Nervous System Part 1 Flashcards

Question

What is a ‘graded potential’ and ‘action potential’.

Answer 1

They are both types of electrical signal in a neuron A graded potential is any electrical impulse that travels around the cell body and dendrites of a neuron. An action potential is any electrical impulse that travels down the axon.

Answer 2

Specific ion channels can open and close when stimulated. Electrical differences across the cell membrane (resting potential),

Answer 3

Ion channels are transmembrane proteins. Na+ and K+ channels are the really important ones. Stimuli that trigger ion channels: - changes in voltage - chemicals (hormones) - mechanical pressure

Answer 4

Neurons at rest possess an ELECTROCHEMICAL gradient across the cell membrane. This is created by the build-up of NEGATIVE ions on the inside of the cell membrane relative to the extracellular fluid which contains more POSITIVE ions The separation of charges create POTENTIAL energy. The resting potential is approximately -70mV. Cells exhibiting a membrane potential are said to be POLARISED or charged.

Answer 5

Inside the neuron in the intracellular fluid we will find an accumulation of - potassium ions (K+) and also, - large negatively charged protein molecules that cannot leave the cell. Overall it carries a negative charge Outside and around the neuron in the extracellular fluid we find an accumulation of sodium ions (Na +) and Chloride ions (Cl-). Overall it carries a positive charge. Therefore we have more positivity outside than we do inside. The inside is negatively charged compared to the outside. This creates a very specific charge in our neurons. In an axon that is at rest and not carrying an electrical signal, the charge in that Neuron will be - 70mV. That is the separation of charge between the inside and the outside. We call this disparity between the inside and the outside, this build up of negative ions on the inside of the cell membrane, relative to the extracellular fluid which contains more positive ions, the resting potential. Why don’t things even up in the concentration gradient through passive transport? Normally it would but in this case as the NA+ as CL- try to move back to equalise the charge, the separation of charges is maintained by the sodium-potassium pump which pumps 3 Na+ out for every 2 K+ it pumps back in (using ATP).

Answer 6

- Depolarisation - Repolarisation

Answer 7

a. Depolarisation Depolarisation is when a positive charge builds up inside the cell - the negative membrane potential (-70mV) becomes positive and reaches +30mV. Step 1: Depolarisation is triggered by stimulation of a nerve ending. Step 2: That stimulation must reach a threshold value -55mV in order to generate an action potential. Step 3: Na+ channels open allowing Na+ to flood into the cell up to about +30mV Step 4: A positive charge builds up inside the cell b. Repolarisation Repolarisation is where we get the restoration of the membrane potential to -70mV. To do this potassium channels now open but much more slowly than Na+ channels. The result is that Na+ channels just start to close as K+ channels open. K+ can flood out of the cell restoring the membrane potential to -70mV

Answer 8

a. Refractory period The time after depolarization and repolarization where we can’t generate another action potential. The reason we can’t generate another action potential is because ions (Na+ and K+) are on the wrong side of the membrane and the charge is all over the place. b. Absolute refractory period Even a really strong stimulus would not be able to generate an action potential because the ions are in the wrong place. c. Relative refractory period The time when you could generate another action potential but the stimulus would have to be bigger than the original stimulus.

Answer 9

ContinuousVS Saltatory Myelination: Unmyelinated VS myelinated Depolarisation: Step-by-step VS Leaps Speed: Slower VS Faster Energy efficiency: Less VS more

Answer 10

At the nodes of Ranvier, there are high concentrations of Na+ gates. This causes the current to appear to jump from node to node (saltatory conduction).

Answer 11

Cold slows down action potentials. Ice pain signal’s are relayed more slowly.

Answer 12

**Synapse receives the depolarising wave** and we get **sodium channels opening** and sodium entering the axon again and again. This causes **calcium channels** to **open** and we get the influx of calcium into the synaptic bulb. Sodium in in droves…then calcium … When **calcium ions are in large quantities** in that synaptic end bulb, they cause the **synaptic vessels** which store the neurotransmitter to **break down** and that process of break down is known as **exocytosis.** Neurotransmitters are released into the synaptic cleft. The **released neurotransmitters diffuse** across this gap (the synaptic cleft) and bind to receptors on the post synaptic neuron. This causes something to happen in the next neuron depending on whether it is excitatory (continues) or inhibitory (stops) .

Answer 13

a. GABA – Amino Acid b. Dopamine - Monoamine c. Acetylcholine – Unique molecule d. Serotonin - Monoamine

Answer 14

Between impulses the transmitter molecules are rapidly removed from the synaptic cleft to prevent continuous stimulation of postsynaptic neurons. There are two types of removal: Re-uptake – the neurotransmitter is reabsorbed back into the presynaptic neuron and restored inside a vesicle ready to be used again. Enzyme degradation – neurotransmitter is broken down by an enzyme (such as MAO) into smaller inactive product which are then reabsorbed by the presynaptic neuron and resynthesised into active neurotransmitter.

Answer 15

Inhibitory GABA is an inhibitory neurotransmitter. It lessens a nerve cell’s ability to receive, create or send chemical messages to other nerve cells. GABA is known for producing a calming effect.

Answer 16

a. Serotonin - Tryptophan b. Dopamine - Tyrosine

Answer 17

It is needed to encourage intestinal motility (peristalsis) and epithelial cell secretion.

Answer 18

**S**leep regulation **P**ain **A**ttention **L**earning and memory **T**hermoregulation GIT intestinal motility

Answer 19

It is particularly abundant in the substantia nigra.

Answer 20

Movement - Patients with Parkinson have a lack of dopamine in the substantia nigra Reward mechanisms – Dopamine released with sugar, alcohol, cocaine Regulating muscle tone Cognition and emotion

Answer 21

Muscle contractions Cognition – Embedding and recalling memory. 90% of Alzheimer’s patients are deficient in ACH

Answer 22

Endorphins are hormones that are released when your body feels pain or stress. They are produced in your brain and act as messengers in your body. Help to * improve mood. * relieve pain * reduce stress Endorphins can be boosted by exercising, eating, having sex, getting a massage and many other ways. Endorphins Dynorphins Enkephalins

Answer 23

Substance P

Answer 24

**S**erotonin. **A**drenaline. **N**oradrenaline. **D**opamine.

Answer 25

**A**drenaline. **N**oradrenaline. **D**opamine.

Answer 26

A junction between two neurons or a neuron and a muscle

Answer 27

In the GIT - 95% of it

Answer 28

Tingling; Numbness; pain >>> in the associated distribution

Answer 29

They carry impulses to and from the spinal cord

Answer 30

**PNS** fibres can regenerate but only if 1. the cell body is intact because that is where the nucleus would be. The nucleus is needed to code for the newly produced axon. 2. Schwann Cells are present **CNS** nerve fibres do not retain the capacity to undergo division/regenerate However….If a patient was to damage an area of tissue within the CNS we can sometimes get neuroplasticity. We adapt and create new pathways

Answer 31

The carpal tunnel is a narrow passageway in the anterior wrist that contains tendons and the median nerve. This median nerve provides sensory information to the hand and controls movements in the hand and fingers The median nerve becomes compressed in the wrist and hand carpal tunnel syndrome.

Answer 32

Pathologies - RA, Hypothyroidism, acromegaly Also – fluid retention due to pregnancy, overuse, posture, using vibrating tools

Answer 33

* Tingling, numbness or pain in the median nerve distribution. * Symptoms are often worse at night * Weakness of grip and weak thumb opposition

Answer 34

Two tests that will reproduce carpal tunnel syndromes if the median nerve is at play: **Tinel's test** (tapping on the median nerve) depolarises the median nerve. If there is damage, by tapping this it will create symptoms very quickly **Phalen’s test** - also reproduces symptoms

Answer 35

The nerve that controls the facial muscles (facial nerve) becomes inflamed or compressed.

Answer 36

Herpes simplex

Answer 37

* Sudden **unilateral** weakness or paralysis of the facial muscles. * Sometimes cannot close eye on affected side * Loss of taste and intolerance to loud noise if severe

Answer 38

Both autoimmune and both interfere with laying down of myelin on axons

Answer 39

Guillain-Barre is a form of post-infectious de- myelinating disease with neuritis. It is associated with acute, ascending, progressive inflammation and demyelination of peripheral nerves. MS is autoimmune inflammatory disease causing demyelination of axons in CNS neurons with damage. T-Lymphocytes attack myelin antigens. Multiple areas of sclerosis (scar tissue) along axons disrupt conduction. MS and GBS are both auto immune and both inflammatory and both demyelinating. MS is in the CNS and GBS in the PNS.

Answer 40

Epstein-Barr in 75% of cases it is autoimmune after an infection like Epstein-Barr

Answer 41

In 75% of cases GBS is triggered by a recent infection (one–three weeks after respiratory / GIT infection or post-vaccination e.g., flu / EBV). Molecular Mimicry is where antibodies formed against virus cross react with lipids in myelin.

Answer 42

Guillain–Barré syndrome ( GBS) is a rapid-onset muscle weakness caused by the immune system damaging the peripheral nervous system. * Sudden, progressive, **bilateral** ascending paralysis. * Paraesthesia (pins and needles)and sensory changes. * Neuropathic pain into legs.

Answer 43

It is an autoimmune, inflammatory and demyelinating disease in the CNS T lymphocytes attack myelin antigens on the CNS, * leading to multiple areas of sclerosis (hardening/scar tissue) along axons, * leading to disruptions in conduction * leading to multiple systems including vision issues, deafness and loss of balance, burning and pulling sensations, tingling and loss of sensation, cognitive changes and depression, weakness, bladder urgency and incontinence

Answer 44

**Relapsing – Remitting:** Most MS follows a relapsing-remitting pattern (85%) where the disease goes from relapse to remission to relapse etc **Primary – Progressive:** Serious from the start and progress from the start. Poor prognosis **Secondary – Progressive**: When it starts as relapsing-remitting and as the disease progresses it becomes progressive

Answer 45

**Vitamin D** Low Vit D is one of the biggest risk factors for MS. **Oligodendrocytes need it to produce myelin**. * Correlation between Vit D deficiency/proximity to the equator and MS * Correlation with other countries that also are known to have Vit D deficiency, for example because they apply a lot of sunscreen or cover skin for religious reasons Eg: Australia and Saudi Arabia **Vitamin B12** B12 normally acts as a co-factor in myelin formation and also has immunomodulatory effects.

Answer 46

Epstein-Barr

Answer 47

MRI Opthalmoscopy

Answer 48

Working down the body … 1. Cognitive changes and depression. 2. Visual symptoms are common: Blindness, loss of vision of one eye and occasional pain (neuritis). Double vision and nystagmus (jerking of eyeball). 3. Deafness and loss of balance. 4. Bladder urgency and incontinence. More general symptoms 1. Paraesthesia - Burning, pulling sensations. - Tingling and loss of sensation. 2. Weakness

Answer 49

The progressive degeneration of motor neurons in the spinal cord, motor cortex and brain stem. MOTOR not sensory therefore no sensory symptoms like tingling/numbness but motor symptoms like paralysis and weakness.

Answer 50

The current hypotheses focus on abnormal mitochondrial function causing oxidative stress in motor neurons. Genetics is also implicated

Answer 51

1. Typically presents as weakness in upper limbs - dropping objects or difficulty manipulating objects. 2. Wasting of hand muscles and tremor of limbs at rest. 3. Later stages can affect the legs (tripping), cause slurred speech, dyspnoea and dysphagia. 4. Death by respiratory failure — typically within 3–5 yrs

Answer 52

a. Alzheimer’s disease (AZ) 50% of dementia diagnosis. Associated with * Degeneration of the cerebral cortex * Reduced acetylcholine production * Deposition of Protein Plaques called beta amyloid plaques b. Vascular dementia 25% of dementia diagnosis * Associated with cardio vascular disease and poor oxygen delivery * Often associated with stroke or multiple strokes cutting off circulation in aregion of the brain * Parkinson's disease.

Answer 53

Alzheimer’s is a neurodegenerative disease of the cerebral cortex. The hippocampus is among the areas first affected. It is where we store memories. As the hippocampus degenerates we lose the ability to recall these memories. Typically, more short term memories. Later as the disease progresses it spreads to the amygdala which is the area of the brain that is active when we are dealing with emotions and longer term memories. Whilst progressing, additional regions of brain become affected. Associated with Beta Amyloid plaques, atrophy of neurons and less acetycholine. Beta amyloid plaques are the key diagnostic feature of alzheimers.

Answer 54

a. Earlier stages of AZ Hippocampus b. Later stages of AZ Amygdala

Answer 55

a. Homocysteine * The Amino acid homocysteine needs to be converted to methionine. This conversion needs B6/9/12 vitamins and thus we accumulate more homocysteine because it isn’t converted * High increases risk. * Facilitate a build-up of toxic β-amyloid and tau in the brain b. Stress * Higher cortisol levels linked to memory issues c. Hormones defiicieny increases risk of cognitive impairment * Oestrogen deficiency can make post menopausal women more prone to learning and memory problems. * Testosterone deficiency in men as it has a neuroprotective effect. * Thyroid hormone deficiency linked to an increased risk of cognitive impairment. d. Heavy metals Thought to degenerate the blood brain barrier and allow some of the other substances to enter through. * Excessive levels of copper (sml qty is beneficial) * Mercury. * Aluminium toxicity (e.g. from vaccines, cans, foil, antiperspirants etc.). e. Chronic inflammation * Such as sugar (and insulin resistance), dairy, gluten. * Leaky gut (promoting inflammation).Gluten is implicated here.

Answer 56

ApoE4 gene

Answer 57

B1, B3, B6, B12, folate, omega-3 fatty acids.

Answer 58

a. Oral bacteria such as P. gingivalis have been identified in tissue biopsies. b. Herpes simplex virus.

Answer 59

a. Early stages of AZ Hippocamous Stage * Slight memory loss (especially short-term) i.e., forgetting recent conversations. * Repeated questions and confusion. * Decreased initiative (↓hobbies, ↓hygiene) b. Later stages of AZ Amygdala Stage * Significant memory loss (incl. long-term memory). * Subtle changes in higher order functions i.e. understand jokes. * Mood disturbances: agitation and aggression. * ‘Loss of sense of self’ — autobiography (left hippocampus). * Difficulty with language, unsteady, depression.

Answer 60

Parkinsons is a progressive neurological movement disorder affecting movement caused by degeneration of dopamine producing neurons in the area of the brain called the substantia nigra located in the mid brain. It leads to an accumulation of abnormal protein plaques (Lewy bodies) within neurons. Alzheimers is also a neurodegenerative disease but it is of the cerebral cortex staring at the hippocampus and moving to the amygdla. It affects memory and emotion. It only affects movement in later stages but this is due to loss of memory. It leads to a build of beta amylin plaque.

Answer 61

* Mitochondrial dysfunction (oxidative stress). *Genetics. * Constipation and diet low in polyunsaturated fats. * Toxic environmental factors: i.e.carbon monoxide, manganese poisoning, exposure to pesticides and herbicides.

Answer 62

* Bradykinesia: Short, shuffling steps (difficulty stopping / starting) * Resting tremor (‘pill rolling’). * Stooped / flexed posture/ arms at side * Lack of normal subconscious movements (swinging arms). * Muscle rigidity, mask-like face * Low/deep voice.

Answer 63

* Genetic disease with a defect on chromosome 4 * An inherited neurodegenerative disorder affecting the basal ganglia * Results in loss of muscle coordination (chorea), cognitive impairment and poor regulation of mood and emotions. Note: The basal ganglia are located in the brain stem, thalamus, and cerebral cortex areas of the brain. This group of structures is important in regulating voluntary movements.

Answer 64

Median Nerve

Answer 65

Facial nerve

Answer 66

A. Multiple sclerosis – 20 to 50 B. Motor neuron disease – 50 - 70

Answer 67

Heavy metals Chronic inflammation – gluten, dairy, sugar Bacteria like gingivitis High homocysteine levels High cortisol levels lots of free radicals lots of atherosclerosis/cardiovascular disease Genetics

Answer 68

Substantia Nigra

Answer 69

Glutamate GABA Seratonin Dopamine Adrenaline and noradrenaline Acetylcholine Nitric Oxide

Answer 70

Glutamate is the most abundant excitatory neurotransmitter released by nerve cells in your brain. It plays a major role in learning and memory. For your brain to function properly, glutamate needs to be present in the right concentration in the right places at the right time. Too much glutamate is associated with such diseases as Parkinson’s disease, Alzheimer’s disease and Huntington’s disease. Primary mode of action: Excitatory Location it works in - CNS Derived from what amino acid - Glutamine Role - Memory, learning

Answer 71

Primary mode of action - Inhibitory Location it works in - Brain Derived from what amino acid - Glutamate together is vitamin B6 dependent Role - Prevents neural overactivity

Answer 72

Primary mode of action - Inhibitory Location it works in - 95% enteric nervous system and 5% CNS Derived from what amino acid - Tryptophan Role - Sleep Attention Intestinal mobility and secretions Pain regulation

Answer 73

Primary mode of action: inhibitory Location it works in: Brain - Substantia Nigra Derived from what amino acid: Tyrosine Role: Reward Cognition Movement Muscle tone

Answer 74

Primary mode of action: Excitatory Location it works in: Sympathetic nervous system; Brain - motor Neurons Derived from what amino acid: Tyrosine Role: mobilise body and brain to take action when danger

Answer 75

Primary mode of action: Excitatory Location it works in: Parasympathetic nervous system CNS motor neuron junction Derived from what amino acid - N/A Role: Muscle contraction cognition

Answer 76

Primary mode of action: Excitatory Location it works in: Smooth muscle Derived from what amino acid: Arginine Role: vasodilation

Answer 77

Autoimmune Genetics Vitamin D and vitamin B 12 deficiency

Answer 78

Graded potentials are changes in membrane potential that vary according to the size of the stimulus, as opposed to being all-or-none Graded Potential: * for short distance, communication * occurs in dendrites and cell body * No threshold * Longer duration Action potential: * for long-distance communication * Occurs along the axon * All or nothing – has a threshold * Shorter duration