L1: Neurons & Neural Networks I: Regulation of Signalling Flashcards
Describe how the Na+/K+ ATPase Pump establishes a concentration gradient within the cell
- Na/K+ ATPase pump uses ATP to actively pump 3 Na+ ions and 2 K+ ions out and into the cell, respectively
- maintaining a more depolarised internal environment
what role do the sodium and potassium channels play in maintaining membrane potential?
- Na+ channels permit rapid influx of sodium into cell upon opening, with resultant depolarisation (more positive)
- K+ channels permit rapid efflux of Na+ out of cell upon opening with resultant hyperpolarisation (more negative)
what two forces are ions under during the establishing of the membrane potential?
- electrostatic force (dependent on charge)
- force of diffusion (dependent on concentration)
describe the direction of travel within a neuron
- dendrites receive incoming signals
- incoming signals converge at cell body (summation effect, if strong enough AP propagates along axon)
- conveyed along axons to transmit signal in form of action potential (AP) to target neuron
describe the simple neural networks (refer to notes for image)
- e.g. sensory terminals in skin responding to temp/touch
- info classically relayed in a primary afferent via dorsal root ganglion (if for body, below the neck) or trigeminal ganglion (above the neck)
- info relayed via spinal cord and conveyed up to brain through secondary afferent/motor tracts
- most info ends up at thalamus, main sensory nuclei within diencephalon, relayed through a number of different nuclei
- output and response (e.g. motor response)
what is the function of the generator potential?
- function to initiate action potentials in neuronal axon
- associated with non-specific cation channels (letting in any positive ion)
what does it mean that the generator potential is modality specific?
within the skin there are different receptors that respond to different modalities so can understand if it’s e.g. chemoreceptors/mechanoreceptors/thermoreceptors etc.
the generator potential is modality specific for what?
mechanoreceptors (high or low threshold)
thermoreceptors (hot or cold)
chemoreceptors
polymodal receptors (nociceptors)
is the generator potential ‘all-or-nothing’ or graded?
graded potentials
is the generator potential transient?
yes but can be sustained
outline the strengths of the generator potential
localised: info on location of stimulus (where is the stimulus)
graded: info on intensity of stimulus (how strong is stimulus)
outline the limitations of the generator potential
- generated by specific modality but doesn’t convey modality specific info
(i.e. once converted into AP it goes into system and if system goes wrong brain can misinterpret info being from wrong place e.g. touch is painful when it shouldn’t be (allodynia))
Draw an action potential graph and label all (9) steps
- resting membrane potential
- depolarising stimuli
- depolarisation reaches threshold: voltage-gated sodium channels (NaV) open and Na+ ions enter neuron
- rapid Na+ entry depolarises neuron further
- NaV channels inactivate and slower (0.5mS) potassium channels (Kv) open
- K+ ions moves out of neuron
- Kv channels remian open and more K+ ions leave neuron, hyperpolarising it
- Kv channels close, some K+ enters cell through leak channels
- Normal membrane potential
Describe the function and the nature of the action potential
function: carry signal from point to point
- highly specific interaction between NaV and Kv (voltage gated Na+ and K+ channels)
- an ‘all-or-nothing’ event
- very brief event (~2-5ms)
outline the strengths of an action potential
- signal size is maintained over distance and branches
- versatile: frequency and pattern encoding
outline the limitations of an action potential
- membrane must be hyperpolarised to start
- system has to be re-primed (refractory period)
what is excitatory postsynaptic potential (EPSP)?
- postsynaptic potential that makes the postsynaptic neuron more likely to fire an AP
(depolarises postsynaptic cell, bringing membrane potential closer to threshold and so firing an AP)
what is inhibitory postsynaptic potential (IPSP)?
- synaptic potential that makes postsynaptic neuron less likely to generate an AP
- (a temporary hyperpolarisation of postsynaptic neuron caused by flow of negatively charged ions (Cl-) into postsynaptic neuron)
Are EPSPs graded or all or nothing?
graded
the amplitude of EPSPs depend on what factors?
- amount of NT released
- number of receptors
- state of receptors
Decay of EPSP depend on what factors?
- dissociation of ligand
- diffusion and uptake (e.g. glutamate)
- desensitisation (e.g. AMPA-type glu receptors
- enzymatic breakdown (e.g. Ach)
How do EPSPs engage in spatial summation?
- occurs when subthreshold EPSPs, occurring simultaneously at different points along postsynaptic membrane combine to cause depolarisation that reaches threshold of excitation
How do EPSPs engage in temporal summation?
occurs when multiple subthreshold EPSPs from one neuron occur close enough in time to combine and trigger action potential at axon hillock (postsynaptic potentials last for ~ 4milliseconds, while AP last for 2 ms)
What two factors are essential for neurotransmitter release?
- depolarisation of terminal
- presence of Ca2+ ions in extracellular fluid
EPSPs contribute to what and so lead to what?
EPSPs contribute to depolarisation leading to generation of action potential
how fast do EPSPs occur?
- normally fast but slow EPSPs occur
- Fast EPSPs (~10-100ms): associated with activation of ligand-gated non-specific (Na+,K+, Ca2+) cation channels .g. glutamate (AMPA, NMDA), ATP (P2X), Ach (nicotinic)
what are the strength of EPSPs?
- versatile:
- different transmitters can act on same postsynaptic cell using different receptors
- different receptors/ion channels can be regulated independently
- independent postsynaptic and presynaptic control of ‘synaptic strength’
what are the limitations of EPSPs?
- metabolically expensive (e.g. making NTs)
- vulnerable to chemical interference (e.g. drugs) - not always bad, can module how neurons signal and increase e.g. serotonin
function and nature of IPSPs?
- function: prevent depolarisation and inhibit the generation of the action potential (opens anion channels e.g. Cl-)
- graded (not ‘all-or-nothing’)
are IPSPs fast or slow? describe..
- normally fast (but slow IPSPs do occurr)
- Fast IPSPs (~10-500ms): activation of ligand-gated (Cl-) anion channels by GABA(subscript A) receptors or glycine
strengths of IPSPs
- versatile:
- different transmitters can act on the same postsynaptic cell using different receptors (e.g. mixed EPSP & IPSP)
- different receptors/ion channels can be regulated independently
- independent postsynaptic and presynaptic control of ‘synaptic strength’
limitations of IPSPs
metabolically expensive and vulnerable to chemical interference (e.g. drugs and toxins)
Neural networks allow for information to be passed through the nervous system as a result of what?
neuronal convergence and divergence
what is convergence?
one postsynaptic neurons receives signals from multiple presynaptic neurons so it can integrate different inputs to make a decision
what is divergence?
when one presynaptic neuron communicates with multiple postsynaptic neurons coordinating their action in a network
divergence in networks is controlled by what?
interneurons
what is lateral inhibition?
- when a neuron excites inhibitory neurons which then inhibit neighbouring neurons in a network
- e.g. used in retina to provide edge enhancement i.e. important in visual acuity
what is feedforward excitation?
one neuron activates a second neuron which may go on to excite a third and so on (activates a pathway)
what is feedback excitation?
when neuron activated by any of its downstream neurons
- once first neuron in circuit stimulated, circuit is self-perpetuating until neuron is switched off (way to maintain a persistent long-standing response to a brief stimulus)
what is feedforward inhibition?
- neuron stimulates an inhibitory neuron which inhibits the next neuron
- used to shut down a pathway
what is feedback inhibition?
- neuron inhibited any of its downstream neurons
- purpose is to terminate/inhibit excitation in a pathway after an effect is achieved
(very common used to maintain homeostasis)
how do feedforward excitatory circuits lead to muscle contraction (e.g. knee-jerk response)?
- brain sends out signals to two feedforward excitatory circuits that control extensor and flexor muscles simultaneously
- these two circuits inhibit each other via inhibitory interneurons so their activation occurs alternatively (not simultaneously)
- producing contraction in one group of muscles and relaxation in the other
