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- You have bunch of neurons in alive in a dish. You are recording from the axon hillock of one neuron while you stimulate an action potential in another neuron that synapses on the neuron you are recording from. One action potential from your presynaptic neuron causes +5 mV depolarization in the postsynaptic neuron’s axon hillock. Threshold for this neuron requires +10 mV. How can you most assuredly achieve threshold for this post-synaptic neuron? Group of answer choices Firing the presynaptic neuron multiple times in close succession Firing the presynaptic neuron plus another random presynaptic neuron that you find in the dish You can’t a +5mV EPSP will never be able to reach a 10mV threshold Firing the presynaptic neuron multiple times but keep the firing events spaced out really far in time.A neuron has a resting membrane potential of -70 milivolts (mV) and a threshold value of -55 mV. Three synapses on the body of this neuron receive the impulses listed below. hyperpolarisation by 5 mV • depolarisation by 15 mV • depolarisation by 10 mV ENTER THE MEMBRANE POTENTIAL AS A NUMBER WITH + OR - IN FRONT OF IT. The final membrane potential will be mV and this cause an action potential becasue it is v than theAn EPSP facilitates depolarization of the postsynaptic membrane by O increasing the permeability of the membrane to K+. O stimulating the Na+-K+ pump. O allowing Cl- to enter the cell. O increasing the permeability of the membrane to Na+. O insulating the hillock region of the axon.
- Opening of ligand-gated Cl- channels causes :-a- inhibition of the postsynaptic neuronb- depolarization of the postsynaptic neuronc- initiation of an action potentiald- block of ligand-gated cation channelsThe absolute refractory period of an action potentialA. only ensures one-way travel down an axon.B. only allows a neuron to ignore a second signal sent that closely follows the first.C. only prevents summation of action potentials within the axonD. ensures one-way travel down an axon and allows a neuron to ignore a second signal sent that closely follows the firstE. ensures one-way travel down an axon, allows a neuron to ignore a second signal sent that closely follows the first, and prevents summation of action potentials within the axonThe giant axon of the squid (Figure Q11–3) occu-pies a unique position in the history of our understandingof cell membrane potentials and nerve action. When anelectrode is stuck into an intact giant axon, the membranepotential registers –70 mV. When the axon, suspended in abath of seawater, is stimulated to conduct a nerve impulse,the membrane potential changes transiently from –70 mVto +40 mV.
- A neuron receives a series of stimuli that increases the membrane permeability of Na', but not enough to cause membrane potential to surpass-55mV. This neuron is said to be O graded. O amplihed. O facilitated. O refractoryIPSP differs from EPSP in :-a- being of shorter durationb- being unable o summate spatiallyc- moving the membrane potential away from thresholdd- depending upon opening of voltage K + channelsWhich statement is true regarding chemical neurotransmission? O An IPSP closer to the soma will diminish the effects of an EPSP on a dendrite Chemical neurotransmission is mediated by gap junctions All neurotransmitter receptors are located on the postsynaptic cell membrane Neurotransmitters remain in the synaptic cleft indefinitely
- rearrange these in the correct order of events in an action potential.Action potentials propagate in one direction because of: O K+ Voltage-gated Channels become inactive for a while O Nat Voltage-gated Channels become inactive for a while O K+ nongated Channels become inactive for a while O Nat nongated Channels become inactive for a whileWhich of the following situations in a neuron results in action potentials that have extended depolarization phases? O None of these result in extended depolarization phase. O Compromising the inactivation mechanism in voltage-gated Na* channels. O Stimulating the voltage-gated K* channels. O Inhibiting the voltage-gated Na* channels. O Compromising the inactivation mechanism in voltage-gated K* channels.