Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
64 Cards in this Set
- Front
- Back
|
Describe the structure and function of the most basic neuron. |
Dendrite > Receive signals Soma > Contains the nucleus Axon hillock > Initiate signal Axon > Conduct signal Synapse > Communicate signal between two cells |
|
|
General form of the synapse:
|
Presynaptic terminal; Mitochondria; Synaptic vesicle (packets of neurotransmitters); Presynaptic density (collection of proteins for locating, exocytosis and recycling synaptic vesicles); Synaptic cleft (gap between pre/post synaptic membranes |
|
|
General form of the dendrites |
Origin in the soma; can be covered in small spines; Majority of neuron area of synaptics |
|
|
In what order does an action potential propagate down a neuron? |
Synapse > Dendrite > Soma > Axon hillock > Axon > Synapse |
|
|
General form of the Axon |
Originates from axon hillock; No or few branches until terminal end; produce synaptic outputs |
|
|
Describe the structure and function of the cell membrane |
It has a biplanar lipid structure non-permeable to ions and the direction and rate of ion movement on charge, chemical gradient of the ion and electrical charge distribution across membrane. |
|
|
Describe the characteristics of ion channels |
Neuronal potentials rely on ion diffusing through ion channels and the permeability of a channel is based on ion selectivity by charge or size. |
|
|
What is the resting membrane/action potentials based on? |
Resting membrane potentials are based on ion channels permeable to Na, K and Cl ions. Action potentials are based on voltage gated ion channels of Na (upstroke) and K (downstroke). Each ion needs its own specific channel. |
|
|
What are synaptic potentials based on? |
Based on ligand gated ion channels. Neurotransmitters get released into the synaptic terminal > bind to the post synaptic receptor sites > opens up integrated ion channel that is simliar to the one that is bound on the receptor > new action potential is generated. Flow through channels depends on concentration and electrical gradient across the membrane. |
|
|
What is Ohms law? |
V = IR or I/G where G is conductance in siemens |
|
|
What is the ion distribution of the K, Na, Cl, and Ca? |
Outside Inside Ionic equilibrium (mV) K 5 100 -80 Na 150 15 62 Cl 150 13 -65 Ca 2 0.0002 123 |
|
|
What is the resting membrane potential range/ what controls it? |
Range is in between -90 -> -45 range and K controls RMP since the permeability of K is high and the ratio of the concentration is high. Increasing extracellular K will depolarise the RMP in K. |
|
|
What are glial cells used for? |
Glial cells buffer changes by storing K and distributing it elsewhere through gap junctions between the glial cells. |
|
|
What are ion pump proteins? |
Ion pump proteins maintain the ion gradient by pumping proteins; Na-K ATPase maintains RMP by moving 3 Na out for every 2 K in. (70% of ATP used)
Ca pump also uses ATP to move Ca out of cytoplasm into internal stores. Cl ions distribute passively but can be transported by Cl cotransporter. |
|
|
How is the RMP maintained? |
Maintained by the flux K, Na, and Cl through non-voltage dependent channels and this ion flux is opposed by ion exchanger pumps. The RMP is the balance between flux and pump activity. |
|
|
What does the RMP set? |
The RMP sets the distance from the action potential threshold and is the driving force for all ion movement.
|
|
|
Small changes in RMP occurs when small changes in ion concentration. True or False? |
False. Large changes in RMP occurs when small changes in ion concentration. Moving the RMP a lot doesn't do a lot to ions. |
|
|
What is the ionic driving force? |
The fact that ions move across the membrane at rate dependant on the RMP and E(ion). |
|
|
Describe the electrical movement in terms of current flow. |
Positively charged ions move into cell, the cell becomes more positive (inward current) and positively charged ions moving out cause the cell to be negative (outward current). Inward > depolarisation Outward > hyperpolarisation |
|
|
What sort of balance of charge is on the inside/outside and why? |
There is a net negative charge on the inside of the cell and net positive charge on the outside of the cell due to the ions on the inside of the cell being large -ve molecules which can't cross the membrane. |
|
|
How do action potentials occur? part 1 |
AP's fired from the soma/axon hillock > Depolarisation happens when resting potential (-60mV) is raised to the threshold (-40mV) > This is due to the integrated sum of responses to all active synaptic inputs |
|
|
How do action potentials occur? part 2 |
Voltage gated ion channels (Na and K) open > Rising phase is due to the opening of the Voltage gated Na channels leads to positive feedback loop of Na voltage gated channels opening > leads to strongly depolarising the cell (momentary positive charge) {Membrane potential moves towards the ionic equilibrium for Na} |
|
|
How do action potentials occur? part 3 |
K channels prevent the MP from reaching the E(Na) > at the AP peak, Na deactivate and no more will open while K channels are open > gradient of Na falls while gradient of K rises (causes undershoot) |
|
|
What does conduction velocity depend on? |
Myelination (Schwann cells {PNS} and oligodendrocytes {CNS}) Axon diameter - wider diameter - faster speed |
|
|
General knowledge about myelination |
> Membrane capacitance is low areas of myelination.
> Nodes of Ranvier allow 'jumping' of the current (saltatory connection) > Few ions channels underneath the myelin sheath > Loss of myelination causes poor nerve impulse conduction (Multiple sclerosis, acute demyelination polyneuritis) |
|
|
What are electrical synapses?
|
> ES allow the flow of electrical current between cells > Flow through connexons (protein ion channels which cross and intercellular gap called a gap junction) > Connexons can allow ions and small molecules > Transmission is fast, bidirectional and failsafe > Uncommon in adult brain but found in cardiac and smooth muscle, glial cells > Opening of connexons can be modulated by Ca levels (low = open, high = closed) |
|
|
What are neurotransmitters? |
Chemicals which relay, amplify and modulate electrical signals between neurons and other cells |
|
|
What conditions must be met for a chemical to be classified as a neurotransmitter? |
> Synthesized endogenously (within the presynaptic neuron) > Availible in sufficient quantity to exert effects on the postsynaptic neuron > Mimic the endogenously-released substance if externally administered > A mechanism for inactivation must be present (clearing the synaptic cleft) |
|
|
What are the two receptors that neurotransmitters act on? |
Ligand gated ion channels and G-protein coupled receptors |
|
|
How do ligand gated ion channels work? |
Neurotransmitter that is excocytosed from pre-synaptic terminal binds to the receptor on the post-synaptic terminal and opens up an integral ion pore |
|
|
How do G-protein coupled receptors work? |
Once neurotransmitter binds to the binding site on the G-protein coupled receptor, activate separate G proteins that once active will then activate other effector proteins (ion channels or enzymes that synthesize different second messenger molecules) |
|
|
What is the difference between Ligand gated ion channel receptors and G-protein coupled receptors? |
LGIC are generally more swift following the release of the neurotransmitter whereas G-protein coupled receptors have a significant delay of a response. |
|
|
What are the three main neurotransmitter groups that make up neurotransmitters? |
Amino acids (Glutamate {EXCITE}, Glycine {INHIB}, GABA {INHIBI}) Amines (ACh {fast excitatory synaptic transmission at all Neuromuscular junctions}, Dopamine, Adrenaline, Noradrenaline, Serotonin, Histamine) |
|
|
What are the basic functions of neurotransmitters? |
All of them mediate slow synaptic transmission at central and peripheral synapses.
Many synapses have both peptides and amines/amino acids and can release both. |
|
|
What are the basic steps of neurotransmitter release? |
1) AP enters the presynapse 2) Depolarisation opens voltage gated Ca channels which enter the terminal 3) Ca triggers the exocytosis of neurotransmitter from vesicle, diffusion across the cleft 4) Transmitter binds to postsynaptic receptors and opens an ion channel 5) Postsynaptic potential is generated. |
|
|
How does vesicle recycling occur? |
1) Vesicle membrane is endocytosed and refilled with neurotransmitter 2) Filled vesicles are repositioned near active zone (base of the presynaptic terminal) 3) Primed for release through ATP-dependent process 4) Ca entering the cell through closely located voltage gated Ca channels triggers fusion of synaptic vesicle membrane with presynaptic membrane |
|
|
How are neurotransmitters synthesised? |
All except peptides are made in the nerve terminal. Amino Acids/Amines: > Enzymes and precursors are transported to nerve terminal > Subject to feedback inhibition > Can be stimulated increase activity Peptides: >Made from precursor proteins in the cell body > Proteases cleave the precursor into appropriate peptides |
|
|
How are neurotransmitters stored? |
All are packaged into vesicles. Amino acids/Amines: > uptake from cytoplasm into vesicle involves a transporter protein in the vesicle membrane powered by the pH gradient. (inside = acidic, outside = neutral) > Transport can be blocked by drugs that block the neurotransmitter release. Peptides: > Packaged into vesicles that bud off the golgi apparatus in the cell body which are transported along the axon to the terminals |
|
|
How does an AP evoked neurotransmitter get released? |
The influx of Ca into the cell is important, blockage of Ca ion channels or removal of extracellular Ca stops the neurotransmitter being released. AP > Ca enters cell > binds to synaptotagmin protein > synaptotagmin allows the vesicle to fuse > release of NT occurs |
|
|
How do synaptic potentials increase? |
They increase in unitary steps. A miniature postsynaptic potential is called a quantum, and a multiple of that single miniature potential leads to larger responses. |
|
|
Most synapses spontaneously release single neurotranmitters without the need of an AP. True or False? |
True. The release of singular vesicles is called a quantum. A synaptic potential contains at least 1 quantum but can have more. |
|
|
Describe how a receptor can be desensitised. |
Receptors are desensitized if a NT is present for a period of time. NT have to be cleared to avoid desensitization. |
|
|
How does a receptor get cleared? |
1) Diffusion into extracellular space. 2) Re-uptake into the nerve terminal through transporters > repackaging/enzymatic breakdown 3) Uptake into glial cells by NT transporters 4) Enzymatic breakdown in synaptic cleft > ex: Acetlycholinesterase breaks down ACh very quickly (nerve gases, pesticides) |
|
|
Describe the general characteristics of ligand gated ion channels. |
> Fast electrical response following the binding of a NT to the receptor site. > Ligand gated ion channels exist for: 1) All amino acid NT 2) Some Amines (ACh acting on Nictonic ACh receptors or Seratonin acting on 5-HT3 receptors) 3) ATP acting on P2x receptors |
|
|
What is an EPSP/EPCP? |
EPSP = excitatory postsynaptic potential EPCP = excitatory postsynaptic current Net effect is depolarisation so excitatory (pushed to threshold) They rely on ligand gated channels permeable to Na, K and sometimes Ca. |
|
|
What types of receptors produce an EPSP? |
Glutamate and nicotinic ACh receptors. (sometimes also ATP P2x and 5TH3 receptors. |
|
|
Properties of ionotropic glutamate receptors: |
The main excitatory NT in the CNS (90%) 4 protein subunits around the pore (lets Na, K, and sometimes Ca through) Three types named after activating chemicals: 1) AMPA: fast rising and falling electrical responses (sometimes Ca) 2) NMDA: slow rising and falling electrical response (always Ca but can be blocked by Mg unless a strong MP is present) 3) Kainate: similar to AMPA. |
|
|
Properties of Inhibitory Postsynaptic potentials an currents: |
Channels are permeable to Cl Hyperpolarisation == inhibitory Inhibitory postsynaptic potentials (IPSPs) are driven by outward current (IPCP) Main types are: GABA and Glycine receptors |
|
|
Properties of GABA, Glycine and Nicotinic receptors: |
Share a common structure (5 protein subunits with a central ion pore) Subunit types alpha, beta, and others in combinations. Different combinations influence channel behavior. Nicotinic permeable to all major cations (Na, Ca, K) GABA and Glycine permeable to Cl. |
|
|
Properties of GABA receptor: |
Many sites for binding of drugs and endogenous factors that affect receptor activity. Target for sedatives which increase GABA currents. Endogenous factors include steroid hormones (progesterone, corticosteroids, testosterone) |
|
|
Characteristics of G-protein coupled receptors: |
Slow synaptic transmission due to delayed activation and long duration. Called metabotropic receptors. (ionotropic == ligand gated) Can open g-protein gated ion channels (K ions)or regulate protein phosphorylation. |
|
|
What is summation? |
Summation is when more than one vesicle is released at a time which leads to summation of many excitatory and inhibitory inputs that leads to an AP threshold being reached in the axon.
It is not a linear process since 1)Dendritic filtering of synaptic as they propogate to the soma 2) Local interactions between potentials - changes in resistance to nearby synapses resulting in threshold being reached more quickly |
|
|
Why is the location of EPSP's and IPSP's important? |
Having a synapse near/on the soma reduces the amount of dendritic filtering occuring and can influence APs. Many neurons have a dense cluster of IPSP's on the soma or at the base of large dendrites. > IPSP's == gatekeeper by hyperpolarizing and shunting the EPSP arriving from distant locations. |
|
|
How does postsynaptic inhibition work? |
Opening of Cl channels can reduce neuronal excitability in two ways: 1) Hyperpolarisation: If RMP is more positive than the ionic equilibrium of Cl, membrane potential will hyperpolarize when Cl channels open.
2) Shunting inhibition: if MP is close to ionic equilibrium, Cl channels will open but MP won't change, and current essentially 'leaks out' therefore shunting the excitatory response. |
|
|
How does presynaptic inhibition work? |
Three synapses are involved. Synapse 1 (axo-axonic synapse) controls Synapse 2 which in turn Synapse 3. By releasing inhibitory neurotransmitters that bind to receptors on synapse 2, synapse 1 controls the the nuerotransmitter release of synapse 2. This works by decreasing excitability in the 2nd synapse by opening K and Cl channels while reducing the number of Ca channels. |
|
|
Difference between pre and post synaptic inhibition? |
Presynaptic inhibition is a more fine control since it controls singular synapses while post synaptic inhibition can control/stop the excitatory response of multiple synapses. |
|
|
Individual synaptic inputs determine whether a neuron fires an AP or not. True or False? |
False. Individual synaptic input rarely determines whether or not a neuron fires an AP. The important thing is that how many synaptic inputs are active over a period of time and relative timing of activation. |
|
|
What is spatial/temporal summation? |
Spatial: Lots of synapses at different locations on the dendritic tree firing that leads to an AP in the post synapse. Temporal: Constant firing of single presynaptic terminal that leads to the post synaptic neuron to reach threshold and fire an AP. |
|
|
What is short term synaptic plasticity? |
Synaptic potentials change when a single neuron is reactivated quickly. (activation needs to be infrequent for it to return to its original amplitude) If it amplitude gets bigger as signals continue (synaptic facilitation) If amplitude gets smaller as signals continue (synaptic depression) |
|
|
What is long term plasticity? |
Refers to the Hebbian model stating that if cell a consistently fires cell B, connection between the cells will be strengthened which is how we learn (memory) |
|
|
What is LTP and LTD? |
LTP == long term potentiation is the persistent increase in synaptic response induced by high frequency stimulation. LTD == Long term depression is the opposite of LTP |
|
|
What is the significance of the hippocampus? |
Removal or damage of the hippocampus can impair memory formation but has no affect on the memory formed prior to the accident. |
|
|
What is necessary for LTP induction? |
Tetanic stimulation is needed for LTP induction. It results in depolarisation due to summation of evoked EPSPs. Only synapses stimulated during the tetanus undergo LTP |
|
|
How does maintenance of LTP occur? |
1) immediate increase in CA1 inputs over 2-3 hours due to s h i t |
