Neurophysiology Flashcards
Are solutes equally distributed between interior and exterior of cells?
No - there is unequal distribution
This creates concentration gradient as cell membrane is almost impermeable
What ions dominate ECF?
Na+ & Cl-
What ions dominate ICF)
K+ & A- (anions)
Define membrane potential
Separation of ions across a membrane (basis for excitable cell function)
Size of potential depends on amount of separation of opposite charges
Opposite charges are attracted to each other
Define resting membrane potential
Neurons at resting membrane potential have constant number of charges separated
Usually ~-70mV
Approximation of resting membrane potential
-70mV
Define polarization
Having a membrane potential - separation of ions across a membrane
Define depolarisation
Decrease in potential
Membrane less negative
Define repolarisation
Return to resting potential after depolarisation
Define hyperpolarisation
Increase in potential
Membrane more negative
Graded potential
Small stimulus –> small number of Na+ channels open –> small influx of Na+
What occurs when Na+ enters cell?
depolarisation
Action potential
A large stimulus causes membrane to reach threshold
Lots of Na+ channels open
Initially overcorrection: hyperpolarisation
Action potential complete after hyperpolarisation begins
After action potential
Na+ - K- pumps restores ions to original concentrations
Pump doesn’t activate after every single AP
- Huge amounts of each ion in each compartment and only relative few involved in AP
All or nothing rule
If the membrane of an excitable tissue is stimulated, it will either respond with a maximal action potential that spreads along the membrane in an undiminished fashion or does not respond at all
All action potentials last for the same amount of time
What determines the strength of AP?
The frequency and area (number of nerves) of APs indicates the strength of signal
What is the ‘trigger zone’ of AP?
Axon hillock (AP is initiated here)
Can AP only move one way?
Yes
Absolute refractory period
Membrane area is already undergoing AP
Na+ channels are open & cannot be triggered to re-open until membrane has returned to res23qting potential (inactivation gates)
Relative refractory period
New AP can be triggered, by stronger than normal stimulus
When original site has recovered, AP moved too far away to trigger another
How is AP conducted?
AP conducted down axon to terminals
AP depolarises adjacent region to threshold, sets off new AP
AP appears to move down the axon (actually triggers identical events down the axon)
Spreads in an undiminished fashion
Signal replicated over long distances
Continguos conduction
Occurs on unmyelinated fibres
AP spreads down axon, along every patch of membrane –> requires a lot of energy to return membrane to resting potential
Saltatory conduction
Occurs in myelinated fibres
Occurs in long distance signals
Myelin = lipid - stops ions passing through (insulator)
Not continuous - ‘Nodes of Ranvier’
AP travels down axon by jumping from node to node
Quicker and requires less energy than continuous conduction
- Small sections of axon stimulated, instead of entire axon
- ~50x faster
- Larger fibre diamter –> faster signal
What could happen if myelin sheath degrades?
MS Signals jump between different pathways Only affects motor neurons Less controlled movements e.g. move arm instead of foot
Classic NTRs
Small rapid acting
E.g. Acetylcholine, Noradrenalin, dopamine, serotonin, glutamate
Neuropeptides (type of NTR)
Larger, slower acting
E.g. insulin, bradykinin, oxytocin
Hormones are a type of neurotransmitter (slow acting)
Synaptic cleft
Gap between neurons
Synaptic knob
Axon terminals end with a slight swelling
Subsynaptic membrane
Membrane of postsynaptic neuron under synaptic knob
Conduction of impulse neuron to neuron junctions
Action potential reaches axon terminal of presynaptic neuron
Stimulates opening of voltage Ca+ channels
Calcium enters synaptic knob
Triggers the movement of NTR to the synaptic cleft via exocytosis of vesicles
NTR binds to specific receptors that are part of the chemically gated channels on synaptic membrane of post synaptic neuron
Specific channel opens
Two main types of chemical synapses (postsynaptic potentials)
1. Excitatory Small depolarisations (influx of positive ions - closer to threshold)
2. Inhibitory Small hyperpolarisations (influx of negative ions - harder to reach AP)
Excitatory synapses
Binding of NTR causes a net increase of positive ions within the cell - triggers a small depolarisation of membrane
Like a graded potential
- One usually not enough to trigger AP
Inhibitory synapses
Binding of NTR opens K+ or Cl- channels
K+ goes out or Cl- comes in
And this causes hyperpolarisation of the cell membrane
Grand postsynaptic potential
Total summation of Excitatory and inhibitory synapses
Temporal summation
Rapid, successive signals from 1 neuron
Spatial summation
Single signals from 100s of neurons
How are NTRs cleaned up from synaptic cleft
Enzymatic destruction or re-uptakes
Diffusion only occasionally
Where is neuromuscular junction located
In the middle of one muscle cell
Terminal button
Axons terminals end in slight swelling
Neuromuscular junction terminology
Motor end plate
Membrane of postsynaptic muscle cell under terminal button
Neuromuscular junction terminology
What NTR is used in neuromuscular junction?
Always acetylcholine
2 Ach molecules bind with nicotinic receptor on motor end plate
Muscle cell depolarisation is called…
End plate potential
Larger than excitatory postsynaptic potential
- is a graded potential
- causes AP in adjacent membrane
In neuromuscular junction Acetylcholine is cleaned up by
Acetylcholinesterase
Reflexes maintain
Posture and balance
Lower motor neurons
Integrate information & innervate muscles
Synapse at NMJ & only release Acetylcholine
- excitatory postsynaptic potential leads to muscle contraction
Reflexes are
automated regulatory mechanisms (ANS)
Simple somatic reflexes occur at
Spinal cord
- usually have protective functions
Somatic spinal reflexes
Automatic control to maintain posture, control movement
Types of spinal reflexes
Stretch reflex
Tendon reflex
Withdrawal reflex
Stretch reflex
Controls the length of skeletal muscles
- smooths movement
- maintains posture
Muscle stretch detected by afferent fibres
Send signal that muscle is stretching
Synapse directly to motor neuron in SC (no interneurons)
Motor neuron triggers muscle contraction to prevent overstretch
Local negative feedback
Tendon reflexes
Inform spinal cord or continual tension
Golgi tendon organs detect stretch - have branched nerve endings interwoven between collagen fibres of the tendon
Muscle fibres contract & pull tendons, changing shape of the entwined Golgi organ
Change in shape increases firing of the sensory fiber
Fibers connected to inhibitory interneurons in spinal cord, which synapse on motor neurons that innervate that muscle
When tendon is greatly stretched it triggers muscle to relax and reduces load
Withdrawal reflex
Automatically withdraws if touch something painful
Sensory nerve endings in skin
These synapse with interneurons in spinal cord
Stimulate motor neurons innervating the limb
Contracts withdrawal muscles - inhibits antagonistic muscles
Pattern generator in spinal cord
Controls motor neuron activity
Coordinates left & right, flexor & extensor, fore & hind limb
Also involve thalamic & midbrain input - increase stimulation of these - increase speed of movement
What regulates change in gait
Midbrain
Postural reflexes:
Vestibulo-ocular reflex
Vestibular placing reflex
The righting reflex
Vestibulo-ocular reflex
Stabilises image on the retina during rapid head rotation
Exterior eye muscles move eyeball with & in opposite direction to a movement of the head
Maintains visual field
Vestibular placing reflex
Shifts centre of gravity to keep the animal stable
Information is received from balance organs (vestibular apparatus) in ears
Coordinates flexion and extension of legs
The righting reflex
Restores posture when falling
Sensors: balance organs, neck muscle spindles & skin pressure
Head position is adjusted first
Then body position is adjusted (relative to head)
Ear organs detect acceleration of fall & trigger leg extension, ready for landing
Upper motor neurons
motor neurons from the cortex or brain stem
Project down spinal cord in tracts called pyramids
Where do upper & lower neurons synapse?
Ventral horn of spinal cord
Pyramidal tracts
Connect cortex to spinal cord via pyramids in medulla oblongata
No synapse
Activates muscles involved in fine motor skills & initiation of voluntary muscle movement
Most fibres cross over to other side of body in medulla
Extrapyramidal tracts
Connect cortex to spinal cord
NOT through medulla
Synapse at brain stem nuclei
Activates larger muscle groups - stabilises posture, balance & smooth movements
Voluntary movement pathway
Primary motor cortex commands muscles to start movements
Cerebellum then gets the plan and minimises difference between intended and actual movements - important in planning and timing of movements (smoothes & coordinates movement)
Basal ganglia and brain stem act together to plan complex movements - creates link between motivation and body movement
(Basal ganglia prepare for movement, inhibit unwanted movement - cerebellum coordinates movement as they are performed)
Sympathetic NS preganglionic fibres
Myelinated & short
Sympathetic NS ganglia located in
Sympathetic trunk
Sympathetic NS postganglionic fibres
Unmyelinated & long
Adrenal medulla
Large combined sympathetic ganglion & gland
Parasympathetic fibres located
Cranial & sacral regions
Sympathetic fibres located
Thoracic & lumbar SC
Parasympathetic preganglionic fibres
Myelinated & long
Parasympathetic postganglionic fibres
Short and unmyelinated
Parasympathetic Ganglia located
Close to target organs
In ANS do all preganglionic and parasympathetic postganglionic neurons release Ach
Yes
What NTR do sympathetic postganglionic neurons release?
Noradrenalin
Adrenal medulla relases
Noradrenalin & adrenalin
Both promote symp NS
Cholinergic receptors
stimulated by acetylcholine
Two types of cholinergic receptors
Nicotinic & muscarinic
Nicotinic receptors
Found on all ANS postganglionic cell bodies
Bind Ach from all preganglionic fibres
Only have excitatory effects E.g. muscle contraction
Muscarnic receptors
Found on all AND effector cell membranes
Bind with Ach from parasympathetic postganglionic fibres
Excitatory or inhibitory
E.g. contract or relax muscle
Adrenergic receptors
Stimulated by noradrenalin
Types of adrenergic receptors
Alpha and Beta receptors
both have subtypes 1 & 2
Alpha receptors
Alpha 1 - found in most sympathetic tissues that are excited by the sympathetic NS - excitatory response
E.g. Systemic vessels constrict - blood diverted away from GIT spincters that need to stop movement of digesta
Alpha 2- Primarily found in the gut - where action is to inhibit digestive secretions
Beta receptors
Beta 1 - found primarily in the heart (also kidney) - excitatory response - e.g. heart beats faster
Beta 2- Found in most tissues that are inhibited (relaxed) by sympathetic NS
E.g. Relax GIT muscles to slow movement of digesta or blood vessels in skeletal muscles that need extra blood
Also stimulates insulin release, lipolysis, glycogenolysis - convert stored energy to usable energy
Antagonistic control
Stimulation vs inhibition
Hypothalamic reflexes
Homeostasis
Highest level of integration
e.g. thirst & water balance
