Nervous System Flashcards
What are axodendritic, axosomatic, and axoaxonic synapses?
-Axodendritic: connecting w the dendrites
-Axosomatic: connecting w the soma/cell body
-Axaoxonic: connecting w the synapse btw two other neurones, often inhibitory, it can block/ cancel out signal
What is Dales law?
Neurons will use the SAME neurotransmitter at all of its synapses
What is the difference between Type I and II synapses?
Type I has asymmetrical membranes and is excitatory
Type II has symmetrical membranes and is inhibitory
What is labelled line code?
each sensory neuron encodes only one stimulus modality
What is rate code?
stimulus intensity encoded by firing rate
What is population code?
stimulus intensity encoded by rate and population code
.# of axons activated can also encode information abt stimulus strength
What is timing code?
central neurons may use spike timing codes as well as spike rate codes for representing information
What is temporal summation?
- A typical input on its own is not enough to activate AP
- If memebrane A is active just once, there is 1 depolarization and it does reach threshold
- If you activate A in quick sucession before it can go to rest then the inputs ‘add up’ or ‘sum’ and may be enough to trigger AP
Detects high frequency firing by upstream neurons
What is spacial summation?
- Activation of A on its own is not enough for AP, and same for B (not enough on its own)
But if A and B are together, happens at same time, then they are enough
Detects coincident firing of upstream neurons
What is inhibition summation?
- activity in synapse C prevents simultaneous activity in A & B from generating an impulse
Enables upstream neurons to prevent downstream firing
What are some main differences between NMJ and central synapses
- NMJ has 1 presynaptic neuron per muscle fibre, vs central has many converging onto one post-syanptic neuron
- NMJ has a ‘safety factor’ vs central has integration
- NMJ’s main NT is ACh, vs central uses lots of different NT
- NMJ EPP is excitatory, vs central can be excitatory or inhibitory
- NMJ AP frequency and the number of recruited fibers determine contraction strength, vs central AP frequency, AP timing, and neuronal identity are important for central representation of information
Where is glutamate synthesised?
- Synthesised in the presynaptic terminal
How is glutamate released?
- Loaded into vesicles in the presynaptic terminal and then released during AP
- Its taken back up by transporters or glilal cells that convert glutamate into glutamine then back to glutamate
How is glutamate/glutamine broken down?
Glutamate turned into glutamine by glutamate synthase in glilal cell
Glutamine broken by phosphate activated glutaminase (turns glutamine to glutamate) in presynaptic terminal
How do ionotrophic glutamate receptors cause excitation?
- Needs spacial summation
- When glutamate binds it triggers Na and K channels to open
(influx of Na and efflux of K)
At typical resting potential, membrane potential is driven towards eq potential= suggests excitatory response
What do AMPA receptors mediate?
The fast component of glutamatergic synaptic current
What do NMDA receptors mediate?
The slow component of glutamatergic synaptic current
AP5 is an antagonist of NMDA receptor and blocks slow component
What are the effects of glutamate on AMPA and NMDA receptors?
AMPA: when glutamate binds, channel opens
NMDA: when glutamate binds, channel opens but Mg2+ blocks channel and only leaves during depolarization
What is the difference between ionotrophic glutamate receptors and metabotrophic glutamate receptors?
- Ionotropic glutamate receptors (iGluRs): membrane ion channels that are gated by glutamate
- Metabotropic glutamte receptors (mGluRs): seven transmembrane domain proteins that couple to G proteins
What evidence suggests that glutamate is important in membrane and plasticity?
- High densities of channels activated by glutamate are found in brain regions associated with learning and memory function
- Mg2+-dependent block enables NMDA receptors to act as coincidence detectors for associative memory
- Block of NMDA receptors by intraventricular infusion of AP-V prevents learning
- Drugs that block the action of glutamate inhibit learning and memory
- Drugs that potentiate the actions of glutamate enhance learning and memory
Whats the difference between cholinergic and glutamatergic synaptic transmission?
Cholingeric: uses nicotinic (Na/K) and muscarinic (G-protein) receptors
Glutamatgeric: uses AMPA (Na/K), NMDA (Na/K/Ca), and mGluR (G-protein) receptors
What are the two main inhibitory neurotransmitters?
GABA
Glycine
GABA and glycine both mediate fast synaptic inhibition through activation of ionotropic receptors.
How is GABA synthesised?
Synthesised from glutamate by glutamic acid decarboxylase in the presynaptic terminal
Released via vesicles into the post-synaptic terminal and then into glilal cells and recycled in the presynaptic terminal
How is GABA broken down?
Broken down in the TCA cycle to glutamate then glycine
What would happen if too much or too little GABA regulation were to occur?
Too much regulation would cause seizures
Too little regulation would cause brain dead
GABA is inhibitory, regulation of inhibition is important
How do GABA receptors cause inhibition?
When GABA binds, Cl- channels open
What is the difference between GABAa and GABAb?
GABAa: ionotrophic (fast), mediates Cl channels
GABAb: metabotrophic (slow), mediates Ca channel closure and K channel opening
Ca2+ channel closure - inhibition of transmitter release.
K+ channel opening- slow IPSP.
Baclofen is a selective GABAB receptor agonist, while 2-hydroxy-saclofen is a selective GABAB receptor antagonist
What does strychnine do?
- competitive antagonist that binds to the α subunit of GABAa receptor (posion if swallowed)
- causes convulsions and asphyxia
What drugs target GABAa receptor and what effects do they have?
Benzos: anxiolytics, anti-convulsants
Ethanol:
Barbiturates:
Neurosteroids:
Benzodiazepines potentiate the action of GABA at GABAA receptors by increasing the probability that the channel opens following the binding of GABA. Only GABAA receptors that contain a γ subunit (in addition to α and β subunits) show potentiation by benzodiazepines. Make amplitude of synaptic current larger, and makes the duration of the synaptic conducters change longer as well
Whats the difference between glycine and GABA synaptic transmission?
Glycine: Cl- channels
GABA: GABAa (Cl-) and GABAb (G-protein)
Whats the difference between glycine and GABA synaptic transmission?
Glycine: Cl- channels
GABA: GABAa (Cl-) and GABAb (G-protein)
