Rs - GPCR and Gq coupled
Bitterness mechanism of taste transduction
Detected by approx. 25 T2Rs
Binds to T2R which is coupled to G-protein Gq
Stimulate phospholipase C into IP3 and activate special type of Na+ ion channel and release Ca2+
Both actions depolarise the taste cell - release ATP and gustatory afferents activated
Sweetness mechanism of taste transduction
Detected by 1 receptor - T1R2 and T1R3 proteins
Binds to dimer receptor formed from T1R2 and T1R3 - coupled to G protein Gq
Stimulate phospholipase C into IP3 and activate special type of Na+ ion channel and release Ca2+
Both actions depolarise the taste cell - release ATP and gustatory afferents activated
Why do we not confuse bitter and sweet tastes
Taste cells express either bitter or sweet receptors - NOT BOTH
Bitter and sweet taste cells connect to different gustatory axons
Umami mechanism of taste transduction
Detected by 1 receptor T1R1 and T1R3
Binds to dimer receptor formed from T1R1 and T1R3
Stimulate phospholipase C into IP3 and activate special type of Na+ ion channel and release Ca2+
Both actions depolarise the taste cell - release ATP and gustatory afferents activated
Central gustatory pathways
Taste cells to gustatory axons
Gustatory nucleus (medulla)
Ventral posterior medial nucleus (thalamus)
Gustatory cortex
Olfactory transduction mechanisms
Bind to odorant receptor proteins on the cilia
Olfactory specific G-protein is activated
Adenylyl cyclase activation increase cAMP formation
cAMP-activated channels open, allowing Na+ and Ca2+ influx
cAMP activated chloride channels open enabling Cl- efflux
Causes membrane depolarisation of olfactory neuron
What is the flow of smell information to the CNS
Olfactory receptor send axons into the olfactory bulb
Olfactory receptor cells express the same receptor proteins project to the same glomeruli in the olfactory bulb
Signals are relayed in the glomeruli and transmitted to higher regions of the brain
Peripheral nerve structure
Nerve = bundle of axons ensheathed in connective tissue
EPINEURIUM = connective tissue ensheathing the whole nerve
Within the nerve axon bundles may be in separate fascicles surrounded by perineurium connective tissue
Dorsal root ganglion cells sensory receptors contain
Large fibers
Small fibers
Are the sensory receptors of the somatosensory system
Structure of large fibers in dorsal root ganglion. And detects…
Large diameter
Myelinated
Fast conduction
Tactile and proprioceptive
Structure of small fibers in dorsal root ganglion. And detects…
Small diameter
Thinly myelinated/unmyelinated
Medium/slow conducting
Temperature, pain, itch, crude touch
Receptors for proprioception
α afferents - large diameter, myelinated, fastest conducting (≤100 m/s)
In Muscle spindles
Receptors for tactile afferents
β afferents: large diameter, myelinated, 2nd fastest conducting (30-70 m/s)
Where are the receptors for tactile afferents found
Superficial: Meissner's corpuscles Merkel's discs Deep: Ruffinni corpuscles Pacinian corpuscles
What fibres are in free nerve endings
Delta fibres - small diameter, thinly myelinated, moderate conduction velocity
C fibres - small diameter, unmyelinated, slow conducting
Cutaneous receptors of the somatosensory system
Meissner corpuscle Pacinian corpuscle Ruffini corpuscles Merkel's disks Free nerve endings
List the 2 major central pathways of the somatosensory system
Dorsal column - medial lembiscal system (DCML) Spinothalamic tract (STT)
What does the dorsal column detect
Mediate discriminative touch, vibration, proprioception
Inputs from from β and α afferent fibres
What does spinothalamic tract detect
Coarse touch, termperature, pain
Inputs from delta and C fibres.
Auditory system pathway
Cochlear nucleus Olivary complex Lateral lemniscus Inferior colliculus Medial geniuculate body Auditory cortex
How does semi-circular canals sense rotation
Rotation cause fluid motion in semi-circular canals
Hair cells register different directions
Cilia connected to the gelatinous cupula
Fluid in canal lags - pull cupula in opposite direction to rotation of head
Cilia displaced - depolarising hair cells
Microtia
Under developed pinna (external ear)
Grade I microtia
less than complete development of the external ear – identifiable structures and a small but present external ear canal
Grade II microtia
partially developed ear – closed stenotic external ear canal producing a conductive hearing loss
Grade III microtia
absence of external ear, external ear canal and ear drum – most common form
Grade IV microtia
absence of total ear or anotia
Glue ear (otitus media/OM)
Fluid fills the middle ear
Impedes motion of ossicles - decrease middle ear gain, increase hearing threshold
Organs of corti
Sits on top of basilar membrane, within scala media
Inner and outer hair cells are mounted on it
Organs of corti in action
Motion of organ of corti on the basilar membrane causes displacement of the sterocilia
How hair cells work
Tip links open ion channels. Increase in K+
K+ influx - depolarise the cell
VGCC open - Ca2+ trigger neurotransmitter release at synapse - trigger action potential in post synapse
How does a Cochlear amplifier work
Outer hair cells are motile – influx of + ions make the outer hair cells contract
Prestin (motor protein of the outer hair cells) in short conformation state
Outer hair cell contracts – pulls the basilar membrane toward the tectorial membrane
Quiet sounds are amplified – loud sounds are not
Tuning is sharper than the passive vibration of the basilar membrane
How does battery driving cochlear hair cells work
• Increase K+ conc. of the endolymph of the Scala media creates a 2x amplification
If it were not potassium rich then inner hair cell output (of the cochlea nerve) would be ½ making sound perceptually quieter
Cochlea amplification would be smaller – making sounds quieter
Declarative memory
Declarative memory consists of facts and events that can be consciously recalled or “declared.” Also known as explicit memory, it is based on the concept that this type of memory consists of information that can be explicitly stored and retrieved.
Types of declarative memory
Working memory – temporary storage, lasting seconds
Short term memories – vulnerable to disruption
Facts and events stored in short term memory
Subset are converted to long term memories
Long term memories – recalled months or years later
Non declarative memory
Procedural memory
Motor skills, habits, striatum
Pre-frontal cortex function
Self-awareness, capacity for planning and problem solving
Memory consolidation
Process of converting short term memories into long term memories
Medial temporal lobes involved
Amnesia
Serious loss of memory and ability to learn
Synaptic plasticity
Biological process by which specific patterns of synaptic activity result in changes in synaptic strength
Trisynaptic circuit
Info flows from entorhinal cortex via performant path to dentate gyrus
Dentate gyrus to neurons of CA3 in hippocampal region
Axon from CA3 to CA1 hippocampal region
Brain rhythms
Distinct patters of neuronal activity that are associated with specific behaviours, arousal level and sleep state
Electroencephalogram
measurement of electrical activity generated by the brain and recorded from the scalp.
Require synchronous activity.
Amplitude - signal depends upon how synchronous activity of a group of cells is
Alertness and wake rhythm
Increase frequency and low amplitude
Non-dreaming sleep rhythm
Low frequency and high amplitude
Collective behaviour
Synchronous rhythms arise from collective behaviours of cortical neurons themselves
Thalamic pacemaker
Connections between excitatory and inhibitory thalamic neurons force each neuron to conform to rhythm of group.
Co-ordinated rhythms passed to cortex by thalamocortical axons
Behaviour of cortical neurons
Rely on collective interactions of cortical neurons - not thalamic pacemaker.
Excitatory and inhibitory interconnections of neurons result in a co-ordinated synchronous pattern of activity
Can be local or spread to larger regions of cerebral cortex
Non-REM sleep
Body capable of involuntary movement - rarely with vivid detailed dreams
Decrease temp, HR, breathing and brain energy consumption
REM sleep
Body immobilised, with vivid detailed dreams.
Decreased temperature, HR, breathing (irregular). Increased brain energy consumption
Brainstem activity during wakefulness
Increased brainstem activity. Several sets of neurons increase rate of firing in anticipation of waking.
Neuron synapse to thalamus and cerebral cortex.
Increase excitatory activity. Supress rhythmic forms of firing in thalamus and cortex during sleep
Brainstem during sleep
Decrease in activity. Neurons decrease rate of firing during sleep. (ACh, 5HT, norephinephrine)
Cholinergic neurons in pons - increase rate of firing to reduce REM sleep
Rhythmic forms of firing to the thalamus block sensory info to cortex
How Adenosine affects sleep
Decrease HR, repiratory rate and BP and smooth muscle tone.
Inhibitory effect on ACh, 5HT = promote wakefulness.
Adenosine antagonists promote wakefulness
How nitric oxide affects sleep
Potent vasodilator - decrease smooth muscle tone and BP
Simulates adenosine release
How inflammatory factors affect sleep
Cytokines stimulate immune system to fight infections
Interleukin 1 levels shown to promote non-REM sleep
How melatonin affects sleep
Hormone secreted by pineal gland at night
Initiate and maintain sleep
What is parabiosis?
And what was the experiement
Sharing of blood circulation between animals.
ob/ob mice - 1 mouse couldn’t produce leptin and 1 could = decrease in obesity
Anorexic response
Increase leptin levels = inhibit eating
Rise in leptin levels detecred by neurons in arcuate nucleus - aMSH & CART to respond to increased levels of leptin
What regions do aMSH and CART project to
Parventricular nucleus, intermediolateral grey matter of spinal cord and the lateral hypothalamus to give rise to :
Humoral, visceromotor and somatic responses
Orexigenic response
Response to decreased leptin levels.
Fall detected by neurons in arcuate nucleus - NPY and AgRP
What does NPY and AgRP act on
Inhibit neurons in paraventricular nucleus - controls release of TSH and ACTH from pituitary
Activate neurons in lateral hypothalamus - stimulate feeding behaviour
AgRP and MC4 receptor
Blocks MC4 = no inhibition of feeding behaviour
aMSH and MC4 receptor
Stimulates MC4 = inhibition of feeding behaviour
Other orexigenic peptides
Melanin concentrating hormone
Orexin
3 phases of satiety
Cephali
gastric
substrate (intestinal)
Cephalic phase
HUNGER
Ghrelin released when stomach is empty - activates NPY/AgRP containing arcuate nucleus
Reward system
DA to neurons project from VTA to nucleus acumbens
DA is released to pre-frontal cortex
Stages of addiction
Acute reinforcement Escalating/compulsive use Dependence Withdrawal protracted withdrawal Recovery
Dependence
Driven by need to self medicate negative withdrawal symtpms - negative reinforcement
Positive reinforcement
anything added that follows a behaviour that makes it more likely that the behaviour will occur again in the future
Negative reinforcement
response or behaviour is strengthened by stopping, removing, or avoiding a negative outcome or aversive stimulus
Hippocampus - role
Memory and learning
Strong memory in those with dependence
Amygdala - role
Emotion
Connection to drug of abuse
Dopamine and reinforcement
Released in the nucleus accumbens is correlated with motivation but not liking
Also, released in anticipation of reward and in movement
Serotonin - food and mood
5HT in hypothalamus
links food with mood - rise anticipation of food, spike during meal, association anorexia nervosa, bulimia with depression
Cerebral organisation of language - Articulation and phonology
Inferior parts of motor homonculus
Broca’s area
Cerebral organisation of language - meaning
Temporal lobes
Densely interconnected - widespread regions associated with cortex
Cerebral organisation of language - syntax
Left inferior frontal gyrus
Cerebral organisation of language - comprehension
Primary auditory cortex temporal lobes left inferior frontal gyrus Arcuate fasciculus Left posterior superior Temporal gyrus
Broca’s aphasia
Difficulty articulating and phonology
Speeh = halting, fragmented, distorted
Comprehension - words, decreased understanding of sentences
Pathologies = middle cerebral artery, infarction, haemorrhagic stroke
Wernicke’s aphasia
Receptive aphasia or sensory aphasia
Speech - fluent, often with meaningless phonological strings
Damage to - posterior regions or language network
Pathologies = penetrate brain injury, cerebral haemorrhage - in region of broca’s area
Conduction aphasia
Difficulty with repetition
Speech = mild fluency and comprehension difficulties
Damage - posterior perisylvian regions and underlying white matter
Pahtologies = lacunar stroke
Non fluent progressive aphasia
Affect syntax and phonology Slow, distorted, agrammatic speech progressive Phonological and grammatical errors in spontaneous speech SIngle word comprehension Pathology = primary tauopathy
Dynamic aphasia
Difficulty planning, initiating and maintaining speech
Speech = fragmented, preservative speech
Damage to anterior left inferior frontal gyrus
Pahtologies = left anterior cerebral artery infarction
Fluent progressive aphasia
Disrupted meaning
Normal speech and produce empty content.
Generic word and pronoun use - spontaneous speech
Single word comprehension difficulties
Pathology = TDP-43 proteinopathy
Logopenic progressive aphasia
Subtle word finding changes - poverty of speech output
Ocassional errors in syntax and phonology - poor sentence repition
Pathology = Alzheimer’s disease
Damage to posterior perisylvian pathology
