Reflexes Flashcards
Physiology
The Reflex Arc (explain)
Skeletal muscles are one of the few systems over which we can exert conscious control and certainly there are no other aspects of body function over which we have such well-developed influence.
It would be wrong to suppose, however, that all skeletal muscle activity is the product of conscious motor control.
Many reflex responses occur as involuntary responses to specific sensory stimuli and take the form of some fixed pattern of motor response, so that stimulus A always tends to produce response B.
These responses, however, may then be modified through conscious controls.
Unconscious, or reflex muscle control is very important and provides the appropriate patterns of background activity allowing for efficient and effective voluntary actions.
Each reflex requires some sort of sensory detector, a sensory nerve pathway (the afferent limb), a motor nerve pathway (the efferent limb) and skeletal muscle fibres which respond to the motor nerve activity.
This set of connected elements is referred to as the reflex arc.
The Stretch Reflex (explain)
This is the simplest reflex in the body since it involves only one nerve-nerve connection (one synapse, a monosynaptic reflex arc).
It is the classical example of a spinal cord reflex, ie, one in which is co-ordinated within
the spinal cord.
The stretch reflex is activated by increases in muscle length (not tension) and leads to contraction in the stretched muscle.
This type of reflex is important in controlling the resting tone in muscles, especially the
extensor muscles of the lower limb which resist gravity.
Any tendency for the knee to buckle, for example, will be
resisted by the stretch this puts on the quadriceps muscles of the upper thigh, which reflexly contract, keeping the leg in its normal standing position.
It is also the reflex which is tested by clinicians when they elicit a knee jerk for example.
The receptor for the stretch reflex is called a muscle spindle and it is a specialised muscle cell which runs parallel with the normal fibres.
Muscle spindles are stretch receptors and increasing the muscle’s length activates
them leading to action potentials being generated in the associated sensory nerve.
These action potentials are conducted to the spinal cord where there is a synapse with the α -motoneurone to the
stretched muscle.
An excitatory neurotransmitter is released producing an action potential in the motor axon which conducts it back to the neuromuscular junction.
Muscle contraction results.
The stretch reflex also influences muscles other than those which were initially stretched.
The sensory nerve has branches in the spinal cord which synapse with another set of neurones known as interneurons (or Renshaw cells).
These are connecting cells and they synapse with α-motorneurones which supply muscles antagonistic in action to the stretched muscle.
The interneurones are inhibitory, so that contraction in these antagonists is inhibited.
This again reduces the degree of stretch in the muscle from which the reflex originates.
Golgi Tendon Organ Reflex (explain)
The Golgi tendon organs are another set of stretch receptors attached in series with the muscle fibres of the
muscle and located, as their name suggests, within the tendon.
Increasing muscle tension tends to activate these
receptors and the sensory afferent is connected by an inhibitory interneurone within the spinal cord to the a-
motoneurones supplying the same muscle.
The reflex seems to be protective, reducing muscle tension before permanent damage to muscle or tendon results.
Withdrawal and Crossed Extensor Reflexes
This is one of the patterns of reflex activity with which we are most familiar since it is induced by painful stimuli such as a pinprick or a hot saucepan, sensations which are rapidly experienced at the conscious level (unlike muscle spindle or Golgi tendon organ output which is communicated to the brain but is not consciously perceived.
It is sometimes referred to as the pain reflex because of this.
It is a more complex reflex than those described above, involving muscle groups on both sides of the body, not just on the side of injury.
Any stimulus which stimulates pain receptors causes a reflex withdrawal of that part of the body from the damaging agent.
If I touch a hot dish I will pull my hand away reflexly due to the excitation of flexor muscles in that arm by polysynaptic connections between the sensory nerves from the pain receptors and the relevant α-
motoneurones.
Other branches of the sensory nerve make connections via inhibitory interneurones to the α -motoneurones supplying the extensor muscles in the arm.
These tend to relax leaving flexion unopposed.
This aspect of the response is the flexor or withdrawal reflex.
Further connections are made to the muscles in the opposite arm and give rise to the crossed extensor reflex.
This is a mirror image of the flexor reflex, with extensors being activated and flexors inhibited.
This reflex follows within 0.5 sec. of the flexor reflex and it causes a rapid straightening of the opposite arm which tends to push the whole body away from the source of trouble.
Similar reflexes are elicited by painful stimuli to the legs and
indeed to any part of the body.
The pain reflex is also a good example of how conscious control can modify reflex actions.
If you pick up a hot dish your reflex response is to drop it, flex your arm and push back.
If the dish contains your dinner, and you have no other prospect of a meal, you can consciously inhibit the reflex, allowing you to transport the dish safely (if somewhat quickly and noisily) to the table.
Transmission at the Neuromuscular Junction (explain)
Although each nerve supplies several, sometimes many, muscle cells, each muscle fibre is innervated by one and only one axon and electrical activity in one muscle fibre does not directly influence the adjacent cells.
Thus, skeletal muscle activity is completely dependent on the activity in the relevant motoneurones.
The mechanisms whereby an action potential in the nerve leads to an action potential in the muscle fibre are corporately referred to as
neuromuscular transmission.
This does not rely on direct electrical transmission since there is an appreciable space
between the end of the nerve and the underlying muscle, the neuromuscular cleft.
This gap is bridged by a chemical transmitter which alters the properties of the underlying muscle membrane (the motor end plate).
This triggers an action potential which is conducted along the muscle membrane and acts as the signal for muscle contraction.
When an action potential reaches the end of the nerve it depolarises the nerve ending or terminal.
This makes the plasma membrane in this small area more permeable to Ca2+ ions which diffuse into the nerve terminal.
This causes the secretory vesicles in the terminal to fuse with the plasma membrane, releasing the neurotransmitter
which they contain (acetyl choline) into the neuromuscular cleft.
The acetyl choline quickly diffuses across the cleft and then binds to specialised receptors (cholinergic receptors) which are attached to a region of muscle plasma
membrane subjacent to the nerve terminal known as the motor end plate.
There are several types of receptor for acetyl choline in different parts of the body but the receptors on skeletal muscle fibres are referred to as nicotinic receptors because they also respond to nicotine.
Once the receptors have been activated they depolarise the membrane, producing a local change in potential which is referred to as the end plate potential.
This tends to depolarise adjacent, normal muscle
membrane and when threshold is reached an action potential is initiated.
This is then conducted over the plasma membrane.
The transmission process is brought to an end by the release of acetyl choline from its receptors and its degradation into acetate and choline.
This reaction depends on the presence of the enzyme acetyl cholinesterase which is attached to the motor end plate membrane.
Once acetyl choline breakdown has occurred, allowing the
motor end plate to repolarise and the muscle to return to its resting state, the process of neuromuscular transmission
is complete.
Medical Interest - Organophosphates (explain)
A group of chemicals that inhibit the actions of cholinesterases, including
acetyl cholinesterase.
This causes ACh to accumulate in the neuromuscluar junction, thus causing uncontrolled contraction and hence muscle fatigue, so that vital functions such as respiration cannot take place.
This group of chemicals has also been exploited in chemical
weapons, several of which act in exactly the same way in humans.
Medical Interest - Botox (explain)
Comes from the bacteria Clostridium Botulinum, which was first found growing in badly-kept sausages (botulus = sausage in Latin) associated with the disease of botulism, which is a progressive paralysis that can result in death.
Its mode of action is to inhibit
the intracellular proteins that enable transmitter-containing vesicles to fuse with the synaptic membrane in neurones.
The extracted toxin has been used for cosmetic purposes, because in small doses injected into facial muscles can relax the muscle and reduce wrinkling in the overlying skin.
It is now being used for a number of medical reasons (eg hyperactive bladder, migraine, muscle spasm, squint), although the mode of action is not always known.
Medical Interest - Neuromuscular Blockers
A group of compounds (indole alkaloids) related to the chemical curare.
These compounds were originally extracted from plants, or from the secretion of frogs that eat the plants and used by indigenous jungle tribes in Central and South America in their hunting with poisoned blow darts or arrows.
They act by binding to the ACh receptors and blocking the actions of Ach, causing muscular weakness and paralysis.
Anaesthetists use these
compounds in surgery to produce muscular relaxation, to enable easier intubation (placing a tube down the throat, across the trachea for artificial respiration), and to reduce the amount of other
anaesthetic drugs needed to maintain unconsciousness (safer).
Medical - Myasthenia Gravis (explain)
The body has, for whatever reason, begun to produce
antibodies that specifically attack Ach receptor proteins in the neuromuscular junction.
This results in a progressive paralysis that can lead to death.
This may first be apparent as a
weakness in the eyelids, causing a notable droopiness when the patient looks up.
It is treatable with drugs that inhibit the actions of anticholinesterase, allowing greater concentrations of Ach in the junction and ensuring a greater proportion of the reduce number of receptors are occupied.
Immunosuppression by drugs or removal of the thymus gland
may also be employed.
