Nervous system Flashcards

(33 cards)

1
Q

What is a ganglion

A

Collection of cell bodies outside of the CNS

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2
Q

Different types of neural processing

A

Divergent, convergent, parallel, serial processing and reverberation (homeostasis)

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3
Q

Types of neurons

A

Bipolar, unipolar, anaxonic, multipolar (single axon, multiple dendrites)

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4
Q

Glial cells in the CNS

A

Oligodendrocytes (myelination), astrocytes (form blood brain barrier, structural support and regulate ion + neurotransmitter), Microglia (immune cells of CNS), Ependymal cells (line ventricle’s)

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5
Q

Glial cells in PNS

A

Schawnn cells (myelination and repair after injury), Satellite cells (surround neuron and cell bodies, regulate O2/Co2, nutrients and transmitter levels)

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6
Q

What is myelination

A

Fatty layer surrounding neurons that increases transduction speed.

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7
Q

What is RMP and how is this achieved

A

-70 mV.
This is achieved by the imbalance of ions. The ICF is much more negatively charged than the ECF. Resting membrane is very permeable to K ions meaning RMP is closet to the Nerest value for K (90). K higher inside and Na higher outside.

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8
Q

Ion flow underlying action potentials

A

Depolarisation opens voltage gated Na channels causing influx due to concentration gradient. This causes further depolarisation causing more Na to open

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9
Q

Action potential propagation in unmyelinated axons

A

The influx of sodium causes a depolarisation in the adjacent part of the axon, causing opening of Na channels. This can only move in one direction due to the inactivated state of the Na channels (refractory period). Remember that even if artificially stimulated a nerve can only give a response at one end due to the release of neurotransmitter.

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10
Q

Saltatory conduction (AP propagation in myelinated axons)

A

Action potentials can jump from one node of Ranvier to another. This is driven by the adjacent spread of depolarisation. Refractory periods are still present.

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11
Q

What are the refractory periods

A

Absolute – No action potential can be generated due to the Na channels being in the inactivated state
Relative – Action potential can be generated if the stimulus is large enough as some Na channels are in the closed state

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12
Q

Factors effecting rate of conduction

A

Temperature, axon diameter and degree of myelination

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13
Q

Contrast action potentials and graded potentials

A

Action – causes by depolarisation, all or nothing response (change frequency for increasing stimulus), always movement of K and Na, constant duration (1-2 ms), refractory period, no summation, propagates throughout membrane without diminishing.
Graded – multiple causes (stimulus, neurotransmitter with receptor, changes in channel permeability), movement of ions across membrane (Na, K, Cl, Ca), magnitude and duration varies with magnitude and duration of triggering event, magnitude decreases with distance, temporal and spatial summation.

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14
Q

Synaptic transmission termination

A

This occurs via the removal of the neurotransmitter which can occur in one of three ways. Breakdown by enzymes, diffusion away from synaptic cleft where it is broken down or the reuptake back into the presynaptic terminal (or astrocytes)

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15
Q

Process of synaptic transmission

A

Action potential propagates down action causing voltage gated calcium channels to open. Influx of calcium causes the release of the neurotransmitter from presynaptic neuron into synaptic cleft. Neurotransmitter then binds to specific chemically gated ion channels that will then let specific ions into the post synaptic neuron, this can cause either a inhibitory or excitatory response.

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16
Q

Summation of synaptic inputs

A

Temporal summation – two EPSPs from the same pre synaptic neuron occur close in time and depolarise
Spatial summation – two EPSPs form different pre synaptic neurons occurs close in time
EPSPs and IPSPs cancel each other out

17
Q

What effects synaptic transmission

A

The type of cell it terminates on (Skeletal, neuron, cardiac), type of chemical release (excitatory or inhibitory) and the type of neurotransmitter receptor on the postsynaptic neuron (ligand gated will cause direct changes to membrane potential while G protein coupled receptor will have an indirect off on this and other cellular functions.

18
Q

What is a ligand gated ion channel

A

Ion channel in membrane that are open through the binding of a ligand (neuro transmitter, chemical messenger). Causes ions to flow in or out and therefore has a direct impact on membrane potential creating a local response that can either be EPSP or IPSP. Has a fast response (10-100 ms)

19
Q

Organisation of muscles

A

Sarcomere →myofibril → muscle fibre → skeletal muscle

20
Q

Components within sarcomere

A

Z line - holds the thin filaments (between 2 of these is referred to as a sarcomere)

M line - proteins that hold the thick filaments

A band - Thick and thin overlap

I band - Thing filaments that dont overlap with thick

H zone - middle of A band where thin dont reach

21
Q

Thick Filament

A

Myosin chains

This is a protein with a long tail and a head which contains the actin binding site

22
Q

Thin Filament

A

Chain of many actin protein molecules

Actin has multiple myosin binding sites which are often blocked by tropomyosin.

Another protein known as troponin binds to tropomyosin and via calcium can move the troponin-tropomyosin complex to expose myosin binding sites.

23
Q

Calcium cross bridges pre req

A

During muscle relaxation, tropomyosin is blocking the myosin binding sites.

However, during excitation calcium is released into the muscle which binds troponin causing it to move the troponin-tropomyosin complex and expose the myosin binding sites. This then causes the cross bridge cycle to occur

24
Q

Calcium cross bridge cycle

A
  1. Myosin head binds to actin
  2. Myosin performs power stroke pulling the thin filament relevant to the thick
  3. Myosin head detaches and “unflexes”
  4. Myosin head is now able to bind to another actin binding site

Multiple of these cross bridges and the flexion of multiple myosin heads allow the thin filament to be moved towards the thick (muscle contraction)
Energy (ATP) required to detach myosin head after power stroke

25
What is a motor unit
Motor neurons and the muscles fibres it innervates The more motor units that are innervated the larger the contraction Neuromuscular junction is where the motoneuron reaches each muscle fibre
26
Muscle contraction triggering
1. Action potential prorogates down the axon 2. Depolarisation from this AP causes opening of voltage gated calcium channels 3. Influx of calcium triggers the release of AcH (Acetylcholine) 4. AcH diffuses across the synapse and binds to nicotinic acetylcholine receptors (ligand gated ion channels) 5. Binding AcH to nicotinic AcH receptors open Na channels allowing influx 6. This influx of NA is always enough to start an action potential (large depolarisation) 7. Depolarisation spreads along muscle fibre, opening voltage gated Na channels 8. Triggering AP in every muscle fiber 9. AcH broken down by the enzyme acetylcholinesterase, this turns off the mechanism and stops muscle spams.
27
What are T tubules
Extensions of surface membrane that go into the muscle fibers that are internal stores of calcium. AP triggered at neuromuscular junction travels into the muscle fiber via T tubule. These are linked to a sarcoplasmic reticulum which surrounds myofibrils and contains calcium (needed for cross bridging)
28
Three factors effecting contractile force
Muscle length relationship, Summation and motor unit recruitment
29
Muscle length tension relationship
Amount a muscle can contract is dependent on its length, maximal contraction potential being at is resting length (optimal crossing over of actin and myosin) At longer muscle lengths there are fewer cross over sites and therefore fewer sites for binding (contraction force will be less). At shorter muscle length actin starts to overlap reducing opportunity for interaction with myosin head and myosin are pushed up against Z lines limiting further shortening.
30
Summation of action potentials
Single AP generates short twitch (contraction). In order to generate longer contractions multiple APs need to arrive from the motoneuron in close succession. If this happens, the contraction summates with the previous contraction resulting in greater contraction. If a very high number of APs arrive the muscle can reach its maximal contraction, this is referred to as tetanus.
31
G protein mediated activation of the IP3/PKC pathway
1. The G protein receptor is activated by the neurotransmitter, activating the G protein, which in turn activates the enzyme phospholipase C (the effector protein) 2. Phospholipase C splits a membrane lipid, PIP2, into IP3 … 3. … and DAG (the second messengers) 4. IP3 triggers release of Ca2+ into the cell, which activates a kinase, calmodulin. DAG activates protein kinase C 5. Calmodulin and protein kinase C phosphorylate other proteins to create a cellular effect
32
G protein mediated activation of the adenylate cyclase/PKA pathway
1. The G protein receptor is activated by the neurotransmitter, activating the G protein, which in turn activates the enzyme adenylate (adenylyl) cyclase (the effector protein). 2. Adenylate cyclase converts ATP into cAMP (the second messenger) 3. cAMP activates protein kinase A 4. Protein kinase A phosphorylates a protein, changing its shape and activity 5. The activated protein generates the cellular response
33
What is tetanus
Sustained maximal contraction, caused by rapid arrival of action potentials meaning the muscle does not have time to rest.