Nervous Coordination Flashcards
(53 cards)
1
Q
Neurones
A
Specialised cells adapted to rapidly carrying electrochemical changes called nerve impulses
2
Q
Resting Membrane Potential
A
- When neurone isn’t being stimulated, outside of membrane is more positively charged
- More positive ions outside of cell
- Voltage when membrane at rest
3
Q
Movement of sodium and potassium ions
A
- Resting potential is created and maintained by sodium-potassium pumps and potassium ion channels in a neurone’s membrane
- Sodium-potassium pumps use active transport to move 3 sodium ions out of the neurone for every 2 potassium ions moved in (ATP needed)
- Potassium ion channels allow facilitated diffusion of potassium ions out of the neurone, down their concentration gradient
- Sodium-potassium pumps move sodium ions out of the neurone, but the membrane isn’t permeable to sodium ions, so they can’t diffuse back in (creates a sodium ion electrochemical gradient because more positive sodium ions outside cell than inside)
- Sodium-potassium pumps also move potassium ions in to the neurone
- When the cell’s at rest, most potassium ion channels are open
- Means that the membrane is permeable to potassium ions, so some diffuse back out through potassium ion channels
- In total, more positive ions move out of cell
- Phospholipid bilayer of axon plasma membrane prevents sodium and potassium ions diffusing across it
4
Q
Sequences that lead to an action potential
A
- Stimulus= excites neurone cell membrane, causing sodium ion channels to open. Membrane becomes more permeable to sodium, so sodium ions diffuse into the neurone down the sodium ion electrochemical gradient. Makes inside of the neurone less negative.
- Depolarisation= if potential difference reaches threshold,more sodium ion channels open so more sodium ions diffuse into the neurone.
- Repolarisation= (+30mV) sodium ion channels close and potassium ion channels open. Membrane is more permeable to potassium so potassium ions diffuse out of the neurone down the potassium ion concentration gradient. This starts to get the membrane back to its resting potential.
- Hyperpolarisation= potassium ion channels are slow to close so there’s a slight ‘overshoot’ where too many potassium ions diffuse out of the neurone. Potential difference becomes more negative than the resting potential.
- Resting potential= ion channel are reset. Sodium-potassium pump returns the membrane to its resting potential by pumping sodium ions out and potassium ions in, and maintains the resting potential until the membrane’s excited by another stimulus.
5
Q
Why are sodium-ion channels voltage-gated?
A
Only open when the potential difference reaches a certain voltage
6
Q
Refractory Period
A
- After an action potential, the neurone cell membrane can’t be excited again straight away
- This is because the ion channels are recovering and they can’t be made to open-sodium ion channels are closed during repolarisation and potassium ion channels are closed during hyperpolarisation
- Period of recovery is called the refractory period
- Refractory period acts as a time delay between one action potential and the next (makes sure action potentials don’t overlap and are discrete impulses)
- Also means there is a limit to the frequency at which the nerve impulses can be transmitted, and that action potentials are unidirectional (they only travel in one direction)
7
Q
Passive and active process
A
- Resting potential is maintained by active transport (active)
- Action potential= movement of sodium ions due to diffusion (passive)
8
Q
Waves of depolarisation
A
- When an action potential happens, some of the sodium ions that enter the neurone diffuse sideways
- Causes sodium ion channels in the next region of the neurone to open and sodium ions diffuse into that part
- Causes a wave of depolarisation to travel along the neurone
- Wave moves away from the parts of the membrane in the refractory period because these parts can’t fire an action potential
- K+ channels open and Na+ channels close
9
Q
All-or-nothing principle
A
- Once threshold is reached, an action potential will always fire with the same change in voltage, no matter how big the stimulus is
- If threshold isn’t reached, an action potential won’t fire
- Bigger stimulus won’t cause a bigger action potential but it will cause them to fire more frequently
- Different neurones have different threshold values
- This principle stops the brain from getting over-stimulated by not responding to very small stimuli
10
Q
Factors that affect speed of conduction
A
Myelination, salatory conduction, axon diameter and temperature
11
Q
Myelination
A
- Some neurones are myelinated (have myelin sheath which is an electrical insulator)
- In the peripheral nervous sytem, the sheath is made of a type of cell called a schwann cell
- Between schwann cells are tiny patches of bare membrane called the nodes of Ranvier
- Sodium ion channels are concentrated at the nodes of Ranvier
12
Q
Structure of a myelinated motor neurone
A
- Dendrons= extensions of cell body which subdivide into dendrites that carry nerve impulses towards cell body.
- Schwann cells= surround axon, protecting it and providing electrical insulation. Carry out phagocytosis and play a part in nerve regeneration. Schwann cells wrap around loads so layers of membrane build up.
- Axon= single fibre that carries nerve impulses away from cell body.
- Cell body= associated with production of proteins and neurotransmitters.
13
Q
Saltatory Conduction
A
- In a myelinated neurone, depolarisation only happens at the nodes of Ranvier (where sodium ions can get through the membrane)
- Neurone’s cytoplasm conducts enough electrical charge to depolarise the next node, so the impulse ‘jumps’ from node to node
- Known as saltatory conduction and it’s really fast
- In a non-myelinated neurone, the impulse travels as a wave along the whole length of the axon membrane (so you get depolarisation along the whole length of the membrane)
- This is slower than saltatory conduction
14
Q
Axon diameter
A
- Action potentials are conducted quicker along axons with bigger diameters beacuse there’s less resistance to the flow of ions than in the cytoplasm of a smaller axon (less leakage of ions and leakage makes membrane potentials harder to maintain)
- With less resistance, depolarisation reaches other parts of the neurone cell membrane quicker
15
Q
Temperature
A
- Energy for active transport comes from respiration which is controlled by enzymes (as well as sodium-potassium pump)
- Enzymes function rapidly at higher temperatures up to a point (can denature)
- Ions can diffuse quickly at higher temperatures
- Temperature also affects speed and strength of muscle contractions
16
Q
Myelin sheath as electrical insulator
A
- Preventing an action potential forming in the part of axon covered in myelin (increases speed of conductance)
17
Q
Hormonal system VS Nervous system
A
18
Q
What is a synapse?
A
- Junction between a neurone and another (or effector cell)
- Space between synapse is called the synaptic cleft
- Presynaptic neurone has a swelling called a synaptic knob (possesses many mitochondria and endoplasmic reticulum that helps make neurotransmitters)
- Contains synaptic vesicles filled with chemicals called neurotransmitters (made in presynaptic neurone)
19
Q
Effect of an action potential
A
- Causes neurotransmitters to be released into the synaptic cleft
- They diffuse across to the postsynaptic membrane and bind to specific receptors
- When neurotransmitters bind to receptors they might trigger an action potential (in a neurone), cause muscle contraction (muscle cell), or cause hormone to be secreted (gland cell)
- Because receptors are only on the postsynaptic membranes, synapses make sure impulses are unidirectional (can only travel in one direction)
- Neurotransmitters are removed from the cleft so the response doesn’t keep happening (taken back into presynaptic neurone or broken down by enzymes-products taken back into neurone)
20
Q
Nerve impulse across cholinergic synapse
A
- Action potential arrives at synaptic knob
- Voltage-gated ion channels open
- Calcium ions diffuse into the synaptic knob (pumped out afterwards by active transport)
- Calcium ions cause the synaptic vesicles to move to and fuse with the presynaptic membrane
- Acetylcholine released by exocytosis
- Acetylcholine diffuses across cleft
- Acetylcholine binds to the receptor sites on the sodium ion channels in the postsynaptic membrane (complementary)
- Sodium channels open
- Sodium ions diffuse across post synaptic membrane into postsynaptic neurone (excitatory postsynaptic potential created)
- EPSPs can combine, reaching the threshold potential
- New action potential created in the postsynaptic neurone
- ACh removed from synaptic cleft so response doesn’t keep occuring
- Broken down by acetylcholinesterase and products are re-absorbed back into presynaptic neurone, ready to make more ACh
21
Q
Exocytosis
A
Vesicle inside cell moves to the cell-surface membrane, fuses with the membrane and releases its contents outside the cell
22
Q
Depolarise
A
Making potential difference across the neurone membrane more positive
23
Q
Hyperpolarise
A
Making potential difference across the membrane more negative
24
Q
Acetylcholine
A
Both excitatory and inhibitory neurotransmitter
25
Excitatory neurotransmitters
Depolarise the postsynaptic membrane, making it fire an action potential if the threshold is reached
26
Inhibitory neurotransmitters
Hyperpolarise the postsynaptic membrane, preventing it from firing an action potential
27
Inhibition
* Synapse where **inhibitory neurotransmitters** are released from the presynaptic membrane following an action potential is called an **inhibitory synapse**
* Presynaptic neurone releases a type of neurotransmitter that **binds** to **chloride ion protein channels** on the postsynaptic neurone
* The neurotransmitter causes the chloride ion protein channels to **open**
* Cl- move into the postsynaptic neurone by **facilitated diffusion**
* The binding of the neurotransmitter causes the opening of nearby potassium protein channels
* Potassium ions move out of the post-synaptic neurone into the **synapse**
* Combined effect of **negatively charged chloride ions moving in** and **positively charged potassium moving out** is to make the inside of the postsynaptic membrane more negative and the outside more positive
* Called **hyperpolarisation** and makes it less likely that a new action potential will be created beacuse a larger influx of sodium ions is needed to produce one
28
Summation at synapses
* If a stimulus is **weak**, only a **small amount** of **neurotransmitter** will be released from a neurone into the synaptic cleft
* Might not be enough to **excite** the **postsynaptic membrane** to the threshold level and stimulate an action potential
* **Summation** is where the effect of neurotransmitters released from many neurones (or one neurone that's stimulated a lot in a short period of time) is **added together**
* Means synapses **accurately** process information, **finely tuning** the response
29
Spatial summation
* Where **2** or **more** presynaptic neurones release their neurotransmitters at the **same time** onto the **same postsynaptic neurone**
* The **small amount** of neurotransmitter released from each of these neurones can be enough **altogether** to reach the **threshold** in the postsynaptic neurone and trigger an **action potential**
* If some neurones release an **inhibitory neurotransmitter** than the total effect of all the neurotransmitters might be **no action potential**
30
Temporal summation
* Where **2** or **more** nerve impulses arrive in **quick succession** from the **same presynaptic neurone**
* Makes an action potential **more likely** because more neurotransmitter is released into the synaptic cleft
31
Neuromuscular junctions
* **Specialised cholinergic synapse** between a **motor neurone** and a **muscle cell**
* Neuromuscular junctions use the neurotransmitter **acetylcholine**, which binds to cholinergic receptors called nicotinic cholinergic receptors
32
Similarities and differences of cholinergic synapse and neuromuscular junctions
**_Similarities_**
* Both release ACh from vesicles in the presynaptic membrane
* ACh then diffuses across the synaptic cleft and binds to cholinergic receptors on the postsynaptic membrane (triggers action potential if threshold is reached)
* Also in both, ACh is broken down in the synaptic cleft by the enzyme AChE
* Use a sodium-potassium pump to repolarise axon
* Have neurotransmitters that are transported by diffusion
**_Differences_**
* N.J: Postsynaptic membrane has lots of folds that form clefts (these store AChE)
* N.J: Postsynaptic membrane has more receptors than other synapses (ACh binds to receptors on membrane of muscle fibre)
* N.J: ACh is always excitatory, so when a motor neurone fires an action potential, it normally triggers a response in a muscle cell (isn't always the case for a synapse between 2 neurones)
33
Drugs at synapses
* Some drugs are the **same shape** as neurotransmitters ao they **mimic** their action at **receptors** (these drugs are called **agonists**)-means more receptors are activated
* Some drugs **block** receptors so they can't be activated by neurotransmitters (these drugs are called **antagonists**)- means fewer receptors (if any) can be activated
* Some drugs **inhibit** the **enzyme** that **breaks** down **neurotransmitters** (means more neurotransmitters in synaptic cleft bind to receptors and they're there for longer)
* Some drugs **stimulate** the **release** of **neurotransmitter** from the presynaptic neurone so more receptors are activated
* Some drugs **inhibit** the **release** of **neurotransmitters** from the presynaptic neurone so fewer receptors are activated
34
Smooth muscle
* Contracts without conscious control
* Found in walls of internal organs apart from heart e.g. stomach, intestine and blood vessels
35
Cardiac muscle
Contracts without conscious control (like smooth muscle) but it's only found in the heart
36
Skeletal muscle
(also called striated, striped or voluntary muscle) is the type of muscle you use to move e.g. the biceps and triceps move the lower arm (conscious)
37
Role of skeletal muscle
* **Skeletal muscles** are attached to **bones** by **tendons**
* **Ligaments** attach bones to other bones, to hold them together
* Pairs of skeletal muscles contract and relax to **move bones** at a joint-the bones of the skeleton are **incompressible** (rigid) so act as levers, giving muscles something to pull against
* Muscles that work together to move a bone are called **antagonistic pairs**
* The **contracting muscle** is called the **agonist** and the **relaxing muscle** is called the **antagonist**
* When your bicep contracts your triceps relaxes (pulls the bone so arm bends at elbow)
* Biceps are agonist and triceps are antagonist
* When triceps contract and bicep relaxes, this pulls the bone so your arm straightens at the elbow
* Triceps is agonist and biceps is antagonist
38
Structure of skeletal muscle
* Skeletal muscle is made up of **large bundles** of **long cells**, called **muscle fibres** (**cell membrane** of muscle fibre is called **sarcolemma**)
* Bits of the sarcolemma **fold inwards** across the muscle fibre and stick into the sarcoplasm (muscle cell's cytoplasm)
* These folds are called **transverse tubules** and help spread **electrical impulses** throughout the sarcoplasm so they reach all parts of the muscle fibre
* A network of internal membranes called the **sarcoplasmic reticulum** runs through the sarcoplasm
* Sarcoplasmic reticulum stores and releases **calcium ions** that are needed for muscle contraction
* Muscle fibres have lots of **mitochondria** to provide the **ATP** that's needed for muscle contraction
* They are **multinucleate** (contain many nuclei) and have lots of long, cylindrical organelles called myofibrils
* **Myofibrils** are made up of **proteins** and are highly specialised for contraction (organelles within the muscle fibre cell)
* Individual muscles are made up of millions of tiny muscle fibres called myofibrils (parallel to maximise force)
* Muscle fibres share nuclei and cytoplasm called sarcoplasm
39
Examination of muscle under optical microscope
* What you see depends on how you have stained your sample
* Longitudinal cross-sections are taken along the length of a structure, whereas transverse cross-sections cut through the structure at a right angle to its length
40
Myofibrils
* Contain bundles of **thick** and **thin myofilaments** that move past each other to make muscles contract
* **Thick** myofilaments are made of the protein **myosin** (long-rod shaped tails with bulbous heads on side) and the **thin** myofilaments are made of the protein **actin** (2 strands twisted around one another)
* **Dark bands** contain thick myosin filaments and some overlapping thin actin filaments (**A-bands**)
* **Light bands** contain thin actin filaments only (**I-bands**)
* Thick and thin filaments **don't overlap**
* A myofibril is made up of many short units called **sacromeres**
* The ends of each sacromere are marked with a **Z-line**
* In the middle of each sacromere is an **M-line**
* M-line is the **middle** of the **myosin filaments**
* Around the M-line is the **H-zone**
* H-zone **only** contains **myosin filaments**
41
Sliding filament theory (muscle contraction)
* **Myosin** and **actin filaments** slide over one another to make the **sacromeres contract**- myofilaments themselves don't contract
* The simultaneous contraction of lots of sacromeres means the **myofibrils** and **muscle fibres** contract
* Sacromeres return to their **original length** as the muscle **relaxes**
* **I-band** becomes **narrower**
* **Z-line** move **closer together** (sacromere shortens)
* **H-zone** becomes **narrower**
* **A-band** remains **same width**
* Width of this band is determined by length of myosin filaments, myosin filaments don't go shorter
* Discounts the theory that muscle contraction is due to filaments themselves shortening
42
Myosin filaments
* (head and tail) Have globular heads that are hinged, so they can move back and forth
* Each myosin head has a binding site for actin and a binding site for ATP
43
Actin filaments
* (globular protein, chains twisted around) Have binding sites for myosin heads, called actin-myosin binding sites
* Another protein called tropomyosin is found between actin filaments
* Helps myofilaments move past each other
44
Binding sites in resting muscles
* For myosin and actin filaments to **slide** past each other, the **myosin head** needs to **bind** to the **actin-myosin binding site** on the **actin filament**
* In a **resting** (unstimulated) muscle the actin-myosin binding site is **blocked** by **tropomyosin**
* This means myofilaments can't slide past each other because the myosin heads can't bind to actin filaments
45
Process of muscle contraction
* **Action potentia**l from a motor neurone stimulates a muscle cell, it **depolarises** the **sarcolemma** (calcium ions diffuse into the synaptic knob, acetylcholine released in synaptic cleft and bind to receptors)
* Depolarisation spreads down the **T-tubules** to the **sarcoplasmic reticulum**
* This causes the sarcoplasmic reticulum to **release stored calcium ions** into the sarcoplasm
* This influx of calcium ions into the sarcoplasm triggers **muscle contraction**
* Calcium ions bind to a **protein** attached to tropomyosin, causing the protein to **change shape** (pulls the attached tropomyosin out of the actin-myosin binding site on the actin filament)
* This **exposes** the **binding site**, which allows the myosin head to bind
* Bond formed is an **actin-myosin cross bridge**
* **Calcium ions** also **activate** the enzyme **ATP hydrolase**, which hydrolyses ATP to provide energy for muscle contraction
* Energy released from ATP causes the **myosin head** to **bend**, which pulls the actin filament along in a kind of rowing action
* Another ATP provides energy to **break** actin-myosin cross bridge, so myosin head **detaches** from the actin filament after it's moved
* The myosin head then returns to it's **starting position**, and **reattaches** to a **different binding site** further along the actin filament
* A new actin-myosin cross bridge is formed and the cycle is repeated (attach,detach)
* Many actin-myosin cross bridges form and break very rapidly, **pulling** the **actin filament** along- which **shorterns** the **sacromere**, causing the muscle to contract
* Cycle will continue as long as calcium ions are present
46
Resting state in muscle contraction
* When the muscle stops being stimulated, calcium ions are **actively transported** back into the **endoplasmic reticulum** using energy from the **hydrolysis** of **ATP**
* This **reabsorption** of the calcium ions allows **tropomyosin** to **block** the actin filament again
* Myosin heads are now unable to bind to actin filaments and contraction ceases (muscle relaxes)
* In this state, force from antagonistic muscles can pull actin filaments out from between myosin (to a point)
47
Aerobic respiration for muscle contraction
* Most ATP is generated via oxidative phosphorylation in the cell's mitochondria
* Only works when there's oxygen so it's good for long periods of low-intensity exercise e.g. long walk
48
Anaerobic respiration for muscle contraction
* ATP is made rapidly by glycolysis
* End product of glycolysis is pyruvate, which is converted to lactate by lactate fermentation
* Lactate can quickly build up in the muscles and cause muscle fatigue
* Good for short periods of hard exercise e.g. 400m sprint
49
ATP-phosphocreatine (PCr) system
* Stored in muscle
* ATP is made by phosphorylating ADP-adding a phosphate group taken from PCr
* PCr is stored inside cells and the ATP-PCr system generates ATP very quickly
* PCr runs out after a few seconds so it's used during short bursts of vigorous exercise e.g. tennis serve
* System is anaerobic and alactic (doesn't form lactate)
* Can't supply energy directly so makes ATP
* Some of creatine gets broken down into creatinine, which is removed from the body via kidneys
* Creatinine levels can be higher in people who exercise regularly and have a high muscle mass
* High creatinine levels also indicate kidney damage
* ADP + PCr = ATP + Cr
50
What is energy used for in muscle contraction?
* Movement of myosin heads
* Reabsorption of calcium ions into the endoplasmic reticulum by active transport
51
What 2 types of muscle fibres are in skeletal muscles?
Slow twitch and fast twitch muscle fibres
52
Slow twitch and fast twitch muscle fibres
**Slow twitch**
* Mitochondria are mainly found near edge of muscle fibres, so there's a short diffusion pathway for oxygen from the blood vessels to the mitochondria
* Numerous mitochondria to produce ATP
* Aerobic to avoid build up of lactic acid which leads to less effective function
**Fast twitch**
* Stores of PCr so energy can be generated quickly when needed
* More powerful contractions
* High concentration of glycogen
* Thicker and more numerous myosin filaments
* High concentration of enzymes involved in anaerobic respiration which provides energy for muscle contraction
53
Active muscle
* Demand for ATP and oxygen
* ATP needs to be generated rapidly
* Achieved by phosphocreatine or glycolysis
