Neuronal communication Flashcards
What is the somatic nervous system
motor nerves from CNS to skeletal muscles. Voluntary control.
What is the autonomic nervous system
nerves from CNS to internal organs e.g., heart
What is an excitatory synapse
electrical activity in presynaptic neuron to increase the excitability of postsynpatic neuron. (Inhibitory – decreases)
What is a chemical synapse
prevent direct electrical propagation of AP from pre – to post - synaptic neuron
What happens when an action potential reaches a synapse
- Pores in cell membrane open allowing influx of Ca2+ into pre-synaptic terminal
- Neurotransmitter is released into synaptic cleft
- Neurotransmitter diffuses across the synaptic cleft and interacts with receptors on the post-synaptic membrane
- the neurotransmitter causes a pore to open allowing an influx of ions into the post-synaptic terminal which is propagated along the dendrite towards the soma
How long is the synaptic delay
~0.5ms
How long is the sypase
20-30nm
What is removed and uptaken at the synapse
enzymes, reuptake by glial cells
Fusion of vesicle with presynaptic membrane - part 1
- Opening of Ca 2+ channels and actin.
- Fusion protein macromolecules (FPMs) separate to allow fusion.
- Vesicle membrane incorporated into presynaptic membrane.
Fusion of vesicle with pre-synaptic membrane - part 2
- Clathrin molecules assist inward movement of the vesicle membrane. Dynamic assists in FPM pairs and pinching the neck of the emerging vesicle.
- Vesicles are now free for recycling.
How are neurotransmitters removed from the synaptic cleft
- Enzymatic breakdown
- Active reuptake (rapid) - pumped back into pre-synaptic terminal
- Active uptake (rapid) - pumped into glial cells
How does novichok poison you
inhibits acetylcholinesterase
Symptoms of novichok poisoning
Symptoms: Spasm, prevents relaxation of muscles (cardiac and respiratory). Cause of death asphyxiation or cardiac arrest
Features of novichok poisoning
Fast acting. Remain poisonous for a long time period
Features of an excitatory post-synaptic potential (EPSP)
fast rise time, slower decay time - depolarising
What causes EPSP
Usually caused by ligand gated channels once neurotransmitter has binded, Na enters to depolarise. G protein couples receptors can also cause this, (neurotransmitters bind)
What are EPSPs and IPSPs
‘mini action potentials’ which cause transient a small transient change in membrane potential of a cell (either aid or hinder action potential formation. They can summate (an opposed to Aps).
Excitatory neurotransmitters
Glutamic acid (most common) and acetylcholine are excitary neurotransmitters and cause influx of Na (EPSP)
Inhibitory neurotransmitters
Glycine and GABA, produce an increase in negative potential (away from action potential threshold). Chloride entering cell of Potassium leaving the cell cause this.
What is convergence of neuronal communication
integrating information from a number of inputs
What is divergence of neuronal communication
response to be felt from a number of effectors
What happens if Ex1 fires twice with sufficient time between the 2
the post synaptic potential has decayed so there is no summation of inputs and no action potential, firing.
When does temporal summation occur
EX1 fires twice in a short time, so can summate sufficient to cause an action potential.
What happens when EX1 and EX2 are fired at the same time
EPSPS can summate and cause an action potential
What can prveent an action potential firing
An inhibitory presynaptic input
Wat do inhibitory neurotransmitters cause
IPSPs which can prevent action potentials firing
Why are action potentials required
for correction functioning of the brain, heart and skeletal muscles.
What is a nerve fibre
the axon of a single neuron
What is a nerve
a bundle of nerve fibres
What is intracellular recording
recording electrical activity across a membrane of one single cell (one electrode is inside the cell and one (earth) is outside).
What is extracellular recording
recording electrical activity from a population of cells (both electrodes are outside of the cell).
Extracellular recording technique
metal, hollow, saline-filled glass or silicon electrodes
Extracellular recording technique
metal, hollow, saline-filled glass or silicon electrodes
Intracellular recording technique
with an electrolyte-filled hollow glass ‘spear’ (<0.1um tip)
Patch recording (with a clean ~ 1 +um tip diameter glass pipette):
Record from slices of brain tissue, kept alive in solution that mimics extracellular fluid (cerebrospinal fluid, CSF) or record from cultured, dissociated cells. Measure voltage or current in the cell. Record action potentials/synaptic communication using electrodes. Ca2+ imaging using a dye.
What is electrophysiology
recording the signals in excitable cells
Patch recordings: Giga seal
Ensures negligible current leaks out under rim of pipette
Reduces the noise
Enables the detection of very small current (picoamps 10^-12 A, pA) flowing through single channels
Brings small electrode onto the cell, positive pressure applied to electrode so there is a clean passage through solution of brain, positive pressure removed and gentle suction pulls cell membrane up to the pipette, further suction rips a whole in cell gaining electrical access to the cell.
Intracellular sharp electrode recordings
In Vivo (intact animals, via skull ‘window’). Measure electrically during behavior. Can introduce fluorescent dyes to help visulaise individual cells dendritic trees
How does a lipid membrane have capacitance
the lipid membrane separates (stores) opposite electric charges and voltage (potential) is produced across the membrane between separated opposite charges, by electrostatic attraction
charge formula
current x time
What is voltage
the electrical driving force for a current
Voltage formula
charge stored/capcaitance
What is capacitance
ability of the membrane to store charge
Positive feed back cycle of action potential
triggering event -> depolarization -> opening of voltage gated Na+ channels -> Influx of Na+
How does tetrodoxtin effect the nervous system
Selectively blocks Na+ channels (prevents action potentials)
Binds to extracellular side
High affinity (blocks at nM concentrations)
Where is tetrodoxtin found
naturally in puffer fish
What does tetraethylammonium (TEA+) affect
TEA+ blocks K+ channels from wither side
Causes paralysis of the skeletal muscles and marked drowsiness
Effects the falling phase – becomes longer and slower falling as K+ efflux is prevented
What is the most widely distributed ion channel
K+ channel
What do voltage sensors do
(detect depolarisation) cause voltage gated ion channels to open allowing Na+ to enter
What causes inactivation of Na+
Hinged lid and allosteric blocking mechanism - cytoplasmic gate is closed more slowly by depolaristaion
What is permeability of the membrane proportional to
number of channels open or total conductance of that channel type.
Max firing rate
Pyramidal neurons (excitary) ~ 300 spikes vs AP duration ~ 1.5ms
What is the conduction velocity
the speed at which propagation of the action potential occurs. Measured in m/s, can range from 1-100 m/s
What is current to produce a given change in voltage proportional to
1/thickness
Is more or less current required with myelinated fibres
less
What is current to produce a given voltage change inversely proportional to
membrane thickness
What does the current flow occur between
the active and adjacent inactive areas
What do nodes of ranvier have
a high Na+ concentration
How do myelinated fibres transmit an action potential
saltatory conduction - current jumps between nodes (increases conduction velocity)
What does myelin prevent
charge through ion channels
What factors effect conduction velocity
- Myelination of the axon (good insulator, increases resistance, decreases conductance?)
- Diameter of the axon (internal resistance)
Pros of myelination
+Speed:20 m/s unmyelinated squid giant axon vs up to 120m/s in myelinated
+Economy: squid giant axon consumes 5000 times more energy than same speed myelinated axon
+Space
Cons of myelination
Metabolic and developmental costs of setting up vulnerable to demyelinating diseases e.g. Multiple Sclerois (CNS). Guillain-Barre syndrome (peripheral nerves)
What do demyelinating conditions do
decrease conduction velocity in affected axons. Can eventually result in block of conduction. Will cause axonal death in the long term
What is multiple sclerosis
disruption in myelin sheath in CNS neurons
Symptoms of multiple sclerosis
numbness and tingling. Progressive muscle weakness. Mobility problems.
What is the cause of multiple sclerosis
genetics, gender and some viral infections
Causes of Guillain Barre syndrome
campylobacter, influenza virus, cytomegalovirus, epstein-barr virus
What happens in Guillain Barre syndrome
Disruption of myelin sheath in PNS neurons
Symptoms of Guillain Barre Syndrome
pins and needles in the hands and feet, limb weakness and uncoordinated movement
Extracellular recordings of action potentials:
From population of neurons. Measure voltage difference between 2 electrodes relative to one another. Stimulate whole nerve. Biphasic compound action potential -
When are action potentials graded
Compound AP recorded from whole nerve is NOT “all or none” they are graded. Graded dependent on size of the stimulus
What is a small stimulus
few fibres – small potential
What is a larger stimulus
more fibres – larger potential
What is a maximum stimulus
all fibers – max potential
What causes a lower action potential threshold
thicker fibers - easier to stimulate an action potential
