Neurology And Neuroscience Flashcards
What is the most abundant cell type in the mammalian brain
Astrocytes
What are the branches of axons called
Collaterals
Name 5 cell types other than neurons found in the CNS/PNS
- Schwann cells
- oligodendrocytes
- Ependyma
- microglia
- astrocytes
Functions of the cerebellum
Posture, balance, motor coordination
Name 3 types of multipolar neurones
Pyramidal cells (pyramid shaped cell body) Purkinje cells (GABA neurons found in cerebellum) Golgi cells (GABA neurons found in cerebellum)
Describe a multipolar neuron
Multiple projections from cell body - one is an axon, the rest are dendrites
Describe a pseudo unipolar neuron
One axon projection which divides into 2
How can you distinguish axons from dendrites
Axons are myelinated
Dendrites are not myelinated
Function of dendrites
Receive signals from other neurons
Describe resting charge of neuronal cell
Negative charge inside compared to outside
Resting membrane potential of -70 mV
Why do people with multiple sclerosis get movement and visual problems
Multiple sclerosis results in the loss of the myelin from the axons of neurons
Visual problems: neurons in eye can’t transmit signals to brain fast enough
Movement problems: neurons in brain can’t transmit signals to muscles fast enough
What are the three types of synaptic organisation
Axodendritic synapse: between axon (presynaptic terminal) of one neuron and dendrites of another neuron
Axosomatic synapse: between axon (presynaptic terminal) of one neuron and soma (cell body) of another neuron
Axoaxonic synapse: between axon (presynaptic terminal) of one neuron and axon of another neuron
What is the sarcoplasmic reticulum, what is its location function and effect
Location = surround myofibrils in sarcoplasm (inside of muscle membrane) Function= stores Ca2+ and releases them when sarcolemma is depolarised Effect = myofibril and muscle contraction
What are T tubules
Continuous with the sarcoplasm and closely connected to sarcoplasmic reticulum and myofibrils.
When action potential depolarises sarcoplasm, it goes through T tubules to depolarise the myofibrils- causes muscle contraction
Describe sequence of events from action potential in pre synaptic terminal to muscle contraction
AP is propagated along membrane by Na+ and K+ voltage gated channels
When AP reaches the pre synaptic membrane, it causes Ca2+ channels to open and Ca2+ influx into the axon. This causes the vesicles contains Ach to fuse with the membrane and release the Ach into synapse
Ach diffuses across synapse and binds to nicotinic Ach receptors on skeletal muscle, causing influx of Na+ which depolarises the sarcolemma - called the End Plate Potential (EPP)
The AP then travels down T tubules which are continuous with the sarcolemma to the myofibrils which are covered by the sarcoplasmic reticulum.
This causes Ca2+ ions to enter the cell thriugh L type calcium channels. They then bind to Ryanodine receotors on the sarcoplasmic reticulum
This causes release of Ca2+ by the sarcoplasmic reticulum which causes the muscle to contract - bind to Troponin C on actin filament, causing Tropomyosin to move and expose actin binding sites. Mysoin binds to actin, muscke fibres can shorten —> muscle contraction
What happens when only a small amount of Ach is released into neuromuscular junction
Get a miniature EPP and muscle movement instead of full contraction
What is Botulism
Botulinum toxin irreversibly disrupts stimulation-induced release from presynaptic terminal Ach - prevents vesicles fusing with presynaptic membrane
Name two autoimmune disorders of the neuromuscular junction
Myasthenia Gravis
Antibodies directed against nicotinic acetyl choline receptors causing them to degrade
Get fatigable muscle weakness (ie becomes worse with repetitive use) facial muscle weakness and droopy eyelids
Lambert-Eaton Myastenic syndrome (LEMS)
Antibodies directed against voltage gated calcium channels causing them to degrade
Get muscle weakness but not so much on the face
Which condition is described below
A 58 year old male presents with generalised fatigue and weakness. He has had
weight loss and difficulty raising his arms above his head. He has pelvic and
shoulder weakness and mild facial muscle weakness.
Lambert-Eaton myasthenia syndrome
Similar presentation to myasthenia graves but mild facial muscle weakness suggests it’s LEMS
Main functions of parietal frontal temporal and occipital lobes
Frontal: executive actions - personality
Occipital: processing visual information
Temporal: contains important structures such as hippocampus (short term memory), amygdala (behaviour), Wernicke’s area (auditory perception and speech)
Parietal: somatic sensory cortex - processing tactile (touch) information
3 structures that make up brain stem in order going down
Midbrain Pons Medulla
Function of Astrocytes
Most common cells in mammalian brain
Structural role
Cell repair, neuronal maturation, neuronal plasticity, synapse formation
Function of oligodendrocytes and Schwann cells
Oligodendrocytes
- myelinate neurons of CNS
- one can myelinate many axons, there many projections from the cell body which can myelinate internodes of many neurons
Schwann cells
- myelinate neurons of PNS
- one can only myelinate one axon segment
Function of Microglia
Immune cells of CNS
similar to macrophages
Ependyma cells
Endothelial cells
Line fluid filled ventricles which regulate production and movement of cerebrospinal fluid
Flux meaning
Flux = The number of molecules
that cross a unit area per unit
of time (number of particles).
i.e. molecules.m-2.s-1
What is overshoot
Membrane potential becomes positive
Describe how the changes in membrane potential affect the ion channels
Depolarisation: ion channel opens and allows flow of ions through
Sustained depolarisation: ion channel is inactivated - no more ions can flow through
Hyper-polarisation/re polarisation: ion channel is closed
What is the refractory period
The period after the peak of the action potential is reached when the Na+ channels are inactivated and closed. During this period they cannot be reactivated and opened so the cell cannot be re stimulated
What is the relative refractory period
Some Na+ channels have recovered from activation and reopened
But a stronger than normal stimulus is required to trigger an action potential
Does the decay of an AP happen quicker in smaller or larger neurone and why
Happens more quickly in a smaller neurone as the smaller diameter means that it has more resistance
Happens even quicker if the neurone is uninsulated as it would have no insulation
What are the three main factors that influence the
movement of ions across the membrane?
Concentration of the ion on both sides of the membrane,
the charge on the ion and the voltage across the
membrane.
The membrane potential
Why is the K+ equilibrium potential negative (e.g. -70mV)
and the Na* equilibrium potential positive(e.g. +40mV)
when both are positive ions?
More K* inside the cell than outside so tend to flow out of
the cell, while more Na* outside the cell than in, therefore
tend to flow into the cell. A potential of -70mV is needed
to attract K* and stop net outward flow, while a positive
charge of +40mV is needed to repel Na* from entering the
cell.
What factors influence the speed of propagation of an action potential
along an axon?
Larger diameter axons have lower resistance, so ions move faster
conduction velocity is proportional to the square root of the axon
diameter.
There is a linear relationship between conduction velocity and myelin
thickness
What is passive propagation
There is a stimulus and further and further down the axon the voltage measured decreases - voltage decays away exponentially down the axon
(The speed of the decay depends on myelination and axon diameter)
Which types of compounds can opioid receptors respond to
Exogenous compounds eg heroin/morphine Endogenous compounds (produced by body) eg endorphins
What are 3 reasons people take heroine. For each effect name the part of the brain contains the opioid receptors that the heroine acts on
Analgesia (pain relief) - Peri-aqueductal region
Euphoria - Ventral tegmental region
Cough suppression - solitary nucleus
4 main protein targets for drugs
Enzymes
Ion channels
Transport proteins
Receptors
2 types of actions of drugs on a target
Enhance activation - stimulate an effect
Prevent activation - block an effect from being produced
Atorvastatin: what is its target type and what type of effect does it have in the target?
Target = enzyme
Action = prevents activation
(inhibits hmg coA reductase)
Lowers cholesterol
Amlodipine: what is its target type and what type of effect does it have in the target?
Target = ion channel
Action: prevents activation
(Blocks Ca2+ channels)
Treats high blood pressure and coronary heart disease
Salbutamol: what is its target type and what type of effect does it have in the target?
Target = receptor
Action = enhances activation
(Activates/Stimulates beta 2 receptors)
Is a short acting beta 2 adrenergic receptor agonist which causes relaxation of airway smooth muscle: treatment for asthma
Citalopram: what is its target type and what type of effect does it have in the target?
Target = transporter protein
Action = prevents activation
(Blocks serotonin re uptake protein)
Treats low mood and panic attacks
Noradrenaline, serotonin and dopamine all have similar structures so their receptors also have similar structures. However, why might selectivity be more important for drugs than for endogenous compounds?
Endogenous compounds like neurotransmitters (domaine, serotonin, noradrenaline) are released from pre synaptic terminal and travel across v short distance of the synapse to post synaptic terminal
So they are very specifically delivered to their drug target, making the selectivity and fact that they are similarly structured (so could theoretically bind to wrong target) less relevant or important.
Drugs are usually taken orally and travel in the blood I order to be distributed to the tissue where they produce the desired effect
But due to their method of administration and transmission they will come into contact with all tissue types
What is an adverse effect
Side effect with negative health consequences
How is drug safety linked to dose
-The safest drugs are the ones where there is a large difference in the dose required to produce a therapeutic effect and the dose required to produce an adverse effect
- as you start to increase the dose, the side effects usually increase as you lose selectivity.
Eg Pramipexole (dopamine agonist - mimics effects of dopamine)
As you increase the dose you can start to see noradrenaline and serotonin side effects too (as dopamine and therefore Pramipexole have similar structure to serotonin and noradrenaline) so bind to their receptors - if there’s enough Pramipexole, enough will bind to generate these side effects
2 types of side effects
Off target side effects Eg Pramipexole (dopamine agonist) activating serotonin and noradrenaline receptors
Unwanted effects on the same target
Eg might want only the domaine effects in a certain part of the brain by taking Pramipexole, but will get effects in all parts of the body and brain that have the dopamine target as the Pramipexole will act in them all
Eg may only want the cough suppression from heroin but will get euphoria and analgesia too as heroin acts all the opioid receptors in all parts of the brain
What are the main 3 steps of signal transmission
Information reception
Information integration (cell body integrates all the different signals it receives from different neurons)
Information transmission - rapid transfer
3 main types of molecules which can be neurotransmitters
1) Amino acids
Eg glutamate, GABA, glycine
2) amines
Eg Noradrenaline
Dopamine
3) neuroproteins
Eg opioid peptides - endorphins, enkephalins
What is the main inhibitory and excitatory neurotransmitter in the brain
Excitatory = glutamate Inhibitory = GABA
Is glycine an excitatory or inhibitor amino acid
Inhibitory
2 ways of inactivating transmitter after signal has been transmitted across synapse
1) enzymatic degradation within the synaptic cleft
2) re uptake of neurotransmitters back 8 to pre synaptic terminal and packaging into vesicles - reuse
Describe the process of neurotransmitter release
Membrane depolarisation
Ca2+ influx
Causes the docking (mediated by vesicular proteins) of vesicles
Followed by priming of vesicles
Followed by fusion of vesicles with membrane
Vesicles release neurotransmitters into synapse by exocytosis
(Process of fusion an exocytosis is mediated by vesicular proteins, proteins in cytoplasm, proteins on membrane)
(Electrochemical transduction is the process up to here from Ca2+ influx and lasts 200 us)
The vesicles are then budded (pinched off) and recycled/reused
What are SNARE proteins, give examples, and what is their role
They are vesicular proteins eg Synapsin, Synaptobrevin, SNAP 25
They are important in mediating process of exocytosis release of neurotransmitter
How does rapid release of neurotransmitters in response to Ca2+ influx happen
Vesicle docking, priming, fusion and neurotransmitter exocytosis are mediated by vesicular proteins, cytoplasm proteins and proteins on membrane
What are neurotoxins and give some examples of how they work
Toxins which interfere with synaptic vesicles and neurotransmitter release
Eg can break down vesicles whilst they’re still in presynaptic terminal
Eg can can cause excessive neurotransmitter release and subsequent depletion of neurotransmitters in pre synaptic nerve terminal
Eg can inhibit neurotransmitter release
Describe the actions of botulinum toxin as a neurotoxin
Made of 2 chains (bi-chained) and acts on cholinergic nerves
One chain binds to presynaptic membrane and one chain penetrates the membrane and cleaves the peptide bonds in the vesicular proteins which inactivates the vesicles - preventing docking, fusion and release of Ach
This causes flaccid paralysis (paralysis due to complete muscle relaxation)
In high conc, it can inhibit all cholinergic transmission and cause respiratory arrest
Describe the effects of Alpha Latrotoxin as a neurotoxin
From black widow spiders
Acts in cholinergic nerves
Stimulates massive release of Acetylcholine until the nerve is completely depleted of Ach
Causes muscular paralysis
Describe effects of Zn2+ endopeptidases
Inhibit neurotransmitter release
Eg Tetanus toxin produced by C tetani
Inhibits releases of 2 main inhibitory neurotransmitters in CNS: glycine and GABA
Causes spasms and paralysis
2 things that release of neurotransmitters is dependent on
ATP
Ca2+
What are Convulsions
When muscles contract and relax quickly causing uncontrollable shaking of the body - seizure activity
What is the telencephalon also known as
Cerebral hemisphere
Fucntion of the parietal lobe
Somatic sensory cortex responsible for processing tactile info
3 main structures of the brainstem in descending order
Midbrain
Pons
Medulla
Where is the brainstem and what is its overall function
Dorsal region of CNS
roles in motor coordination, balance and posture
What are the functions of oligodendrocytes and schwann cells and whats the difference between them
Bith are myelin producing cells
Oligodendrocytes work in CNS and each one is capable of myelinating a number of axons
Schwann cells work in PNS and each on meylinates only one axon segment
What is a microglial cell
Performs immune function in CNS
What is ependymal cell
Epithelial cells that line the fluid filled ventricles regulating the production and movement of csf