Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PHYSIOLOGY 2 > NEURO > Flashcards

NEURO Flashcards

1
Q

White matter

A

Axonal structure

Connects different part of the cortex together and connects cortical matter to the deep grey matter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How does magnetic resonance imaging work

A

Body has tiny magnets - brain is 75% water

Hydrogens have protons - causes it to have magnetic moment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What does the image intensity depend on in T2 weighted images

A

T2 - more fluid = brighter signalling.

Water content, tissue structure, blood flow, perfusion, diffusion and paramagnetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is T1 weighted images related to

A

Time it takes for the magnetisation to realign with the magnetic field

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Why do white and grey matter have different relaxation time?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What does diffusion MRI measure

A

Measures how freely water diffuses in a variety of directions - what is the max and min diffusion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How does functional magnetic resonance work

A

Venous side is paramagnetic - variation in magnetic field so decrease in MR signal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How does positron emission tomography work

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Microtubules

A

Polymer of the protein tubulin – located in axons and dendrites and important in axoplasmic transport

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Microfilaments

A

Polymer of the protein actin – found throughout the neuron but particularly abundant in axons and dendrites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Neurofilaments

A

A type of intermediate filament – particularly abundant in axons and important in regulating axonal shape

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Glial cells

A

‘Support cells’ within the nervous system and can be classified into 4 categories based on structure and function.
Can myelinate axons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Astrocytes

A

Most numerous type of glial cell within the human brain.

Regulate extracellular environment in the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Microglia

A

Accounts 5-15% of total CNS cell number - broadly distributed in brain and spinal cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Function of microglia

A

Phagocytosis of neuronal and glial debris
Synaptic connection remodelling
Directing neuronal migration during brain development.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Ependymal cells

A

Lines the ventricular system and acts as a physical barrier separating brain tissue from CSF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Oligodendrocytes and schwann cells

A

Function to provide myelin - a membranous sheath around axons to neurons in the nervous system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Oligodendrocytes

A

Situated in CNS - myelinate many axons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Schwann cells

A

Situated in the peripheral NS - myelinate only single axon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Glutamate synthesis

A

Glutamine into glutamate
By enzyme glutaminase - phosphate activated.
Transported into vesicles by VGLUT - counter transport with H+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Degradation of glutamate

A

Glutamate reabsorbed from synaptic cleft into glial cell via EAAT
Glutamate into glutamine by glutamine synthetase
Then move through SN1 and SAT2 into neuron.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Consequences of glutamate signalling in the brain

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Excitotoxicity

A

Pathological process by which excessive excitatory stimulation leads to neuronal damage and death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Mechanism of long term potentiation (LTP)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Memantine

A

Low affinity NMDA receptor antagonist that blocks the NMDA receptor ion channel to reduce glutamate mediated neurotoxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Glutamate

A

Major excitatory neurotransmitter in CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

GABA

A

Major inhibitory neurotransmitter in CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Synthesis of GABA

A

Glutamate converted in GABA by GLUTAMATE DECARBOXYLASE

Has a co-factor - PYRIDOXAL PHOSPHATE.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Degradation of GABA

A

GABA converted into Succinic semialdehyde by GABA transaminase
Then becomes succinic acid by SUCCINIC SEMIALDEHYDE DEHYDROGENASE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

GABA A receptors

A

Ionotropic

Ligand gated Cl- channel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

GABA B receptors

A

Metabotropic

G protein coupled receptors - lead to efflux of K+ and prevent entrance of Ca2+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Cerebellum

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Purkinje cells

A

Class of GABAergic neurons - send projections deep to cerebellar neurons.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Epilepsy

A

Brain disorder characterised by periodic and unpredictable seizures mediated by the rhythmic firing of of large groups of neurons.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

GABA A receptor enhancers

A

Barbiturates

Benzodiazepines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

GAT blockers

A

Tiagabine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

GABA transaminase inhibitor

A

Vigabatrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

GAD modulators

A

Gabapentin Valproate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Glycine

A

2nd major inhibitory neurotransmitter in CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Synthesis of Glycine

A

3-phosphoglycerate converted into serine converted into Glycine
By SERINE HYDROXYMETHYL TRANSFERASE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Degradation of glycine

A

Various enzymes responsible for the breakdown of glycine.

Glycine into serine = SERINE HYDROXYMETHYL-TRANSFERASE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Glycine receptor

A

Ligand gated Cl- channel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Hyperekplexia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

List the 4 main systems in Monoamine system

A

Noradrenergic locus coeruleus
Serotonergic Raphe Nuclei
Dopaminergic substantia Nigra and ventral tegmental area
Cholinergic basal forebrain and brain stem complexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

List the 4 systems with common principles in monoamine system

A

Small set of neurons at core
Arise from brain stem
1 neuron influences many others
Synapses release transmitter molecules into extracellular fluid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Synthesis of Noradrenaline

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Regulation of noradrenaline

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is dopamine involved with

A

Movement
Inhibition of prolactin release
Memory consolidation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Where are D1 and D2 receptors found

A

Striatum, limbic system, thalamus, and hypothalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Where are D3 receptors found

A

Limbic system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Where are D4 receptors found

A

Cortex and limbic system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Main pathways of Dopamine

A

Substantia nigra to basal ganglia

Midbrain to limbic cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Termination of Noradrenaline

A

Neuronal uptake and MAO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Termination of Dopamine

A

MAO, neuronal uptake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Serotonin function

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

5-HT1 receptors

A

inhibitory, limbic system – mood, migraine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

5-HT2 receptors

A

excitatory, hallucinogenic, limbic system & cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

5-HT3

A

excitatory, medulla – vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

5-HT4

A

Presynaptic facilitation (ACh) - cognitive enhancement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

5-HT6 and 5-HT7

A

Novel targets, cognition, sleep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Synthesis of serotonin

A

Tryptophan into 5 hydroxytryptophan by TRYPTOPHAN HYDROXYLASE
hydroxytrptophan into serotonin by DOPA DECARBOXYLASE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Pharmacological effects of amphetamine like drugs

A

Increase alertness and locomotion stimulation.
Euphoria/excitement
Anorexia
Decrease physical and mental fatigue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Cocaine pharmacological effects

A

Euphoria
Locomotor stimulation
Heightened pleasure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Effects of MDMA

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Where does the pituitary lie

A

In the bony cavity (sell turcica or pituitary fossa) in the sphenoid bone
Connected to hypothalamus by a stalk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What are the key nuclei where neuroendocrine secretory cells are in the hypothalamus

A

Medial
pre-optic
arcuate
paraventricular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Function of TRH/TSH

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Where is vasopressin and oxytocin synthesised

A

Supraoptic and paraventricular nuclei

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Mechanism of Tyrosine kinase

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Laron syndrome

A

Mutation in GH receptor

Defective hormone binding or decrease efficiency of receptor dimerization leading to GH resistance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What happens when oxytocin and GnRH bind to GPCRs

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Cytoplasmic/nuclear receptors

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Disorders of neuro-hormone production

A 
Pituitary adenoma
Hypothyroidism
Hyperthyroidism
Addison's disease
Cushing's syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Pituitary adenoma

A 
Too much GH – gigantism & acromegaly
Too much ACTH excess cortisol secretion (Cushing syndrome)
Hypogonadism & infertility
Hypopituitarism
Too much PRL (hyperprolactinaemia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Hypothyroidism

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Hyperthyroidism - Grave’s disease

A

Autoimmune disease - antibodies attack thyroid gland and mimic TSH to thyroids make too much thyroid hormone
Goitre
Complications = heart failure, osteoperosis

77
Q

Goitre

A

Enlarged thyroid gland

Difficulty breathing, anxiety, irritability, difficulty sleeping, weight loss

78
Q

Addison’s disease

A

Adrenals do not secrete enough steroids - most common cause = autoimmune
fatigue, muscle weakness, decrease appetite, low BP, nausea

79
Q

Cushing’s syndrome

A

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)

80
Q

Primary visual pathway

A 
Retina 
Optic nerve
Optic chiasm
Optic tract
Lateral geniculate nucleus
Optic radiation
Primary visual cortex (area 17)
81
Q

Cones

A

Day vision
Does not fire action potentials - no voltage gated channels
Synaptic terminal secretes glutamate - release depends on level of depolarisation

82
Q

Cones response to increased light

A

Hyperpolarises - more negative

Na+ close and synaptic transmission stops - no release of glutamate

83
Q

Cones response to decrease light

A

Depolarise

More Na+ open and glutamate opens

84
Q

Initiation of light response

CONES

A

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

85
Q

Amplifying biochemical cascade

CONES

A

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+

86
Q

Termination of response

CONES

A

G proteins inactivate automatically
Stop photopigment from activating more G proteins - cascade biochemical events remove the activated retinal.
Allow 2nd enzyme to rebuild cGMP

87
Q

Peripheral vision

A

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

88
Q

Central vision

A

Fovea specialised for high resolution
Only cone photoreceptors, primarily red and green.
Which are narrow and closely packed

89
Q

Fovea centralis

A

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

90
Q

How do photoreceptors adapt to changes in illumination

A

When light strikes a photoreceptor there is a strong response.
Same position = receptor adapts and resets - go back to resting potential

91
Q

Retina function and adaptation

A

Set up to look at relative brightness

Adaptation = retina responding changes in brightness over time

92
Q

Retina circuitry

A

Pull out changes in brightness from 1 place to neighbouring place - does that with lateral inhibitions

93
Q

Central photoreceptor response to decreased illumination

A

Depolarised

Bipolar and ganglion cells depolarised by excitatory synapses

94
Q

Central photoreceptor response to increased illumination

A

Hyperpolarised

Bipolar cell depolarised by inverting synapse, excites ganglion cell

95
Q

Classes of retinal ganglion cells

A

Parvocellular

Magnocellular

96
Q

Parvocellular features/function

A

Small field with strong surround. Fine resolution
Accurately follows changes in light
Needs stable image

97
Q

Magnocellular features/function

A

More convergence
Large field with weak surround, Coarse resolution
Transient response to change
Responds well to fast movements

98
Q

Parietal visual areas encode…

A

Encode information about location and movement

99
Q

Cortical area processes…

A

Processes colour

100
Q

Inderotemporal visual areas encode….

A

Encode information about object identity

101
Q

Saltiness mechanism of taste transduction

A

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

102
Q

Sourness mechanism of taste transduction

A

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

103
Q

What mechanism does bitterness, sweetness and umami use

A

GPCR mechanisms via T1 and T2 taste receptors

T1Rs and T2Rs - GPCR and Gq coupled

104
Q

Bitterness mechanism of taste transduction

A

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

105
Q

Sweetness mechanism of taste transduction

A

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

106
Q

Why do we not confuse bitter and sweet tastes

A

Taste cells express either bitter or sweet receptors - NOT BOTH
Bitter and sweet taste cells connect to different gustatory axons

107
Q

Umami mechanism of taste transduction

A

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

108
Q

Central gustatory pathways

A

Taste cells to gustatory axons
Gustatory nucleus (medulla)
Ventral posterior medial nucleus (thalamus)
Gustatory cortex

109
Q

Olfactory transduction mechanisms

A

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

110
Q

What is the flow of smell information to the CNS

A

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

111
Q

Peripheral nerve structure

A

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

112
Q

Dorsal root ganglion cells sensory receptors contain

A

Large fibers
Small fibers
Are the sensory receptors of the somatosensory system

113
Q

Structure of large fibers in dorsal root ganglion. And detects…

A

Large diameter
Myelinated
Fast conduction
Tactile and proprioceptive

114
Q

Structure of small fibers in dorsal root ganglion. And detects…

A

Small diameter
Thinly myelinated/unmyelinated
Medium/slow conducting
Temperature, pain, itch, crude touch

115
Q

Receptors for proprioception

A

α afferents - large diameter, myelinated, fastest conducting (≤100 m/s)
In Muscle spindles

116
Q

Receptors for tactile afferents

A

β afferents: large diameter, myelinated, 2nd fastest conducting (30-70 m/s)

117
Q

Where are the receptors for tactile afferents found

A 
Superficial:
Meissner's corpuscles
Merkel's discs
Deep:
Ruffinni corpuscles
Pacinian corpuscles
118
Q

What fibres are in free nerve endings

A

Delta fibres - small diameter, thinly myelinated, moderate conduction velocity
C fibres - small diameter, unmyelinated, slow conducting

119
Q

Cutaneous receptors of the somatosensory system

A 
Meissner corpuscle
Pacinian corpuscle
Ruffini corpuscles
Merkel's disks
Free nerve endings
120
Q

List the 2 major central pathways of the somatosensory system

A 
Dorsal column - medial lembiscal system (DCML)
Spinothalamic tract (STT)
121
Q

What does the dorsal column detect

A

Mediate discriminative touch, vibration, proprioception

Inputs from from β and α afferent fibres

122
Q

What does spinothalamic tract detect

A

Coarse touch, termperature, pain

Inputs from delta and C fibres.

123
Q

Auditory system pathway

A 
Cochlear nucleus 
Olivary complex
Lateral lemniscus
Inferior colliculus
Medial geniuculate body
Auditory cortex
124
Q

How does semi-circular canals sense rotation

A

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

125
Q

Microtia

A

Under developed pinna (external ear)

126
Q

Grade I microtia

A

less than complete development of the external ear – identifiable structures and a small but present external ear canal

127
Q

Grade II microtia

A

partially developed ear – closed stenotic external ear canal producing a conductive hearing loss

128
Q

Grade III microtia

A

absence of external ear, external ear canal and ear drum – most common form

129
Q

Grade IV microtia

A

absence of total ear or anotia

130
Q

Glue ear (otitus media/OM)

A

Fluid fills the middle ear

Impedes motion of ossicles - decrease middle ear gain, increase hearing threshold

131
Q

Organs of corti

A

Sits on top of basilar membrane, within scala media

Inner and outer hair cells are mounted on it

132
Q

Organs of corti in action

A

Motion of organ of corti on the basilar membrane causes displacement of the sterocilia

133
Q

How hair cells work

A

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

134
Q

How does a Cochlear amplifier work

A

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

135
Q

How does battery driving cochlear hair cells work

A

• 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

136
Q

Declarative memory

A

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.

137
Q

Types of declarative memory

A

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

138
Q

Non declarative memory

A

Procedural memory

Motor skills, habits, striatum

139
Q

Pre-frontal cortex function

A

Self-awareness, capacity for planning and problem solving

140
Q

Memory consolidation

A

Process of converting short term memories into long term memories
Medial temporal lobes involved

141
Q

Amnesia

A

Serious loss of memory and ability to learn

142
Q

Synaptic plasticity

A

Biological process by which specific patterns of synaptic activity result in changes in synaptic strength

143
Q

Trisynaptic circuit

A

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

144
Q

Brain rhythms

A

Distinct patters of neuronal activity that are associated with specific behaviours, arousal level and sleep state

145
Q

Electroencephalogram

A

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

146
Q

Alertness and wake rhythm

A

Increase frequency and low amplitude

147
Q

Non-dreaming sleep rhythm

A

Low frequency and high amplitude

148
Q

Collective behaviour

A

Synchronous rhythms arise from collective behaviours of cortical neurons themselves

149
Q

Thalamic pacemaker

A

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

150
Q

Behaviour of cortical neurons

A

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

151
Q

Non-REM sleep

A

Body capable of involuntary movement - rarely with vivid detailed dreams
Decrease temp, HR, breathing and brain energy consumption

152
Q

REM sleep

A

Body immobilised, with vivid detailed dreams.

Decreased temperature, HR, breathing (irregular). Increased brain energy consumption

153
Q

Brainstem activity during wakefulness

A

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

154
Q

Brainstem during sleep

A

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

155
Q

How Adenosine affects sleep

A

Decrease HR, repiratory rate and BP and smooth muscle tone.
Inhibitory effect on ACh, 5HT = promote wakefulness.
Adenosine antagonists promote wakefulness

156
Q

How nitric oxide affects sleep

A

Potent vasodilator - decrease smooth muscle tone and BP

Simulates adenosine release

157
Q

How inflammatory factors affect sleep

A

Cytokines stimulate immune system to fight infections

Interleukin 1 levels shown to promote non-REM sleep

158
Q

How melatonin affects sleep

A

Hormone secreted by pineal gland at night

Initiate and maintain sleep

159
Q

What is parabiosis?

And what was the experiement

A

Sharing of blood circulation between animals.

ob/ob mice - 1 mouse couldn’t produce leptin and 1 could = decrease in obesity

160
Q

Anorexic response

A

Increase leptin levels = inhibit eating

Rise in leptin levels detecred by neurons in arcuate nucleus - aMSH & CART to respond to increased levels of leptin

161
Q

What regions do aMSH and CART project to

A

Parventricular nucleus, intermediolateral grey matter of spinal cord and the lateral hypothalamus to give rise to :
Humoral, visceromotor and somatic responses

162
Q

Orexigenic response

A

Response to decreased leptin levels.

Fall detected by neurons in arcuate nucleus - NPY and AgRP

163
Q

What does NPY and AgRP act on

A

Inhibit neurons in paraventricular nucleus - controls release of TSH and ACTH from pituitary
Activate neurons in lateral hypothalamus - stimulate feeding behaviour

164
Q

AgRP and MC4 receptor

A

Blocks MC4 = no inhibition of feeding behaviour

165
Q

aMSH and MC4 receptor

A

Stimulates MC4 = inhibition of feeding behaviour

166
Q

Other orexigenic peptides

A

Melanin concentrating hormone

Orexin

167
Q

3 phases of satiety

A

Cephali
gastric
substrate (intestinal)

168
Q

Cephalic phase

A

HUNGER

Ghrelin released when stomach is empty - activates NPY/AgRP containing arcuate nucleus

169
Q

Reward system

A

DA to neurons project from VTA to nucleus acumbens

DA is released to pre-frontal cortex

170
Q

Stages of addiction

A 
Acute reinforcement
Escalating/compulsive use
Dependence
Withdrawal
protracted withdrawal
Recovery
171
Q

Dependence

A

Driven by need to self medicate negative withdrawal symtpms - negative reinforcement

172
Q

Positive reinforcement

A

anything added that follows a behaviour that makes it more likely that the behaviour will occur again in the future

173
Q

Negative reinforcement

A

response or behaviour is strengthened by stopping, removing, or avoiding a negative outcome or aversive stimulus

174
Q

Hippocampus - role

A

Memory and learning

Strong memory in those with dependence

175
Q

Amygdala - role

A

Emotion

Connection to drug of abuse

176
Q

Dopamine and reinforcement

A

Released in the nucleus accumbens is correlated with motivation but not liking
Also, released in anticipation of reward and in movement

177
Q

Serotonin - food and mood

A

5HT in hypothalamus
links food with mood - rise anticipation of food, spike during meal, association anorexia nervosa, bulimia with depression

178
Q

Cerebral organisation of language - Articulation and phonology

A

Inferior parts of motor homonculus

Broca’s area

179
Q

Cerebral organisation of language - meaning

A

Temporal lobes

Densely interconnected - widespread regions associated with cortex

180
Q

Cerebral organisation of language - syntax

A

Left inferior frontal gyrus

181
Q

Cerebral organisation of language - comprehension

A 
Primary auditory cortex
temporal lobes
left inferior frontal gyrus
Arcuate fasciculus
Left posterior superior
Temporal gyrus
182
Q

Broca’s aphasia

A

Difficulty articulating and phonology
Speeh = halting, fragmented, distorted
Comprehension - words, decreased understanding of sentences
Pathologies = middle cerebral artery, infarction, haemorrhagic stroke

183
Q

Wernicke’s aphasia

A

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

184
Q

Conduction aphasia

A

Difficulty with repetition
Speech = mild fluency and comprehension difficulties
Damage - posterior perisylvian regions and underlying white matter
Pahtologies = lacunar stroke

185
Q

Non fluent progressive aphasia

A 
Affect syntax and phonology
Slow, distorted, agrammatic speech 
progressive
Phonological and grammatical errors in spontaneous speech
SIngle word comprehension
Pathology = primary tauopathy
186
Q

Dynamic aphasia

A

Difficulty planning, initiating and maintaining speech
Speech = fragmented, preservative speech
Damage to anterior left inferior frontal gyrus
Pahtologies = left anterior cerebral artery infarction

187
Q

Fluent progressive aphasia

A

Disrupted meaning
Normal speech and produce empty content.
Generic word and pronoun use - spontaneous speech
Single word comprehension difficulties
Pathology = TDP-43 proteinopathy

188
Q

Logopenic progressive aphasia

A

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

PHYSIOLOGY 2 (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions