Neurons and related cells Flashcards
Describe the basic structure of a neuron
- Dendrites are projections which collect information from adjoining cells
- Dendrites send this information to the cell body (soma) which contains the nucleus (site of protein production)
- The axon hillock is a small lump just beyond the cell body which is where action potentials are generated
- Action potentials travel down the axon (which is often covered by a myelin sheath)
- The axon leads into terminal branches, which form synapses with other cells (other neurons or effector cells)
- Terminal branches end in terminal boutons
What is the main difference between neurons in the somatic and autonomic nervous systems?
somatic = the cell body is in the CNS. they have long, heavily myelinated axons which release ACh at skeletal muscles
autonomic = depends on the subdivision
- sympathetic neurons = 2nd order neuron has a cell body in the CNS, releases ACh to a non-myelinated post-ganglionic neuron (with a cell body in the dorsal root ganglion) which releases norepinephrine at a smooth muscle/gland/cardiac muscle.
- parasympathetic neurons = same as above but the post-ganglionic neuron releases ACh.
Define axonal transport
the transport of proteins (including neurotransmitters) from where they are made in the nucleus of a neuron to the terminal branches where they are needed. This happens as kinesin molecules walk transport vesicles down the axon via the cytoskeleton. this process requires ATP.
What is the resting membrane potential of a neuron?
The potential difference in charge across the membrane. It sits at about -70mv in most neurons. It is maintained by a series of ion channels and pumps which maintain consistent levels of Na+ and K+ ions inside and outside the cell.
How is resting membrane potential maintained?
- K+ leakage channels allow potassium ions to leave the cell down their electrochemical gradient
- Na+ leakage channels allow sodium ions to enter the cell down their electrochemical gradient.
- Ion pumps maintain the balance by moving K+ back INTO the cell and Na+ back OUT OF the cell. These require ATP as they move ions against their electrochemical gradient.
As more K+ leaves the cell than Na+ enters, a negative resting potential of -70mv is maintained
What are graded potentials?
A graded potential is a localised change in membrane potential (caused by signals received at a synapse). They are ‘graded’ as the strength of the potential difference across the membrane depends on the strength of the incoming stimulus. They can be depolarisations or hyperpolarisations.
Define depolarisation
Where the membrane potential gets less negative/closer to 0
Define hyperpolarisation
Where the membrane potential gets more negative/further from 0
Describe the process of summation (in creating an action potential)
Excitatory stimuli depolarise a neuron (bring it closer to an action potential threshold) whereas inhibitory stimuli hyperpolarise a neuron (take it further away from an action potential threshold). Neurons receive constant inputs from different neurons/cells which they integrate to determine whether an action potential is reached.
- Temporal summation = a rapidly firing pre-synaptic neuron sends many excitatory signals in close succession so threshold is reached
- spatial summation = multiple excitatory signals are received from different presynaptic neurons so threshold is reached.
Inhibitory and excitatory impulses can cancel each other out.
What is the threshold for an action potential?
Usually around -55mv
Define an action potential
A brief change in membrane potential in an area of membrane that is depolarised by local currents. They are a negative wave of electrical excitation that travels down the axon at speeds ranging from 1-2m/s to 150m/s. They are ALL OR NOTHING events that either happen if the depolarisation threshold is met or don’t happen if it is not.
Describe the process of an action potential (electrochemically)
Resting state/resting potential = all voltage-gated Na+ and K+ channels are closed (resting potential = -70mv)
Depolarisation = Na+ channels open, allowing entry of Na+ ions into the cell down their electrochemical gradient, making the inside of the cell more positive (reaches a maximum magnitude of around +30mv)
Repolarisation = Na+ channels are inactivated/blocked so that no more Na+ ions can enter the cell. K+ channels open, allowing K+ ions to leave the cell, making the membrane potential more negative (it overshoots slightly resulting in hyperpolarisation)
Hyperpolarisation = Na+ channels reset, some K+ channels remain open and there is a gradual return to resting state
Describe the propagation of an action potential along an axon
- Action potentials are generated by an influx of Na+ ions into a localised area of the membrane
- This creates a wave of depolarisation in adjacent areas of the axon, causing an influx of Na+ ions in these areas, which in turn triggers an action potential to occur there.
the signal is not ‘conducted’ but rather propagated through a cascade of adjacently occuring action potentials.
What are some factors that affect velocity of an action potential?
- axon diameter (the larger the diameter the faster the action potential travels)
- degree of myelination (more myelin = faster action potential) this is due to saltatory conduction (action potentials only generated in between myelin sheaths - in the nodes of Ranvier, and so the action potential can skip large parts of the axon)
What are the stages of synaptic transmission?
- action potential arrives at the presynaptic terminal bouton
- depolarisation from arriving action potential causes voltage-gated Ca2+ channels in the axon terminal to open, Calcium ions flood into the neuron.
- calcium ions interact with SNARE protein complexes which cause the synaptic vesicles containing neurotransmitters to be released into the synaptic cleft via exocytosis
- neurotransmitters diffuse across the synaptic cleft and fuse with specific receptors on the post-synaptic membrane
- binding of the neurotransmitter causes the receptors to change shape and open ion channels, creating graded potentials in the post-synaptic membrane
- neurotransmitter effects are terminated through reuptake (either into the pre-synaptic neuron or by glial cells such as astrocytes or satellite cells), degradation by enzymes or diffusion away from the synapse.
What are glial cells?
glial cells, or neuroglia, are cells which support and maintain neurons.
Which glial cells are found in the PNS?
satellite cells = surround neuron cell bodies in the PNS, maintain blood supply to neurons, maintain chemical environment and guide the formation of new synapses
schwann cells = wrap around nerves to form the myelin sheath which increases transmission speeds of action potentials. also vital for regeneration of damaged nerve cells in the PNS.
Which glial cells are found in the CNS
Astrocytes = most abundant, branching cell. They wrap around capillaries, maintaining blood supply to neurons. They maintain the chemical environment by controlling reuptake of Na+ and K+ ions. They also guide formation of new synapses and nerve growth. (They may also be involved in some higher brain functions as there is evidence that they can communicate with each other and respond to local nerve impulses)
Microglial cells = migrate towards injured/damaged neurons. transform into macrophage like cells which phagocytose micro-organisms or debris. the immune system of the CNS.
Ependymal cells = these are ciliated cells which line the fluid filled spaces in the brain. they help to regulate cerebro-spinal fluid production and the rhythmic beating of their cilia helps to move it through the ventricles of the brain.
Oligodendrocytes = produce the myelin sheaths that covers longer nerves within the CNS.
Describe the structure of a nerve
A nerve is a bundle of axons found in the PNS. Axons are surrounded by a myelin sheath, and each is also covered by a thin membrane called the endoneurium. bundles of axons are grouped together by the perineurium to form a fascicle. Groups of fascicles are grouped by another membrane called the epineurium. nerves are heavily vascularised (vasi nervorum) and have their own nerve supply (nervi nervorum)
What are the effects of ageing on nerve health?
In the CNS, the normal process of ageing leads to neuronal atrophy, loss of myelination, noisy processing and dopamine loss. In the PNS, nerve ageing leads to declined axonal transport, axonal atrophy, myelin loss and impaired regeneration.
What are the common types of nerve injury?
Neuropraxia = neurons remain in tact but there is some blunt force damage which may damage the myelin sheath etc which leads to temporary slower conduction speeds.
Axonotmesis = severance of axons caused by heavier trauma. distal to the point of damage, the axon may die but is likely able to regrow. could result in some loss of movement and sensation distal to point of damage.
Neurotmesis = severe severance of the nerve. it is very rare for full regrowth to occur in this instance leading to loss of sensation and motor function. painful neuroma may develop at the point of damage (bundles of axons which try to regrow but cannot reach their intended target)
Ischemic damage (lack of oxygen supply to nervous tissue) = cellular respiration stops, cells depolarise causing a massive calcium influx leading to excitotoxicity (phenomenon where exposure to excitatory neurotransmitters (primarily glutamate) in high doses for prolonged periods starts a cascade of neurotoxicity which eventually leads to cell death)
Describe Seddons classification scheme of nerve damage
A way of classifying the severity of localised nerve damage.
There are three grades/stages:
Neurapraxia = mildest injury to a nerve, caused by transient compression or stretch. Loss of nerve
function results from conduction block. Paralysis of muscles innervated by the nerve is complete but
some sensation may be preserved. Autonomic function may also be preserved. This type of injury will
recover completely providing the cause, for example, ongoing compression, is removed.
axonotmesis = more severe blunt injury to a nerve. This is sufficient to cause axon
degeneration but the connective tissue layers of the nerve including the endoneurial tubes remain intact.
Clinical examination reveals complete loss of motor, sensory, and autonomic function. Since axons distal to the site of injury have undergone Wallerian degeneration conduction is lost both at and distal to the site of injury. Providing the cause is removed, uncomplicated regeneration of axons occurs along the same pathway will occur, with recovery of function progressing from proximal to distal.
neurotmesis = nerve is completely divided or so badly disorganized that recovery
cannot occur. All the connective tissue layers of the nerve as well as the axons are disrupted. There is
axon degeneration distal to the injury. Neurotmesis may be caused by laceration or high energy traction
injuries sufficient to rupture the nerve. complete functional recovery never occurs with this type of injury.
define neuropraxia
Neurapraxia is the mildest injury to a nerve, caused by transient compression or stretch. Loss of nerve
function results from conduction block. Paralysis of muscles innervated by the nerve is complete but
some sensation may be preserved. Autonomic function may also be preserved. This type of injury will
recover completely providing the cause, for example, ongoing compression, is removed.
define axonotmesis
severe blunt injury to a nerve. This is sufficient to cause axon degeneration but the connective tissue layers of the nerve including the endoneurial tubes remain intact.
Clinical examination reveals complete loss of motor, sensory, and autonomic function. Since axons distal to the site of injury have undergone Wallerian degeneration conduction is lost both at and distal to the site of injury. Providing the cause is removed, uncomplicated regeneration of axons occurs along the same pathway will occur, with recovery of function progressing from proximal to distal.
