SfM - How Nerves Work Flashcards
what are the components of the CNS?
brain
spinal cord
peripheral nerves
what are the components of the peripheral NS?
nerves & ganglia outside the brain and spinal cord
somatic/autonomic NS
what are the main regions of the brain?
- cerebrum (frontal, temporal, parietal, occipital lobes)
- cerebellum
- diencephalon (thalamus, hypothalamus)
- brainstem (midbrain, pons, medulla)
- meninges
how many spinal nerves are there?
- 31
8 cervical, 12 thoracic, 5 lumbar, 5 sacral, 1 coccygeal
what is the organisation of spinal cord?
spinal cord –> root –> ganglion –> ramus –> nerve
where are sensory fibres located?
sensory fibres are found only in dorsal side (dorsal root)
where are motor fibres located?
motor fibres are found only in ventral side (ventral ramus)
when do the fibres mix?
Fibres mix in the ramus and go onto create the spinal nerves
what are the main regions of a neurone?
dendrites, cell body, axon hillock, axon, synapse
what is the role of astrocytes?
maintain the external environment for the neurones, produce blood-brain barrier
what is an oligodendrocyte?
forms myelin sheaths in the CNS
what is the role of microglia?
phagocytic hoovers mopping up infection
what is the resting membrane potential?
-70mV
what are the main factors that influence the RMP?
- mainly the leaky K+ channels
Na+K+ pump has influence but it is closer the K equilibrium
what happens if there is higher extracellular K conc?
- reduces concentration gradient
- so K+ enters cell
- therefore RMP reduced
- causes depolarisation
- unregulated AP firing
- All muscles in body contract, atrial fibrillation
- brain is protected from high K+ - blood brain barrier (astrocytes)
How does the Na/K pump influence RMP?
- open Na channels = cell depolarises
- open (more) K channels = depolarisation/hyperpolarisation
- open Cl channels = cell hyperpolarisation
- open Ca channels = cell depolarises
definitions of
- depolarisation
- repolarisation
- hyperpolarisation
- membrane potential becomes more + (moves closer to Na+ equilibrium +60)
- MP moves from a more +ve to a more -ve value (closer to RMP -70)
- MP overshoots, surpassing RMP (closer to K+ equilibrium -90)
what is the role of a graded potential?
graded potentials are changes in membrane potential that vary in size - related to size of the stimulus
examples of graded potentials
- generator potentials - sensory receptors
- postsynaptic potentials - synapses
- endplate potentials - NMJ
are graded potentials decremental?
Following some local stimulus, ion channels open creating a potential difference. This current leaks out along the rest of the membrane, meaning that the further away from initial site of depolarisation you go, the smaller the membrane potential.
how are graded potentials graded?
- if you have a stronger stimulus initially = more channels opened –> bigger current flow & bigger potential
can graded potentials be depolarising?
- GPs can be depolarising or hyperpolarising
- can excite or inhibit a cell for firing an AP
- more likely to fire an AP = excitatory - EPSP
- less likely to fire AP = inhibitory - IPSP
what ions are involved in IPSP/EPSP?
K+ leaves = hyperpolarise = IPSP
Cl- enters = hyperpolarise = IPSP
Na+ enters = depolarise = EPSP
Ca2+ enters = depolarise = EPSP
what generates fast IPSP?
GABA binds to ionotropic GABA receptors triggers opening of ion-pore = hyperpolarisation
what generates slow IPSP?
GABAb is a metabotropic receptor which activates K+ channels, K+ leaves cell - becomes more -ve
what generates fast EPSP?
glutamate binds to ionotropic Na+K+ - huge Na influx -> depolarisation
what generates slow EPSP?
Glutamate binds to leaky K+ channels (metabotropic R) and closes them –> depolarisation = Slow EPSP
can graded potentials summate?
yes, graded potentials can add onto each other
- important in synaptic integration for AP generation
what do spatial summation and temporal summation mean?
- spatial summation - when multiple presynaptic neurons release NT and is enough to evoke AP
- Temporal summation - when one presynaptic neurone releases NT many times enough to evoke AP
what does synaptic integration mean?
- process of summing all neuronal inputs together to determine if initial segment (axon hillock) reaches threshold for AP generation
what are the main characteristics of APs?
- threshold of -55mv
- are all or none
- can only encode stimulus intensity in frequency
- self-propagate
what does self-propagation mean?
- AP can efficiently travel to next bit and open voltage-dependent Na+ channels - elicits an AP in the next neuron
is there back flow of AP?
there is some backflow of current but doesn’t evoke an AP as the previous channels are kept in refractory state
why are APs not decremental?
- myelin sheath prevents current leaking out
what cells produce myelin?
- PNS - Schwann cells
- CNS - oligodendrocytes
what is the role of saltatory conduction?
- saltatory conduction is involved in speeding up conduction
- propagates AP in Nodes of Ranvier
- NoR are uninsulated, meaning ions can be exchanges to regenerate APs
what is the effect of demyelination?
- MS & Guillain-Barre Syndrome are diseases of demyelination
- damage of myelin sheath means AP will leak out = local current decays quicker = fails to depolarise next node to threshold = conduction fails
what is a compound action potential?
- signal recorded (extracellularly) from a large population neuronal axons
- have a mixture of small/large non-/myelinated axons
- this means that different APs will arrive at different speeds (fastest arrive first as a wave, then 2nd fastest…)
what are the characteristics of a fast conductor?
- myelination
- large diameter
examples
all A-fibres are myelinated and fairly large diameter (involved in proprioception, motoneurons, touch, fast pain)
steps to evoke an AP
- AP comes down axon (mediated by Na+ channels)
- AP opens voltage gated Ca2+ channels in presynaptic terminal
- Triggers fusion of vesicles (Ca2+ dependent exocytosis)
- Acetylcholine released and diffuses across cleft
- Binds to nicotinic ACh receptors - evokes GRADED post-synaptic potentials by opening channels
- Opens ligand-gated Na+/K+ channels - more Na+ flows in
- Evokes local graded excitatory end plate potential
- EPP depolarises adjacent membrane to threshold
- Opens voltage-gated Na+ channels - evoking new AP
- ACh removed by acetylcholinesterase
how can toxins impact APs?
- tetrodotoxin - blocks Na+ channels = blocks AP
- joro spider toxin - blocks Ca2+ = stops NT release
- botulinum toxin - disrupts release machinery = blocks NT release
- curare - blocks ACh receptors = prevents EPP
- anticholinesterases - block ACh breakdown = increase transmission at NMJ
what are the differences with CNS synapses?
- have a wider variety of neurotransmitters (ACh, nor/epinephrine, dopamine, glutamate…)
- have a range of small post-synaptic potentials (fast EPSPs - ionotropic, slow EPSPs - metabotropic), fast/slow IPSPs)
- variation of anatomical arrangement of synapse (axo-somatic/axo-dendritic/axo-axonal)
- variations on connectivity of neurones (convergence = many neurones synapse onto 1 neurone, divergence = one neurone synapses onto many neurons, feedback inhibition - presence of inhibitory interneuron)
