Communication and receptors Flashcards

1
Q

What are the two sections of the nervous system ?

A

Central nervous system and peripheral nervous system.

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2
Q

What are the sections of the peripheral nervous system?

A

Somatic
Autonomic
Enteric

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3
Q

Parts of the brain

A

Meninges (membrane surrounding the brain) The brain is wrapped in a natural membrane called meninges.
This membrane is important in protecting the brain because your brain is not attached by ligaments to the skull instead it floats in cerebrospinal fluid.
Gyrus vs sulcus (high and low parts respectively)
Cerebellum (back of the head)
Cerebrum (consisting of the frontal lobe, temporal lobe, parietal lobe and occipital lobe)
Diencephalon (main region for receiving sensory information, contain the thalamus and hypothalamus)
Brainstem (containing the midbrain, pons and medulla oblongata)

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4
Q

What are the different spinal nerves?

A

The spinal cord has spinal nerves coming out of it. There are 31 pairs of spinal nerves. This is made up of 8 cervical (neck, shoulders & arms), 12 thoracic (chest & abdomen), 5 lumbar (hips & legs), 5 sacral (genitalia & gastrointestinal tract) and 1 coccygeal.

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5
Q

What is the difference between white and grey matter?

A

The spinal-chord is made up of white and grey matter. The white matter is where the dendrites are, and the grey matter is where the cell bodies are.

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6
Q

Describe the path of a signal through the spinal chord

A

Sensory signals come in through the dorsal root (passed through the dorsal root ganglion) into the dorsal horn. The signal then travels to and from the brain through spinal tracts before leaving the ventral horn via the ventral root as motor neurons.

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7
Q

What are the somatic and autonomic nervous system?

A

The autonomic nervous system controls involuntary movement while the somatic nervous system controls voluntary movement.
The autonomic nerves have a synapse while the somatic nerves don’t.

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8
Q

What is controlled by the somatic and then the autonomic NS?

A

Smooth muscle, cardiac muscle and glands are controlled involuntarily by the autonomic nervous system.
Skeletal muscle is controlled voluntarily by the somatic NS

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9
Q

Compare the NMJ is the somatic and autonomic NS

A

Somatic;
Specialised
Ionotropic
always excites

Autonomic;
Less specialised
Metabotropic
Excite or inhibit

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10
Q

Describe the sympathetic NS

A

The sympathetic controls fight or flight involuntary behaviour
Sympathetic outflow is from the thoracolumbar (T1-L2) regions
Sympathetic ganglia lie close to spinal cord and are found in the sympathetic trunk (paravertebral ganglia) or in collateral (prevertebral) ganglia
Releases acetylcholine (which acts on cholinergic receptors such as nicotinic and muscarinic receptors) and Noradrenaline ( which acts on adrenergic receptors such as  receptors  receptors)

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11
Q

Describe the parasympathetic NS

A

Parasympathetic controlled rest and digest involuntary behaviour.
Parasympathetic outflow is from the cranial (III, VII, IX, X) and sacral (S2-4) regions.
Parasympathetic ganglia lie close to, or within, the target
Releases acetylcholine only that act on cholinergic receptors such as nicotinic and muscarinic receptors

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12
Q

What are the exceptions to sympathetic and parasympathetic NS?

A

Adrenal medulla releases adrenaline and noradrenaline into the blood.

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13
Q

Effects of the sympathetic NS

A

The pupil of the eye is dilated by the NA acting on 1 contracting the radial muscle.
Ejaculation is caused by NA causing the activation of 1 receptors on smooth muscle of urethra causing the contraction of smooth muscles.
Blood flow decreases as a result of NA activating 1 receptors on smooth muscle of vessels making them contract.
Urination is stopped by the contraction of smooth muscle activated by NA acting on 1 receptors on smooth muscle of sphincter.
Enzyme rich salivary secretion is activated by NA acting on  receptors
The heart rate is increased as a result of NA activating 1 receptors on the pacemaker cells.
The strength of contraction increases as a result of NA activating 1 receptors on the myocytes
The eyes focus is shifted far away by NA acting on 2 receptors relaxing the ciliary muscle.
The airway is dilated as a result of NA activating 2 receptors on smooth muscle of airways causing muscles to relax.
Blood flow is also increased by NA activating 2 receptors on smooth muscle of vessels making the muscles relax.
Reduced pressure in the bladder is activated by NA acting on 2 receptors on smooth muscle of bladder wall which causes them to relax.

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14
Q

Effects of the parasympathetic NS

A

The pupil of the eyes is contracted by AcH activating muscarinic receptors on sphincter muscle of the iris.
AcH has little effect on the smooth muscle (blood flow rate)
Erection is causes by AcH activating muscarinic receptors on smooth muscle of corpus cavernosum which relaxes smooth muscle.
Urination is caused by activation of muscarinic receptors on the sphincter which causes the relaxation of smooth muscle.
Watery secretion stimulated by AcH activating muscarinic receptors.
The heart rate decreases as a result of AcH activating muscarinic receptors on pacemaker cells
AcH has little effect on the strength of contraction as it has little effect on myocytes.
The focus of the eye is shifted close up by AcH activating muscarinic receptors contacting the ciliary muscle.
The airway constricts as a result of AcH activating muscarinic receptors which make smooth muscle contract.
Bladder pressure is increased by AcH acting on muscarinic receptors on the bladder wall causing smooth muscle to contract.

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15
Q

What is the acronym for remembering the effects of the parasympathetic and sympathetic NS

A
eye, ejaculation, flow, urination 
Salvia 
Heart 
Strength 
Eye, airway, flow, urination
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16
Q

How is the autonomic NS controlled?

A

Autonomic reflexes. i.e. baroreceptor reflex. Baroreceptors detect blood pressure, the integrating centre looks at the information, coordinates a sympathetic and parasympathetic outflow to vary heart rate, strength of contraction, and constriction of blood vessels accordingly.

Plus central control. From the hypothalamus it co-ordinates autonomic, somatic and endocrine activity, eg defence response.

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17
Q

How can the unique differences in the pathways be used?

A

Therapeutically i.e.
Salbutamol is a B2 agonist this can be given to dilate the airway without affecting the heart.
Atenolol is a B1 antagonist that can be given to decrease heart rate without affecting the airway.

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18
Q

What can muscarinic agonists be used to treat?

A

glaucoma (high intra occular pressure). Aqueous humour normally drains through the trabecular network into the canal of Schlem the muscarinic agonists contract the ciliary muscle supporting the lens and contracts the sphincter muscle of the pupil increasing the rate of drainage.

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19
Q

What are the two types of cells in he CNS

A

Neurons

Gila

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20
Q

What are the parts of neurons

A
  1. Cell body (soma) this contains the nucleus
  2. Dendrites these receive information
  3. Initial segment (axon hillock ) this part triggers action potential
  4. Axon sends action potential
  5. Axon (presynaptic) terminals release transmitter
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21
Q

What are the different types of neurons?

A

Afferent (sensory) neurones (found in the Peripheral nervous system) pass there signal on to the Interneurones (Found in the Central nervous system) which in tern pass the signal onto Efferent (motor) neurones (which are found in the Peripheral nervous system)

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22
Q

What are the different types of gila ?

A
  1. Astrocytes. Astrocytes maintain the external environment for the neurones. They are surround blood vessels & produce the blood brain barrier.
  2. Oligodendrocytes. Oligodendrocytes form myelin sheaths in the CNS (= Schwann cells in the PNS).
  3. Microglia. Microglia are phagocytic hoovers mopping up infection.
  4. Ependymal cells. Ependymal cells Produce the cerebrospinal fluid.
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23
Q

What are the different types of membrane potetnial?

A
  1. Resting membrane potential. Keeps cell ready to respond.
  2. Graded potentials. Decide when an action potential should be fired
  3. Action potentials. Transmit signals over long distances
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24
Q

What is the resting membrane potential?

A

Inside -70mV compared to outside.
An equilibrium is reached when the electrical gradient is equal and opposite to the concentration gradient. i.e. the rate at which the ions are leaving the cell to move down there concentration gradient is the same as the number of ions moving into the cell down there electrical gradient.

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25
Q

What processes work to maintain the resting membrane potential?

A

Leaky potassium channels. These channels allow potassium to move out of the cell down its concentration gradient. This makes the outside of the cell more positive and so creating a potential difference.

A sodium potassium pump. This pump moves 2 potassium into the cell for ever 3 sodium out of the cell. However because there is usually a similar concentration of potassium inside the cell as sodium outside the cell the charges on each side of the membrane is still fairly similar. The pump contributes about 5mV to the total 70mV gradient.

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26
Q

What is a graded potential? what are the different types of generator potentials?

A

A graded potential occurs when a neurotransmitter synapses with a neuron.
There are different types of graded potentials;

  1. Generator potentials which occurs are the sensory receptors
  2. Postsynaptic potentials which occur at the synapses.
  3. Endplate potentials which occur at the neuromuscular junction.
  4. Pacemaker potentials which occurs in pacemaker tissue.
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27
Q

What are the different features of graded potentials

A

Graded potentials are graded. A small stimulus will trigger a few channels to open and evoke the small response. While a strong stimulus will trigger many channels to open evoking a large response.
The amplitude of a graded potentials is a measure of its strength (or intensity)

  1. Graded potentials are decremental. Graded potentials get smaller as they travel along the membrane. It is just like water leaking from a leaking hose, your axons are very leaky.
    So graded potentials are only useful over very short distances. That is why graded potentials are also called local potentials.
  2. Graded potentials can summate. A single neurone will have many of synapses each producing their own postsynaptic potential.
    If two occur at the same time, they can add to together. If the sum is big enough then an action potential can occur.
  3. Graded potentials can be depolarising or hyperpolarising.
    Neurotransmitters can open channels that depolarise (excite – shown in red) the cell or hyperpolarise the cell (inhibit – shown in the green). Depolarising pushes the potential near the action potential firing threshold.
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28
Q

What are the types of synaptic integration

A

temporal summation

spatial summation

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29
Q

What are the different types of synaptic integration

A

Axo-dendritic
Axo-somatic
Axo-axonic

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30
Q

What changes cause a hyperpolarising postsynaptic potentials

A

Opening of cl channels

opening the K channels

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31
Q

What changes cause a depolarizing postsynaptic potentials

A

Opening of a monovalent cation channel

Closing of a K

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32
Q

What are isotropic and metatropic receptors?

A

Fast responses occur when neurotransmitters bind to isotropic receptors. Slow responses occur when neurotransmitters bind to metatrope receptors.

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33
Q

Describe an action potential

A

-

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34
Q

What are the features of an action potential?

A
  1. They have a threshold. Only once’s you have met the threshold does a action potential occur.
  2. Are all-or-none. Either there is an action potential or there isn’t.
  3. The intensity of a stimulus will be showing the frequency or firing (not amplitude). You cant get a weak or strong action potential it is just an action potential.
  4. Have a refractory period. The rest period between firing.
  5. Are self-propagating.
  6. Travel slowly
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35
Q

How can you make action potentials travel faster?

A
  1. Large axons. Just like water flows more easily through a large pile signals move faster down as large axon. Some animals like the quiz have invested fully in this however this would just take up two much room in a human.
  2. Myelination
    Schwann cells in the PNS and oligodendrocytes in the CNS wrap myelin around sections of the axon.
    This increases membrane resistance, and reduces membrane capacitance which results in less current being wasted.
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36
Q

What disease is associated with myelination?

A

Multiple sclerosis causes demyelination in the CNS and Guillain-Barre syndrome in the PNS.
This results in membrane resistance decreasing and the capacitance increasing. More current is lost between nodes and conduction fails.

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37
Q

What is a compound action potential?

A

The compound action potential
Humans have both small and large unmyelinated and myelinated axons, all conducting at different speeds.

Extracellular recording from a nerve (a bundle of axons) will therefore generate a “compound” action potential

This gives a classification of axons based on their conduction velocity. There conduction speed correlates with their anatomy, and their function

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38
Q

What are the different waves in an compound AP?

A

Large myelination - Proprioception and motoneurons
Large myelinated - Touch and pressure
Small myelinated - Motoneurons of muscle spindles
Smallest myelination - Touch, cold,
Unmyelinated - Warmth

39
Q

What is a NMJ?

A

The Neuromuscular junction is the synapse between the motor neurone and skeletal muscle.
This allow for muscle contraction.
The neuromuscular junction is innervated by the somatic nervous system. It uses the neurotransmitter acetylcholine which acts on a vary of different receptors. In the NMJ it acts on nicotinic receptors.

40
Q

Describe what happens at a NMJ

A

Action potential invades terminal
This activates voltage gated Ca2+-channels allowing Ca2+ to enter the cell.
Triggering Ca2+-dependent exocytosis of pre-packaged vesicles of neurotransmitter ACh.
ACh diffuses across cleft and binds to nicotinic receptors.
This binding of ACh opens ligand-gated Na+/K+ channels
This evokes graded (local) potential (the end plate potential)
This almost always depolarises adjacent membrane to threshold as it the potential is unusually large.
Which opens voltage-gated Na+ channels in the skeletal muscle membrane which evokes new AP
ACh is removed by acetylcholinesterase

41
Q

How can a NMJ be inhibited?

A
  1. Inhibit choline transporter (eg hemicholinium)
  2. Block voltage gated Ca2+ channels (eg black widow spider venom)
  3. Block vesicle fusion (eg botulinium toxins)
  4. Use non-depolarising nicotinic receptor blockers (eg d-tubocurarine)
  5. Use depolarising nicotinic receptor blockers (eg suxamethoneum = succinylcholine)
42
Q

How can a NMJ be increased?

A

There are also ways to potentiate (increase) transmission such as blocking acetylcholinesterase (eg eserine) or prolong the life of ACh i.e. Anti-cholinesterases

43
Q

How can these increases and inhibitions be used clinically?

A

Non-depolarising or depolarising blockers used for paralysis during
surgical procedures
electroconvulsive therapy
controlling spasms in tetanus

Botulinum toxin used for
treating muscle spasm
cosmetic procedures

Anti-cholinesterases used for
treating myasthenic syndromes
reversing action of non-depolarising blockers
countering botulinum poisoning

44
Q

How are NMJ different in the CNS and PNS?

A

The range of neurotransmitters is much greater in the CNS.
The range of post synaptic potentials is much greater in the CNS (in the PNS there is only ever a fast EPSP, but in the CNS there can be a fast or slow EPSP or IPSP)
Small postsynaptic potentials. Enables synaptic integration.
A verity of different synapses (Axo-dendritic, Axo-somatic and Axo-axonal). Note in the NMJ its just synapsed directly onto the muscle and so these types of synapses don’t occur.
Types of synaptic connectivity. In the NMJ it is just convergent where as in the CNS it can be convergent, divergent and can also contain contact inhibition. It can also be a monosynaptic or polysynaptic pathways
Synaptic plasticity exists in the CNS and not in the PNS.

45
Q

What are the functions of muscle

A

Generate force & movement

Allow us to express & regulate ourselves

46
Q

Describe skeletal muscle

A

Straited skeletal muscle exists in multinucleated cells which form fibres. These cells are packed full of protein and therefore there nucleuses are pushed out to the side of the cells. Myoblasts produce skeletal muscle in infants however are not found in adults. In adults muscle is repaired by satellite cells. When one part of skeletal muscle is damaged the muscle around the damage site undergo hypertrophy, making themselves bigger by depositing more protein) to compensate. Atrophy is the opposite of hypertrophy. Skeletal muscle has a very rich blood supply. Too much hypertrophy can cut off your blood supply causing ischemia.

47
Q

Describe cardiac muscle

A

Straited cardiac muscles exists as single cells. They are strong and full of protein and good at conducting electricity. Cardiac cells have intercalating discs which help them to conduct electricity efficiently. When someone has a heart attach cardiac cell protein leaks out the cells and so cardiac vitals can be taken to see if there is any cardiac protein in the blood.

48
Q

Describe smooth muscle

A

Smooth muscle is much smaller than skeletal or cardiac muscle. They are not as strong but they form in layers which gives them a lot of force. They are not as packed with protein and therefore there are no striated effect and the nucleus is still very visible.

49
Q

What is atrophy and hypertrophy?

A

Exercise however causes hypertrophy ( mass). Aerobic exercise results in an increase in mitochondria, increase in vascularisation, a small increase in fibre diameter. Anaerobic (strength) exercise results in an increase in diameter and increase in glycolysis.

Therefore exercise type determines type of muscle fibres you have (though remember we are also very limited by genetics).

50
Q

Describe the structure of skeletal muscle

A

Myofibrils contain basic repeating units called sarcomeres which contain thick myosin filaments and thin actin filaments. These two filaments are interwound together and slide and pull on each other. It is this motion that creates muscle contraction and is called the myosin cross bridge.

There are also other proteins found in striated muscle that help to ensure that these filaments interact in a nice regular repeated way. Tinin is an example of a helper protein.

51
Q

What is the myosin cross bridge?

A

The head of a myosin molecule hydrolyses ATP into ADP and Pi. This changes the position of the head.
The myosin head can then bind to the actin filament which causes the Pi to be released. This causes the myosin head to change formation pulling the actin and releasing a ADP. The myosin head then can bind to another ATP which detaches it from the actin filament

52
Q

How is the myosin cross bridge controlled?

A

The cross-bridge cycle is regulated in a few ways;

  1. Release of calcium. The amount and speed of release can both be used to regulate.
  2. Tropomyosin is a protein on the actin that partially covers myosin binding site therefore preventing myosin from binding.
  3. Troponin holds tropomyosin in blocking position. This is called a co-operative block. Calcium binds to troponin. Troponin alters shape – pulls tropomyosin away. Remove calcium – blocks sites again
53
Q

What is excitation -contraction coupling ?

A

Taking an electric signal (change in membrane potential causes by the NMJ) and converting it into a mechanical force (muscle contraction) is known as excitation contraction coupling.

The action potential travels along the muscle membranes and down transverse tubules (passages that run deep into the muscle carrying the electrical command from the nerve to the core of the muscle). The change in membrane potential triggers the release of Ca2+ from the lateral sac of the sarcoplasmic reticulum via the ryanodine receptor which applies the signal. The sarcoplasmic reticulum is a fine mesh network. Calcium then binds to troponin allowing myosin to bind to actin.

54
Q

What is a motor unit?

A

A motor unit is the area of muscle (many muscle fibres) supplied by one nerve.
The muscle fibres within a unit may be scattered throughout muscle.
Therefore, if one motor neuron dies the affected fibres are scattered throughout the muscle and so it less noticeable than if all the fibres were close together.

55
Q

Muscle mechanics terminology

A

TENSION is the force exerted by muscle

LOAD is the force exerted on muscle

ISOMETRIC (e.g. weightlifting) Contraction with constant length

ISOTONIC (or concentric) (e.g. running) Contraction with shortening length

LENGTHENING (e.g. sitting down) Contraction with increasing length

56
Q

What is a twitch contraction?

A

A single action potential through the NMJ would causes a twitch in a muscle.
The time before contraction starts is called the latent period.
The time between the start of tension and the time of peak tension is called the contraction time. The contraction times of muscles varies quite a lot (10-100ms). It is dependant on the [Ca2+]. As load increases, contraction velocity and distance shortened decreases
Isometric has shorter latent period than isotonic, but longer contraction event.

57
Q

What is tetanus?

A

An action potential is 1-2ms long, but twitch may last up to 100ms therefore you usually get more than one AP during contraction. These add up which is known as summation.
Tetanic tension is greater than twitch tension since [Ca2+] never gets low enough to allow troponin/tropomyosin to re-block myosin binding sites.

58
Q

What is fatigue?

A

Repeated muscle stimulation results in muscle fatigue.
The rate at which muscle fatigues depends on fibre type, length of contraction and fitness of individual.
If fatigued muscle is rested then it can contract again.
Fatigue is used as a safety feature to prevents muscles using up vast amounts of ATP, which would cause rigor.
There are a couple of things that causes fatigue. During high intensity, short duration exercises conduction failure can occur due to [K+] results in depolarisation or there is an increase in lactic acid concentration results in acidifies proteins or there is an increase in ADP and Pi concentration inhibits X-bridge cycle, delaying myosin detachment from actin filaments.
During long-term, low intensity exercise there is a decrease in muscle glycogen, blood glucose and it causes dehydration which all causes fatigue.
There is also a level on central command fatigue (fatigue of the central nervous system) cerebral cortex cannot excite motor neurons. There is no “will to win”.

59
Q

Classifications of skeletal muscle

A

There are different types of muscle fibre. They can be fast shortening (myosin has high ATPase activity), or they can be slow shortening (myosin has a low ATPase activity).
Fibres can have one of two ATP forming pathways can be oxidative or glycolytic. Oxidative fibres are red and have a small diameter. They have an increases mitochondria which increases oxidative phosphorylation. This in tern increases the O2 and nutrients delivery. They also contain myoglobin which also increase O2 delivery.
Glycolytic fibres are white with large diameters. They have few mitochondria. They have an increased enzyme and glycogen and a lower blood supply.
Muscle fibres can also be slow oxidative (I)  resist fatigue, Fast oxidative (IIa)  intermediate resistance to fatigue or Fast glycolytic (IIb)  fatigue quickly.

60
Q

Describe smooth muscles structure

A

Smooth muscle is spindle-shape, mononucleate and divide through life (therefore it is able to repair itself). Smooth muscles is found in lining organs and vessels (e.g. GI tract, uterus, airways, ducts) and is controlled by the autonomic nervous system.
Smooth muscle has thick myosin and thin actin filaments, like skeletal muscle however, filaments arranged diagonally across cells and are anchored to membranes and cell structures by dense bodies (like Z-lines). Filaments still slide together to contract cell.
In reality the pattern would be more random than this.

61
Q

What are the two types of smooth muscle

A

Smooth muscle exists in single or multiunits.
A single Unit (GIT, uterus, small blood vessels) has;
Many cells linked by gap junctions
Signals travel between cells
Contract synchronously
May contain pacemaker cells
Stretch evokes contraction

A Multiunit (airways, large arteries, hairs) has
Few or no gap junctions
Richly innervated by ANS
Don’t respond to stretch

62
Q

Describe the smooth muscle X bridge cycle activation

A

Ca binds to calmodulin
Ca calmodulin complex binds to myosin light chain kinase
This phosphorylates the myosin X bridge
Contraction

63
Q

Where does Ca come from in smooth muscle?

A

The sarcoplasmic Reticulum (SR) is still acting like a storage system. There is however less SR in smooth muscle than in skeletal.
Ca2+ can also taken from outside the cell using voltage-activated Ca2+ channels (VACC’s)

Ca2+ is removed from cytosol by pumping Ca2+ back into SR and out of cell by Ca2+-ATPases (slower process than in skeletal muscle)

In skeletal muscle 1 AP releases enough Ca2+ to saturate all troponin sites. In smooth muscle only some sites activated. Therefore, there is the potential to grade contraction depending on number of AP’s that reach cells. Smooth muscle has tone i.e a basal level of Ca2+ in cells causes a constant level of tension

64
Q

What are sensory receptor’s?

A

Humans have five senses and there are sensory receptors for each of these senses.
These receptors reserve information from the environment and pass it to sensory neurons which transmit the information to the brain.
There are many different types of stimulus, the type of stimulus is called the stimulus modality i.e. temperature or pain.
Receptors are sensitive to one type of stimulus i.e. light. This stimulus is known as the adequate stimulus. However a receptor may still respond to other forms of stimulus if the signal is particularly intense.

65
Q

What is the role of sensory receptors?

A

Inform your brain about the internal and external environment
Are nerve endings which can be specialized non-neural
Convert different stimuli into Action Potentials. (transducers)

66
Q

What are the main types of sensory receptor?

A
  • Mechanoreceptors: Stimulated by mechanical stimuli give us skin sensations of touch and pressure
  • Proprioceptors: Are a form of mechanoreceptors in joints and muscles. They signal information about body or limb position.
  • Nociceptors: respond to painful stimuli (heat and tissue damage)
67
Q

What is an adequate stimulus?

A

An adequate stimulus causes a graded membrane potential change (only a few mV). This change is called a receptor potential or generator potential.
The adequate stimulus in cutaneous (skin) mechanoreceptors and proprioceptors causes membrane deformation which activates stretch sensitive ion channels resulting in ions flowing across the membrane and change the membrane potential locally.
The response can be graded, large stimulus causes more action potential firing.

68
Q

How do mechanoreceptors work?

A

Mechanoreceptors respond to signals in different ways. Some mechanoreceptors continue firing action potentials for as long as the stimulus persists. However others adapt and only fire APs when the stimulus starts, ends or changes.

Rapidly/Moderately adapting receptors include Pacinian corpuscles and Meissner’s corpuscles. Slowly-adapting receptors include Merkel’s discs and Ruffini endings. Here action potentials are fired in a burst this is followed by regular action potential firings.

Note nociceptors which detecting painful stimuli, they do not adapt this is because it is important not to ignore painful stimuli.

69
Q

How do Pacinian corpuscle work?

A

The skin is packed with mechanoreceptors for touch. Their information (vibration, stretch, texture, pain) depends on the properties of nerve endings and of accessory, non-neuronal structures.
One example is the Pacinian corpuscle that detect pressure and vibration. It is contains a myelinated nerve with a naked nerve ending. It is enclosed by a connective tissue capsule of layered membrane lamellae and each layer is separated by fluid ( it is a bit like a spongy onion).

70
Q

What is acuity?

A

The ability to locate a stimulus on the skin and differentiate it from another close by is called acuity.
Some parts of the body will have high acuity while others will have low acuity. Low acuity is a result of high levels of convergence.

Convergence or low acuity allows sub-threshold stimuli from different receptive fields to summate at the secondary neuron, forming a larger secondary receptive field and initiating Action Potentials.

71
Q

What is lateral inhibition ?

A

Lateral inhibition helps us to identify a stimulus very specifically.
Think about a sharp pencil tip on your finger. It will push sharply at the central point but it will also deform a sizeable surrounding area however you can localise it precisely, even with your eyes closed.
The harder the stimulus the greater the lateral inhibition that will occur.
Therefore we can say that lateral inhibition “sharpens or cleans up” sensory information
Lateral inhibition is widespread in the spinal cord.

72
Q

What are the three types of proprioceptor?

A
  1. Muscle spindles – which monitor muscle length and rate of change of muscle length - they control reflexes and voluntary movements.
  2. Golgi tendon organs – which monitor tension on tendons. Tension is produced by muscle contraction, so monitoring muscle tension.
  3. Joint receptors – which monitor joint angle, rate of angular movement and tension on the joint.
73
Q

What is kinasethesia?

A

the ability to perceive limb and body position and movement in space. We are able to do this because of proprioception.

74
Q

Describe muscle fibres

A

Muscle fibres. Muscle contains extrafusal and intrafusal muscles fibres. The extrafusal fibres are skeletal muscle and the intrafusal fibres are proprioceptors.
There are two kinds of intrafusal fibre. Nuclear bag fibres - bag shaped with nuclei collected together and nuclear chain fibres - nuclei lined up in a chain.
Muscle fibres have contractile ends (middle cannot contract) which are innervated by gamma motors. When gamma motors fire the ends contract.
When the extrafusal muscle stretches the muscle fibres can feel the stretch and signal that to the brain. However when the muscle fibres contract the contractile ends of the intrafusal muscle fibres must also contract to allow the intrafusal muscle fibres to continue communicating with the brain (keep the nervous fibres tight). This is called the 𝛼−𝛾 co-activation.

75
Q

Describe the Golgi tendon organ

A

Golgi tendon organ (GTO) has nerve endings that mingle with the tendon bundles at ends of muscles allowing the monitoring of the tension of the tendons.
Muscle contraction increases the tension in the tendons this stretches the nerve endings of the GTO and initiates APs in the group 1b afferent fibre from the GTO.

76
Q

What is a simple spinal reflex?

A

Spinal reflexes are simple building blocks for movements. The simplest reflex of all is the stretch reflex which is found in all muscles. For example the patellar tendon or knee-jerk reflex uses information from muscle spindles which monitor muscle length. Or in the arms. Here a sharp tap to an inelastic tendon causes transmitted of signal to muscle fibres they are more elastic and stretch. This activates 1a afferent sensory nerves in the muscle spindle which increases the number of APs.

77
Q

What is a stretch reflex?

A

When a reflex signal is sent it will synapse directly with a motor neuron which causes the contraction of the agonist muscle required in the desired action. However a branch of the same sensory neuron will also synapse with an interneuron which will synapse with another motor neuron which will inhibit the contraction of the antagonist muscle. This duel action is known as reciprocal inhibition.
The spinal fibres will also travel up to the thalamus and somatosensory cortex to tell the about the length of the muscle.

78
Q

What is an inverse stretch reflex?

A

Here APs fired from the 1b nerves in the Golgi Tendon Organ causes the of signals that decreases agonist contraction strength and increase antagonist contraction strength. (It also sends signal to the brain). This is a protective mechanisms to prevent muscle damage and can be see in the clasp knife reflex where greatly increasing tension leads to collapse of resistance (like in a spring-loaded knife opening up).

79
Q

What is a flexor or withdrawal reflex

A

Reflexes as a result of pain are called flexor or withdrawal reflexes.
These reflexes are polysynaptic and protective as they withdraw part of the body away from the painful stimuli and towards the body.
These painful stimuli are detected by nociceptor nerves and cause;
An increase in activity of the flexor muscles
Antagonist extensors to be inhibited (flexors reflex causes ipsilateral flexion in pain responses)
Excite contralateral extensors
Inhibit the contralateral flexors. This helps to maintain an upright posture by extending the limb opposite the flexed one to bear the shift in body weight.
Sensory information to ascends to the brain (contralateral spinothalamic tract).

80
Q

Can reflexes be overridden?

A

Reflexes can be over-ridden consciously. For example if you ask someone to hold an ever increasing load the load would eventually cause a reflex from the Golgi tendon organs causing you to drop the load. However if the load was something precious like a child then the reflex can be overridden.
When you think ‘I don’t want to drop this’ it causes excitation to descend to the  motoneurones of the contracting muscle. This overrides the inhibition from the GTOs and maintains muscle contraction.
The EPSPs sent form the brain will combine with the IPSPs sent from the GTOs to prevent the muscle from reaching threshold and relaxing.

Withdrawl reflexes can also be over-ridden if you are touching a hot plate but think about how dropping the hot plate will burn your leg then that will help you to over-ride the reflex.
Similarly, anticipating pain can increase the vigour of the withdrawal reflex when a painful stimulus arrives.

81
Q

What is facilitation?

A

The more powerful the pain the more muscles are recruited and the response gets larger.

If one finger touches a hot plate your hand withdraws quickly but if your whole hand contacted a hot surface, you would withdraw your whole arm, extend the contralateral arm…. and probably jump away!

The enhancement of sensory input like this is called Facilitation.

82
Q

intro to intracellular communication

A

Intracellular communication is vital for life. This communication is carried out by chemical signals (hormones and neurotransmitters) from one cell acting on specific receptors on another cell that results in coordination.
Signals act on specific respecters. Different types of cells might have the same receptor. The binding of the signal molecule to this receptor however might cause a different effect in these different types of cell.
The cellular response of signalling molecules can be hugely varied.
The process by which a cell responds to a signalling molecule is called transuding

83
Q

What are hydrophobic signalling molecules

A

Some signalling molecules are lipid soluble (hydrophobic) which means they dissolve through the lipid bilayer of the plasma membrane.
There receptors therefore are intracellular, found in either the cytosol, or in the nucleus.
For example nitric oxide is a lipid soluble signal molecules that binds to soluble guanylyl cyclase in the cytosol and generates cGMP as 2nd messenger that regulates cell activity.
Steroid hormones are another example and there receptor is often a transcription factor that regulates transcription in the nucleus.

84
Q

What are the different types of hydrophilic receptors?

A
  1. Receptor-channels. Also called ionotropic receptors eg nicotinic ACh receptors
  2. G protein coupled receptors (GPCRs). These are also called metabotropic receptors. They do all their work via a middle man, the G protein.
  3. Receptor-enzymes. receptors with intrinsic enzymic activity, eg insulin receptors, or bound to an enzyme, eg cytokine receptors
  4. Integrin receptors. receptors that interact with the cytoskeleton
85
Q

What are the ways in which G protenis work?

A
  1. May couple direct to ion channels. Affects membrane potential and firing of action potentials.
  2. Or they may couple to adenylyl cyclase. This Produces cAMP as 2nd messenger, Regulates protein kinase A activity and phosphorylates target proteins and changes their activity
  3. . May couple to phospholipase C. Produces IP3 and DAG as 2nd messengers, which releases Ca2+ and regulates protein kinase C activity which then phosphorylates target proteins and changes their activity
86
Q

Why is Ca so useful?

A

Ca2+ is a very important secondary messenger.

Sources of Ca2+
from internal stores via IP3- or Ca2+-stimulated release Ca2+ from sarcoplasmic reticulum
from outside the cell via voltage-gated or ligand-gated Ca2+ channels
via inhibition of Ca2+ transport out of the cell
Effects of Ca2+
directly affects target protein (eg PKC)
binds to calmodulin which then activates target protein (eg Ca2+-calmodulin dependent kinase - CamKinase)
works via some other Ca2+ binding protein (eg troponin)

87
Q

What is pharmacology?

A

Pharmacology is the study of the way living systems are affected by chemical agents.
Chemical agents includes endogenous agents made by the body i.e. neurotransmitters and hormones drugs and also includes exogenous agents i.e. drugs.

88
Q

What is a drug?

A

A drug is any chemical agent that affects a biological system
There are many sources of drugs;
Natural products from plants (i.e. caffeine)
Synthetic drugs generated by pharmaceutical industry
Biotechnology using living systems to make therapeutic agents
Gene therapy to introduce new DNA?

89
Q

What is EC50?

A

EC50 is the drug concentration that produced half the

max response.

90
Q

What is affinity?

A

Affinity is determined by strength of chemical attraction between drug and receptor - low EC50 indicates high affinity

91
Q

What is efficacy?

A

Efficacy is determined by how good the drug is at activating the receptor

92
Q

What are the different types of drug?

A
Full agonist (High affinity and efficacy) 
Partial agonist (high affinely and some efficacy) 
Antagonist (High affinity and no efficacy)
93
Q

What are selective agonists and selective antagonists?

A

Selective agonists are drugs that activate only some of those receptors
eg salbutamol - a 2-agonist

Selective antagonists are drugs that block only some of those receptors
eg propranolol - a 1 and 2-antagonist

94
Q

What are the 4 different effects of adrenaline?

A

Alpha 1 dilates pupil
alpha 2 inhibits gastric secretion
beta 1 increases heart rate
beta 2 dilates airways