Nerves and muscles Flashcards
Divisions of the nervous system
Central Nervous System (CNS)
• Brain
• Spinal cord
Peripheral Nervous System (PNS): 2 Divisions
Somatic Nervous System
Autonomic Nervous System (ANS)
(1) Sympathetic
(2)Parasympathetic
(3) EntericNeurones- Characteristics
- High metabolic rate
- Brains – ‘grey matter’
- Many dendrites – signal inputs
- One axon – signal conduction
- Many synaptic terminals – signal output
Structural classes of neurones- 3 of them
Multipolar neurone (a single long axon and many dendrites emerging from cell body- motorneurones)
Unipolar neurone (pseudo-unipolar) (found in sensory ganglia)
Bipolar neurone (found in sensory structures e.g. retina)
Organisation within the spinal cord
White matter mostly contains myelinated axons, and grey matter mostly cell bodies, this accounts for the different staining.
What happens when white and grey matter is stained with Weigert’s stain (stains myelin)
White matter stains dark- has most myelin as mostly axons
Grey matter stains pale- as mostly cell bodies.
What is a group of nerve cells called in the CNS and PNS?
A group of nerve cells is called a nucleus in the CNS but a ganglion in the PNS.
What is a bundle of axons called in the CNS and PNS?
A bundle of axons in the CNS is a tract, in the PNS a nerve.
What are ganglia? What types are there in the PNS?
Ganglia are neuronal cell bodies (ganglion cells) & supporting neuroglia (satellite cells)
Two types of ganglia in the PNS:
• sensory ganglia: cell bodies of sensory (afferent) neurons
• autonomic ganglia: cell bodies of motor (efferent) neurons from the autonomic nervous system
Structure of peripheral nerves
Three layers of connective tissue around the myelin sheath of each myelinated nerve fibre.– epineurium (covers the whole nerve), perineurium (covers a fascicle) and endoneurium (covers individual nerve axons).
What are neurolgia and what do they do?
Neuroglia (Glia or Glial cells)
Traditionally considered as supporting cells for neurones
Recent work – regulate neurone metabolism & function (energy supply & transmitter levels)
Repair & recovery from injury
Regulate blood-brain barrier
Destroy pathogens and remove dead neurones
Glial cell dysfunction implicated in neurological disorders- examples
Autism, schizophrenia or neurodegeneration
Main types of neurolgia in the CNS
Astrocytes- involved in metabolic exchange between neurons and blood
Oligodendrocytes- myelinate axons
Microglia- immune defence- become phagocytic
Ependyma- lining cells or ventricles and central spinal canal, produce CSF
Neurodegenerative problems
- MS (multiple sclerosis)
- ALD (adrenoleukodystrophy)
- ALS (motor neurone disease)
Main types of neuroglia in the PNS- Schwann cells
Schwann cell: similar in function to oligodendrocytes i.e. the Schwann cells provide myelination to axons in the peripheral nervous system (PNS). They also have phagocytotic activity and clear cellular debris that allows for regrowth of PNS neurons.
Main types of neuroglia in the PNS-Satellite cells
Satellite cells - small cells that surround neurons in sensory, sympathetic, and parasympathetic ganglia. These cells help regulate the external chemical environment. They are similar to astrocytes and are highly sensitive to injury and inflammation.
Process of Myelination
Myelination of axons
- Oligodendrocytes myelinate in CNS; Schwann cells myelinate in PNS
- Wrap axon in spiral of concentric layers of fatty myelinated membrane
- Insulation for axons to aid impulse transmission
- Gaps between adjacent cells – Nodes of Ranvier
Non-myelinated axons
Non-myelinated nerves have a supporting Schwann cell
Axon is embedded in a channel called the mesaxon, where the Schwann cell is right next to the axon.
A single Schwann cell supports several axons
Demyelinating Diseases consequences
- A demyelinating disease –a condition that results in damage to the myelin sheath
- Consequences of myelin damage: nerve impulses slow/stop, causing neurological problems
- Deficiency in sensation, movement, cognition, or other functions specific to the nerves involved
- Extensive myelin loss is usually followed by axonal degeneration and often cell body degeneration
Classification of demyelinating diseases- Demyelinating myelinoclastic diseases and demyelinating leukodystrophic (dysmyelinating) diseases
Divided on basis of the cause
- Demyelinating myelinoclastic diseases – secondary: healthy myelin is destroyed by a toxic (eg, alcohol), infectious agents, chemical or autoimmune substance
- Demyelinating leukodystrophic (dysmyelinating) diseases – primary: myelin is abnormal and degenerates; caused by genetics, some idiopathic.
What is MS
• Common demyelinating disease of the CNS
• Aetiology – autoimmune in nature
• Environmental/genetic factors lead to loss of tolerance to self-proteins
• Inflammation and injury to the myelin sheath and nerve fibres
-multiple areas of scarring (sclerosis i.e. lesions/plaques).
• Physical, mental, psychiatric problems
What is the somatic NS?
- often called voluntary nervous system
- has somatic motor neurones- efferent motor neurones/ motoneurones
- innervates and controls voluntary, striated muscles
- has sensory neurones- sensory afferent neurones
What is the autonomic NS?
• Involuntary nervous system. • Controls: – heart rate – blood pressure – respiration – sweat glands – gut movements
• Sympathetic-speeds things up • Parasympathetic-calms things down – anatomical and functional divisions – antagonistic actions – both have efferent (motor) and afferent (sensory) components
Classification of Nerve Fibres
Systems based on fibre diameter and conduction velocity (how fast the impulses travel down the axon)
Classification of sensory receptors
- By location within the body.
• Exteroceptors – external surface
• Interoceptors – internal organs
• Proprioceptors – internal, but concerned with position of muscles, tendons, joints. - By stimulus type detected.
• Mechanoreceptors – touch, pressure, vibration, stretch
• Thermoreceptors – hot, cold, temperature change
• Photoreceptors - light
• Chemoreceptors – chemicals
• Nociceptors – pain (usually chemicals)
Spinal cord reflex pathway
- Sensory receptor - site of stimulus action
- Sensory neurone - transmits afferent information to the CNS
- Integration centre - one or more synapses within CNS (may also signal up to brain)
- Motor neurone - conducts efferent impulses to the effector organ
- Effector - muscle fibre (or gland) that responds to impulses
4 factors that contribute to the resting membrane potential
- charged intracellular proteins- large negative charged proteins trapped in cell- negative cell compared outisde
- the Na+/K+ pump- 3 Na ions out cell, 2 K ions in cell. Cell becomes more negative
- potassium ions- 2 K in cell but large negative gradient cell drags back K
- sodium ions- inward flow Na- cell becomes more positive
Factors that contribute to the resting membrane potential- Effect of intracellular proteins
Large negatively charged intracellular proteins cannot cross the cell membrane to leave the cell interior and so contribute to its negativity.
Large protein molecules within the cytoplasm of the cell are too big to pass through channels in the membrane and have a predominance of negatively charged groups on their surface. This lack of membrane permeability means they are trapped within the cell and cause it to be negatively charged with respect to the extracellular fluid.
Factors that contribute to the resting membrane potential- Effect of the sodium/potassium ion pump
The Na+/K+ pump moves 3 Na+ ions out for every 2 K+ ions in. Thus inside of the cell gets more negative.
Factors that contribute to the resting membrane potential- Effect of potassium ion gradients
K+ tends to leak out of the cell down [gradient], but cell’s negative charges inside tend to pull K+ back in. Eventually, in theory, fluxes become balanced so K+ distribution will be in equilibrium.
Although the concentration gradient for K+ ions means that they tend to diffuse out of the cell through the K+ selective channels, the large negatively charged protein molecules trapped within the cell cause an electrical gradient, which tends to pull the K+ ions back in.
Factors that contribute to the resting membrane potential- Effect of sodium ion gradients
The membrane is only slightly permeable to Na+, so its effects on resting potential are small. The net inward diffusion of Na+ slightly adds to the positivity of the cell.
Note that in the case of sodium ions both the concentration and electrical gradients operate in the same direction to cause inward flow of ions.
The net effect of this is to bring the resting potential back up to about -65 mV.
Phases of the action potential
Phase 1:
• Na+ channels open
• Na+ enters nerve cell
• Membrane potential rises towards zero
Phase 2: Depolarisation • If threshold potential reached, voltage gated Na+ channels open • Na+ ions flow into cell • Action potential spike results
Phase 3:
Repolarisation
• Na+ channels close when Na+ equilibrium potential is reached
• Voltage gated K+ channels open and K+ ions flow out of cell
• Membrane potential reverses
Phase 4:
Hyperpolarisation
• K+ ions continue to flow out of cell while Na+ channels closed
• Hyperpolarisation results
Steps of an AP
- Resting state: all voltage gated Na+ and K+ channels closed
- Depolarising phase: Na+ channel fast activation gates open
- Overshoot phase: inactivation gates of Na+ channels start to close and activation gates of K+ channels begin to open
- Repolarising phase: inactivation gates of Na+ channels closed and K+ channels open
- Undershoot phase (after potential): K+ channels still remain open, Na+ channels closed
- Resting state: all voltage gated Na+ and K+ channels closed
“All-or-nothing” action potential- how it works
- All excitable cells have a threshold membrane potential
- Membrane has to be depolarised beyond threshold for an AP to be generated
- Further increase above threshold -> higher AP frequency not larger AP amplitude
- A neurone either fires or it does not, regardless of signal size – “all-or-nothing”
Action Potential Refractory Periods- are there AP?
During the absolute refractory period no further action potentials can be elicited. This ensures action potential propagation is unidirectional. During the relative refractory period a larger stimulus can result in action potential.
This refractory period means that an action potential can only travel along the axon from cell body to axon terminal, not in the opposite direction. AP can’t summate. It cannot reverberate (i.e. go backwards towards its point of origin – normally the point where the axon joins the nerve cell body).
Non-myelinated axon- how AP moves along
Non-myelinated axon:
Na+ influx depolarises area in front of it and triggers voltage gated Na + channels to open.
Causes AP in next membrane.
Membrane behind impulse in refractory.
Impluse can only go forward along axon.
Myelinated axon
Nodes of Ranvier are the only areas where current can pass through membrane.
Nodes are only areas where membrane can depolarise.
Impulse travels in ‘jump’ not slow flow.
Sensory receptors
Sensory neurone endings, often modified to form specialised sensory receptors, which are ‘tuned’ to specific signals or sensory modalities, i.e., different forms of energy (light, vibration, chemicals, etc.). Sensory transduction is the conversion of environmental or internal signals into electrochemical energy.
Detection of stimulus by receptor causes a receptor potential
• Graded electrotonic response (not action potential)
• Causes action potential
• Specific signals – rate and pattern of action potential firing – decoded in CNS
Sensory receptors in muscles
Where is the muscle spindle located?
Where is the Golgi Tendon Organ located?
- Both are proprioceptors and mechanoreceptors
- The muscle spindle is located within the muscle and stimulated when the muscle is passively stretched.
- The Golgi Tendon Organ is located in the tendon and responds to tension (it is stimulated when associated muscle contracts or is stretched).
Muscle spindle- what is it needed for?
- When a muscle is stretched passively the spindle is activated and so initiates a reflex
- When the muscle contracts and shortens it is switched off
- Protects muscle being overstretched
Golgi Tendon Organ- what is it for?
- GTO is active during both passive stretch and active contraction
- It is a tension detector that protects muscle against excess load
- Function to protect the muscle and connective tissue from injury
- Stimulated by excessive tension during muscle contraction or passive stretch
- Causes a reflex inhibition of the muscle-relaxation
- Helps prevent excessive muscle contraction or passive muscle stretch i.e. Inverse stretch reflex
Two types of synapses- what are they?
Neurones communicate via synapses (synaptic junctions) of which there are 2 types:
• Electrical synapses – direct passage of current via ions flowing through gap junctions
• Chemical synapses – release of vesicles containing chemical transmitter which has an effect on receptors on a target cell
Electrical synapse- how are they formed?
Formed by interlocking connexon channels of adjacent neurones. Connexons comprise connexin proteins.
How do chemical synapses for?
- Interface for chemical communication between neurones
- Release of transmitter from synaptic vesicles on arrival of an action potential in the terminal ‘bouton’ of neuronal axon
Neurotransmitter
Neurotransmitter- a substance that is released at a synapse by one neurone that affects another cell, either neuron or effector organ, in a specific manner
Neuromodulator
Neuromodulator – a substance that is released and modifies the action of a transmitter, but doesn’t have a direct action itself
Neuroactive substance
Neuroactive substance – a neutral term if a substance is known to have an effect in the CNS but its precise action is not known
