Q&A Hero

Q: Endocannabinoids are retrograde neurotransmitters, meaning they are A. released from presynaptic neurons and diffuse to the postsynaptic neuron. B. released from postsynaptic neurons and diffuse to the presynaptic neuron. C. released from presynaptic neurons and diffuse back to the presynaptic cell body. D. None apply.

Q: Endogenous cannabinoids have effects similar to the active ingredient in A. cocaine. B. nicotine. C. amphetamines. D. marijuana.

Q: The most common neurotransmitter in the brain is A. glycine. B. acetylcholine. C. serotonin. D. GABA.

Q: The capacity of synapses for alteration at the molecular level is termed as A. synaptic modulation. B. synaptic alteration. C. synaptic capacitance. D. synaptic plasticity.

Q: Which of the following is NOT a type of glutamate receptor? A. NMDA receptor B. muscarinic receptor C. kainate receptor D. All of the choices are correct.

Q: Excitatory postsynaptic potentials are produced by A. glycine. B. glutamic acid. C. gamma-aminobutyric acid. D. benzodiazepines.

Q: Which of the following is NOT an action needed for glutamate to open ion channels? A. NMDA receptor must bind to glycine B. the membrane must be partially depolarized from the action of a different neurotransmitter C. Cl- must pass through the open channel D. Mg2+ is released from NMDA channel to open it

Q: Glycine and GABA stimulate opening of Cl- channels.

Q: Where is glycine released? A. in the PNS B. at skeletal muscleds C. in the CNS D. at the diaphragm

Q: Glycine is released at extensor muscles when flexor muscles are contracting.

Q: Benzodiazepines act by increasing ________ activity. A. GABA B. glutamate C. ACh D. enkephalin

Q: Which poison inhibits glycine receptors? A. strychnine B. curare C. tetrodotoxin D. All of the choices are correct.

Q: The nigrostriatal dopamine system is located in part of the midbrain known as the substantia nigra and is degenerated in the disease myasthenia gravis.

Q: Parkinson's disease is associated with the loss of dopaminergic neurons.

Q: Neuroleptics, which are used to treat schizophrenia, are A. dopamine agonists. B. ACh antagonists. C. dopamine antagonists. D. glutamate agonists.

Q: Addictive drugs, as well as nicotine, activate dopamine release in the A. nucleus accumbens. B. corpus striatum. C. basal nuclei. D. corpus callosum.

Q: The mesolimbic dopamine neurons arise in the midbrain and terminate in the A. nucleus accumbens. B. corpus striatum. C. basal nuclei. D. corpus callosum.

Q: Cocaine blocks the release of dopamine, norepinephrine, and serotonin.

Q: Which of the following is NOT true of norepinephrine? A. released in both the CNS and PNS B. released by sympathetic neurons to smooth muscle, cardiac muscle, and glands C. amphetamines stimulate norepinephrine pathways D. causes depression in the CNS

Q: Mutation of the N-methyl-D-aspartate (NMDA) receptor would affect the ability of ____________ to regulate neural function. A. acetylcholine B. epinephrine C. glutamate D. nitric oxide

Q: What neurotransmitter is used by neurons with cell bodies in the raphe nuclei along the midline of the brainstem? A. serotonin B. dopamine C. glycine D. GABA

Q: The __________ dopamine system may be involved in emotional reward and drug addiction. A. nigrostriatal B. mesolimbic C. amygdala D. dentate

Q: Serotonin is degraded in presynaptic neurons by monoamine oxidase.

Q: Which of the following is NOT classified as a catecholamine? A. norepinephrine B. epinephrine C. histamine D. dopamine

Q: What amino acid are dopamine, norepinephrine, and epinephrine derived from? A. histidine B. tyrosine C. tryptophan D. serine

Q: Serotonin is derived from the amino acid tryptophan and is an important neurotransmitter.

Q: Which of the following is NOT true of histamine? A. it is derived from the amino acid histidine B. acts as a hormone that stimulates gastric secretion C. acts as a neurotransmitter in the brain to cause drowsiness D. acts as a regulator in inflammation and allergies

Q: Norepinephrine binding to a receptor stimulates the activity of adenylate cyclase.

Q: Serotonin is synthesized from the amino acid A. alanine. B. glycine. C. tryptophan. D. serine.

Q: MAO inhibitors may cause hypertensive crisis by a person eating foods rich in A. phenylalanine. B. tyramine. C. glutamic acid. D. tryptophan.

Q: Catecholamines activate postsynaptic cells by A. inhibition of adenylate cyclase. B. increased Ca2+ influx into the target cell. C. inhibition of calmodulin. D. increased production of cyclic AMP.

Q: What type of autonomic fibers release ACh at effectors? A. parasympathetic B. sympathetic C. somatic D. sensory

Q: Release of ACh at parasympathetic effectors is always stimulatory.

Q: At what region of the neuron are action potentials first produced? A. dendrites B. cell body C. initial segment of an axon D. axon hillock

Q: What is present at the axon hillock that allows the production of action potentials? A. voltage-gated channels B. ligand-gated channels C. muscarinic receptors D. chemical-gated channels

Q: What is NOT true of conduction through dendrites and cell bodies of neurons? A. they are EPSPs B. they are spread by cable properties C. they can summate to reach threshold D. they are action potentials

Q: What is the action of the binding of muscarine to its receptors in the digestive system? A. alpha subunits bind to K+ channels, close them, leading to depolarization. B. alpha subunits bind to K+ channels, open them, leading to hyperpolarization. C. beta-gamma subunits bind to K+ channels, close them, leading to depolarization. D. beta-gamma subunits bind to K+ channels, open them, leading to hyperpolarization.

Q: ____________ is an acetylcholinesterase antagonist used to treat myasthenia gravis. A. Neostigmine B. Muscarine C. Naloxone D. Nitric oxide

Q: Curare is a competitive ACh antagonist at _____________ ACh receptors. A. muscarinic B. NMDA C. kainate D. nicotinic

Q: Cholinergic fibers use ____ as the neurotransmitter. A. norepinephrine B. acetylcholine C. dopamine D. serotonin

Q: Alzheimer's disease is associated with the loss of cholinergic fibers that end at the hippocampus and cerebral cortex.

Q: What do muscarine and nicotine have in common? A. They are both antagonists for their respective receptors. B. They are both agonists for their respective receptors. C. They both activate-protein coupled channels. D. They have nothing in common.

Q: Atropine is an antagonist to nicotine.

Q: Nicotinic receptors utilize G-proteins to regulate the opening of ion channels.

Q: Which of the following is NOT true of nicotinic-gated channels? A. The binding of ACh allows diffusion of Na+ into and K+ out of the neuron. B. Only EPSPs are generated. C. Only action potentials are generated. D. Summation can occur because of a graded response.

Q: What is the predominant affect of stimulation of nicotinic-gated channels? A. stimulation due to outflow of K+ ions B. inhibition due to outflow of K+ ions C. stimulation due to influx of Na+ ions D. inhibition due to influx of Cl- ions

Q: Muscarinic ACh receptors act through ____________ activation of K+ channels. A. cGMP B. G-protein C. M-protein D. ATP

Q: Acetylcholine usually induces an excitatory postsynaptic potential when binding to ________ receptors and an inhibitory postsynaptic potential when binding to some ____________ receptors. A. NMDA, nicotinic B. nicotinic, muscarinic C. muscarinic, NMDA D. muscarinic, nicotinic

Q: Acetylcholine can induce hyperpolarization by A. binding to nicotinic receptors. B. binding to muscarinic receptors. C. binding to a-adrenergic receptors. D. binding to b-adrenergic receptors.

Q: If the binding of muscarine to its receptor in the heart causes the beta-gamma complex of the G-protein to bind to a K+ channel, A. the K+ channel will close, leading to depolarization. B. the K+ channel will open, leading to depolarization. C. the K+ channel will close, leading to hyperpolarization and inhibition. D. the K+ channel will open, leading to hyperpolarization and inhibition.

Q: Acetylcholine A. is always an excitatory neurotransmitter. B. can bind to adrenergic receptors. C. is an inhibitory neurotransmitter released by motor neurons. D. can bind to nicotinic receptors.

Q: Muscarinic ACh receptors are found in all of the following locations EXCEPT A. skeletal muscle B. smooth muscle C. cardiac muscle D. glands

Q: Ligand-gated channels, when activated, allow only Na+ to move into the neuron.

Q: What action produces an IPSP on the postsynaptic membrane? A. influx of Na+ ions B. opening of Ca2+ channels into the neuron C. outflow of K+ ions D. opening of Cl- channels into the neuron

Q: Once an EPSP is created on the postsynaptic neuron, a new action potential is produced down the axon.

Q: An EPSP is conducted decrementally to the axon hillock, where voltage-gated Na+ and K+ channels are opened to created an action potential in the first segment of the axon.

Q: The nicotinic ACh receptor is a ligand-gated channel.

Q: An inhibitory postsynaptic potential would be produced by a neurotransmitter opening Cl- channels.

Q: In a ligand-gated channel, the neurotransmitter receptor and the channel are separate proteins.

Q: Botulism toxin prevents release of ACh, causing A. flaccid paralysis. B. hemiplegia. C. spastic paralysis. D. None apply.

Q: A lack of extracellular Ca2+ would cause increased release of neurotransmitters.

Q: Neurotransmitter release would be inhibited by A. stimulating repolarization of the axon terminal. B. blocking Ca2+ influx in the axon terminal. C. blocking repolarization of the axon terminal. D. stimulating protein kinase activity.

Q: Neurotransmitter release can be inhibited by damaging the SNARE complex.

Q: Hyperpolarization in the postsynaptic cell is caused by A. excitatory postsynaptic potentials. B. inhibitory postsynaptic potentials. C. movement of K+ out of the cell. D. Inhibitory postsynaptic potentials and movement of K+ out of the cell are correct.

Q: Neurotransmitters A. are released by endocytosis. B. all bind to the same receptor. C. usually regulate ion channels. D. are actively transported across the synaptic cleft.

Q: The binding of a neurotransmitter to its receptor protein causes ion channels to open in the post-synaptic membrane. What type of gates are these? A. chemically-regulated gates B. voltage-regulated gates C. ligand-regulated gates D. Chemically-regulated gates and ligand-regulated gates are correct.

Q: Which of the following effect(s) acetylcholine synaptic transmission? A. curare B. botulinum toxin C. strychnine D. curare and botulinum toxin.

Q: Which of the following is NOT true of EPSPs? A. they are graded responses B. they are capable of summation C. they have a refractory period D. they are initiated by neurotransmitters

Q: Conduction of an action potential in a myelinated axon is called A. point to point conduction. B. saltatory conduction. C. refractory conduction. D. cable conduction.

Q: The greater the number of depolarization regions on an axon, the faster the action potential will be conducted.

Q: In a myelinated axon, Na+ channels are A. along the whole length of the axon. B. every 5 mm. C. concentrated at the nodes of Ranvier. D. less numerous at the nodes of Ranvier.

Q: ______ synapses occur between axons of presynaptic cells and dendrites of postynaptic cells. A. Axodendritic B. Axosomatic C. Myoneural D. Axoaxonic

Q: Chemicals that stimulate action potentials in postsynaptic cells are called A. hormones. B. enzymes. C. neurotransmitters. D. neurotrophins

Q: Chemical synapses A. have a delayed impulse transmission. B. utilize gap junctions. C. occur when two nerve cells are in direct contact with each other. D. do not require the release of neurotransmitters.

Q: Most synapses in the body are electrical.

Q: Electrical synapses are functionally linked by tight junctions.

Q: What type of proteins are present in gap junctions that form water-filled channels between neurons? A. connexins B. myelin C. terminal boutons D. cell adhesion molecules (CAMs)

Q: What type of proteins are present at chemical synapses to ensure the close proximity of the presynaptic and postsynaptic membranes? A. connexins B. myelin C. terminal boutons D. cell adhesion molecules (CAMs)

Q: Synaptic vesicles are docked to the plasma membrane of the axon terminal by a protein complex called A. boutons. B. connexins. C. synaptotagmins. D. SNARE.

Q: Neurotransmitter release from synaptic vesicles is caused by Ca2+-synaptotagmin complex interruption of the SNARE complex.