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13 Nov 2018

Which one of the following is an experimental evidence that demonstrates the reverse-transport model of amphetamine action? At high concentration of amphetamine,

a. it shows saturation kinetics when all the transporters are occupied and reversed.

b. it requires Ca++ ions entry to release neuotransmitters.

c. it requires action potential firings at the pre-synaptic terminal

. d. it is broken down by the COMT enzyme at the synapse, rendering it useless.

e. it is synthesized by the presynaptic neuron

33. When the reuptake of dopamine is blocked by the Ritalin™ or cocaine molecule, what would happen?

a. increase in dopamine synthesis by the presynaptic neuron

b. decrease in dopamine synthesis by the presynaptic neuron

c. dopamine level at the synaptic cleft would be prolonged

d. dopamine level at the synaptic cleft would be decreased

e. enhance the release of dopamine from the presynaptic terminal.

Which experiment is used to prove that release of dopamine induced by amphetamine is not coming from vesicular release? a. dopamine is released by activation of action potentials in the presynaptic neuron without amphetamine. b. dopamine release only in the presence of magnesium. c. dopamine release is dependent on depolarization of post-synaptic cell. d. dopamine release from axon terminal can occur in Ca++ free medium. e. dopamine release is quantal in amount.

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15 Nov 2018
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(b)Prevent the cell from reaching the threshold to trigger an action potential

(c)Prevent or prolong the falling phase

(d)None of the above

The hyperpolarization phase of the action potential is due to:

(a)The opening of voltage-gated Cl- channels

(b)Prolonged opening of voltage gated K+ channels

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(d)Rapid inactivation of voltage-gated K+ channels

The period when it is difficult to initiate another action potential for several milliseconds due to voltage-gated sodium channel inactivation is referred to as the:

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(b)Absolute refractory period

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Benzodiazepines such as Valium allosterically regulate GABA receptors by:

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(c)Blocking the action of the endogenous transmitter

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(d)Cl- outflow and hyperpolarization

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(d)An antagonist of the acetylcholine metabotropic receptor

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