Block 5 Neuro Embryo And Transmitters MCQ's
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The myelin sheaths surrounding cranial and spinal nerves are formed by which of the following cells?
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Astrocytes
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Schwann cells
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Microglial cells
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Neuroglial cells
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Oligodendrocytes
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Each neurotransmitter can directly or indirectly influence neurons in a specific portion of the brain, thereby affecting behavior. Neurotransmitters such as monoamines appear in the embryo before the neurons are differentiated. Take up these 8 questions from block five where 8 involve the embryo and 9 are on Neuro transmitters to learn more.
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- 2.
The pons and cerebellum are derived from the walls of which structure?
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Metencephalon
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Telencephalon
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Diencephalon
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Mesencephalon
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Myelencephalon
Correct Answer
A. MetencephalonExplanation
The pons and cerebellum are derived from the walls of the metencephalon. The metencephalon is one of the five major divisions of the developing brain, and it gives rise to various structures including the pons and cerebellum. The pons is a part of the brainstem that helps to relay signals between the cerebrum and the cerebellum, while the cerebellum is responsible for coordinating voluntary movements, balance, and posture. Therefore, the correct answer is Metencephalon.Rate this question:
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- 3.
The nucleus of the fourth cranial nerve, an exclusively motor nerve, which exits from the dorsum of the brainstem and innervates a muscle that moves the eyeball, is derived from which embryonic location?
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Alar plate of the metencephalon
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Alar plate of the myelencephalon
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Basal plate of the mesencephalon
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Basal plate of the diencephalon
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Intermediolateral position near the sulcus limitans of the rhombencephalon
Correct Answer
A. Basal plate of the mesencephalonExplanation
The correct answer is "Basal plate of the mesencephalon." The fourth cranial nerve, also known as the trochlear nerve, is a motor nerve that innervates a muscle that moves the eyeball. The nucleus of this nerve is derived from the basal plate of the mesencephalon, which is a region in the developing brain.Rate this question:
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- 4.
Which of the following is a derivative of the epaxial musculature?
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Rectus femoris
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Biceps brachii
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Trapezius
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Innermost intercostal
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Rectus capitis posterior minor
Correct Answer
A. Rectus capitis posterior minorExplanation
Rectus capitis posterior minor is a derivative of the epaxial musculature. The epaxial musculature refers to the muscles that are located posteriorly to the vertebral column. The rectus capitis posterior minor is a small muscle located in the back of the neck, which falls within this category. It helps to extend and rotate the head. The other options, such as Rectus femoris, Biceps brachii, Trapezius, and Innermost intercostal, are not derivatives of the epaxial musculature.Rate this question:
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- 5.
Nerve tracts running through the caudal medulla develop ventral to the sulcus limitans and eventually form the pyramids. Based on the position of their embryological development, what is the functional association of the pyramids?
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Somatic sensory
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Visceral sensory
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Special sensory
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Motor
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Sympathetic
Correct Answer
A. MotorExplanation
The pyramids are formed by nerve tracts running through the caudal medulla, which develop ventral to the sulcus limitans. Based on their position of embryological development, the functional association of the pyramids is motor. This suggests that the pyramids are involved in carrying motor signals from the brain to the muscles, allowing for voluntary movement and control of body functions.Rate this question:
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- 6.
DiGeorge Syndrome is a suite of congenital craniofacial malformations associated with immunological defects due to failure of the thymus gland to differentiate and calcium metabolic defects related to failed parathyroid gland development. What is the primary embryological cause of this syndrome?
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Failure of development of Rathke's pouch
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Lack of migration of ectoderm through the primitive streak
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Lack of normal development and migration of neural crest cells
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Failure of descent of the thyroid gland primordium
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Lack of normal closure of the cervical sinus
Correct Answer
A. Lack of normal development and migration of neural crest cellsExplanation
DiGeorge Syndrome is primarily caused by the lack of normal development and migration of neural crest cells. Neural crest cells are a group of cells that originate from the neural tube during embryonic development and migrate to different parts of the body, including the thymus gland and parathyroid glands. In DiGeorge Syndrome, the neural crest cells fail to properly develop and migrate, leading to the malformation of craniofacial structures and the failure of the thymus gland and parathyroid glands to function properly. This results in the immunological defects and calcium metabolic defects associated with the syndrome.Rate this question:
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- 7.
Failure of closure of the cranial neuropore causes which serious congenital malformation?
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Meroanencephaly
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Rachischisis
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Myelocele
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Spina bifida occulta
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Spina bifida cystica
Correct Answer
A. MeroanencephalyExplanation
Meroanencephaly is a serious congenital malformation caused by the failure of closure of the cranial neuropore. This condition is characterized by the absence of the cerebral hemispheres and the presence of a rudimentary brainstem. It is a severe form of neural tube defect that leads to significant neurological abnormalities and is usually incompatible with life.Rate this question:
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- 8.
A young child is diagnosed with a communicating or non obstructive hydrocephalus. Which of the following is the most likely cause of this condition?
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Blockage of the foramen of Monroe
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Blockage of the aqueduct of sylvius
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Blockage of the foramen of Megendie in 4th ventricle
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Blockage of the arachnoid villi
Correct Answer
A. Blockage of the arachnoid villiExplanation
Blockage of the arachnoid villi is the most likely cause of communicating or non-obstructive hydrocephalus. The arachnoid villi are responsible for reabsorbing cerebrospinal fluid (CSF) from the subarachnoid space into the bloodstream. If there is a blockage in the arachnoid villi, it can prevent the proper drainage of CSF, leading to an accumulation of fluid and subsequent hydrocephalus. This condition is often seen in young children and can result from various factors such as infection, inflammation, or congenital abnormalities affecting the arachnoid villi.Rate this question:
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- 9.
During the process of chemical neurotransmission, by what mechanism do most non-peptide neurotransmitters previously released into the synaptic cleft leave the Synaptic cleft?
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Endocytosis into the postsynaptic neuron
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Endocytosis into the presynaptic neuron
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Secondary active transport into the presynaptic neuron
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Secondary active transport into the postsynaptic neuron
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Diffusion out of the side of the synaptic cleft
Correct Answer
A. Secondary active transport into the presynaptic neuronExplanation
Most non-peptide neurotransmitters are taken back up into the presynaptic neuron through a process called secondary active transport. This means that the neurotransmitter is transported against its concentration gradient using energy derived from the electrochemical gradient of another molecule, such as sodium or calcium. This allows for efficient reuptake of the neurotransmitter, preventing excessive accumulation in the synaptic cleft and allowing for precise control of neuronal signaling.Rate this question:
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- 10.
Two cells synapse onto the cell body of an axon in the central nervous system. One cell releases glutamate that binds to NMDA-R and the other release GABA that binds to GABA„-R. They both receive action potentials at their presynaptic axon terminals at the same time. Which of the following is true?
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NMDA-R is a metabotropic postsynaptic receptor
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Postsynaptic responses through the NMDA-R and the GABAA-R will summate and always reach threshold causing an action potential to fire,
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GABA will also bind to and activate glycine receptors (GlyR).
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Cl- ions influxing through the GABAA-R will cause an IPSP that reduces the amplitude of the EPSP depolarizing graded potentials in the postsynaptic cell.
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Na+ ions influxing through the NMDA-R will cause hyperpolarizing graded potentials in the postsynaptic cell.
Correct Answer
A. Cl- ions influxing through the GABAA-R will cause an IPSP that reduces the amplitude of the EPSP depolarizing graded potentials in the postsynaptic cell.Explanation
When the presynaptic axon terminals of both cells receive action potentials simultaneously, the cell that releases GABA will bind to and activate GABAA receptors. The influx of Cl- ions through the GABAA receptors will cause an inhibitory postsynaptic potential (IPSP), which reduces the amplitude of the excitatory postsynaptic potential (EPSP) depolarizing graded potentials in the postsynaptic cell. This means that the EPSP will be less likely to reach the threshold for firing an action potential. Therefore, the statement "Cl- ions influxing through the GABAA-R will cause an IPSP that reduces the amplitude of the EPSP depolarizing graded potentials in the postsynaptic cell" is true.Rate this question:
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- 11.
Seizures are fundamentally the result of too much excitatory neuronal activity in the brain. Imagine that you wanted to design a new drug to reduce the severity of seizures. Which of the following approaches would make the most sense?
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Potentiate the effect of glutamate at glutamatergic receptors
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Block GABA receptors
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Open calcium channels
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Block the glial based uptake of glutamate from the synaptic cleft
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Open chloride channels
Correct Answer
A. Open chloride channelsExplanation
Opening chloride channels would make the most sense in designing a new drug to reduce the severity of seizures. Opening chloride channels would allow chloride ions to enter the neuron, hyperpolarizing the cell and making it less likely to fire an action potential. This would help to counteract the excessive excitatory activity in the brain that leads to seizures.Rate this question:
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- 12.
G-aminobutyric acid (GABA) is the most important inhibitory neurotransmitter in the brain. GABA suppresses anxiety, and a deficiency of GABA causes anxiety. You work for a secret service that wants to develop an anxiety-inducing drug for interrogations. The best strategy to accomplish this aim would be a drug that
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Inhibits GABA decarboxylase
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Keeps the GABA-operated chloride channel open
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Inhibits glutamate decarboxylase
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Inhibits GABA transaminase
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Inhibits COMT
Correct Answer
A. Inhibits glutamate decarboxylaseExplanation
Inhibiting glutamate decarboxylase would be the best strategy to develop an anxiety-inducing drug for interrogations. Glutamate decarboxylase is responsible for converting glutamate into GABA, the inhibitory neurotransmitter that suppresses anxiety. By inhibiting glutamate decarboxylase, the production of GABA would be reduced, leading to a deficiency of GABA and ultimately causing anxiety.Rate this question:
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- 13.
The synthesis of the neurotransmitter norepinephrine can be prevented by a drug that inhibits:
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Choline-acetyl transferase
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Tyrosinase
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Monoamine oxidase
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Catechol-O-methyl transferase
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Tyrosine hydroxylase
Correct Answer
A. Tyrosine hydroxylaseExplanation
Tyrosine hydroxylase is an enzyme involved in the production of norepinephrine, a neurotransmitter. If a drug inhibits this enzyme, it will prevent the synthesis of norepinephrine. Therefore, the correct answer is Tyrosine hydroxylase.Rate this question:
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- 14.
Increased activity of the neurotransmitter dopamine at synapses in the mesolimbic dopamine system is known to cause euphoria. To get a good euphoriant effect, you should therefore design drugs that
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Inhibit the sodium cotransporter for dopamine in the nerve terminal
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Inhibit the transporter that pumps dopamine into synaptic vesicles
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Inhibit tyrosine hydroxylase
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Induce enhanced expression of catechol-O-methyl-transferase (COMT)
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Block voltage-gated calcium channels in the nerve terminals
Correct Answer
A. Inhibit the sodium cotransporter for dopamine in the nerve terminalExplanation
Inhibiting the sodium cotransporter for dopamine in the nerve terminal would prevent the reuptake of dopamine back into the nerve terminal, leading to increased dopamine levels in the synapse. This increased activity of dopamine at synapses in the mesolimbic dopamine system is known to cause euphoria. Therefore, designing drugs that inhibit this cotransporter would result in a good euphoriant effect.Rate this question:
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- 15.
All traders at the New York Stock Exchange suddenly get sick with vomiting, excessive salivation, diarrhea, and severe bradycardia. 500 of them die within 2 hours. It turns out that this incident had been caused by a disgruntled former employee who poured 5 gallons of the organophosphorus compound sarin into the air conditioning system of the building. The stock traders died because of
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Too much acetylcholine in their synaptic clefts
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A shortage of acetylcholine at central and peripheral synapses
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Excessive sensitivity of receptors for the neurotransmitter GABA
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Inability to synthesize the neurotransmitter GABA
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Inability to degrade dopamine, norepinephrine and 5-hydroxytryptamine
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Karma is punishing them for their greed
Correct Answer
A. Too much acetylcholine in their synaptic cleftsExplanation
The correct answer is "too much acetylcholine in their synaptic clefts." Sarin is an organophosphorus compound that acts as a potent acetylcholinesterase inhibitor. Acetylcholinesterase is responsible for breaking down acetylcholine in the synaptic cleft, allowing for proper neurotransmission. When sarin inhibits acetylcholinesterase, acetylcholine builds up in the synaptic cleft, leading to overstimulation of cholinergic receptors. This excessive stimulation results in the symptoms described, such as vomiting, excessive salivation, diarrhea, and severe bradycardia. The high levels of acetylcholine can also cause respiratory failure and ultimately lead to death.Rate this question:
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- 16.
A 46 year old male hunter accidentally stuck himself while preparing his arrows for hunting. History revealed that curare (d-tubocurarine) was present in his arrows. A significant finding on examination was paralysis in the arm that he stuck himself. Which of the following best explains the mechanism of the paralysis seen?
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Increased anti-acetylcholinesterase activity
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Blockage of Na+ channels and subsequent repolarization
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Blockage of K++ gated channels and subsequent depolarization
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Competitive inhibition of binding to nicotinic cholinergic receptors
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Competitive inhibition of binding to muscarinic cholinergic receptors
Correct Answer
A. Competitive inhibition of binding to nicotinic cholinergic receptorsExplanation
Curare is a naturally occurring plant extract that acts as a competitive inhibitor of nicotinic cholinergic receptors. These receptors are responsible for transmitting signals from motor neurons to muscles, leading to muscle contraction. By competitively inhibiting the binding of acetylcholine to these receptors, curare prevents the transmission of signals and causes muscle paralysis. This explains the mechanism of paralysis seen in the hunter who accidentally stuck himself with arrows containing curare.Rate this question:
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- 17.
Which of the following, if used as a neurotransmitter at a chemical synapse, is most likely to have a delayed onset and end of action in the postsynaptic neuron?
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Acetylcholine
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Norepinephrine
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Epinephrine
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Vasoactive intestinal peptide
Correct Answer
A. Vasoactive intestinal peptideExplanation
Vasoactive intestinal peptide (VIP) is most likely to have a delayed onset and end of action in the postsynaptic neuron. This is because VIP is a neuropeptide neurotransmitter, which means it is released in larger quantities and has a slower rate of diffusion compared to small molecule neurotransmitters like acetylcholine, norepinephrine, and epinephrine. Neuropeptides typically have longer-lasting effects due to their slower clearance from the synapse, resulting in a delayed onset and end of action in the postsynaptic neuron.Rate this question:
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- 18.
At the neuromuscular junction of skeletal muscle, which of the following proteins is neither present on nor attached to the motor end plate?
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Nicotinic acetylcholine receptor
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Voltage-gated sodium channel
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Acetylcholine esterase
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Sodium-potassium pump
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Ligand-gated sodium-potassium cotransporter
Correct Answer
A. Voltage-gated sodium channelExplanation
The correct answer is voltage-gated sodium channel. The voltage-gated sodium channel is not present on or attached to the motor end plate at the neuromuscular junction of skeletal muscle. The motor end plate contains the nicotinic acetylcholine receptor, which is responsible for receiving the acetylcholine signal, acetylcholinesterase, which breaks down acetylcholine to terminate the signal, and the sodium-potassium pump, which helps maintain the resting membrane potential. The ligand-gated sodium-potassium cotransporter is not relevant to the neuromuscular junction.Rate this question:
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- 19.
Catecholamine biosynthesis involves dopamine (DA), epinephrine (Epi), norepinephrine (Norepi) and L-DOPA (DOPA). In what sequence are these products formed?
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Epi --> Norepi --> DOPA --> DA
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DOPA --> Epi --> Norepi --> DA
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DOPA --> DA --> Norepi --> Epi
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DA --> DOPA --> Epi -->Norepi
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Epi --> Norepi --> DA --> DOPA
Correct Answer
A. DOPA --> DA --> Norepi --> EpiExplanation
Catecholamine biosynthesis begins with the formation of L-DOPA (DOPA), which is then converted into dopamine (DA). Next, DA is converted into norepinephrine (Norepi), and finally, norepinephrine is converted into epinephrine (Epi). Therefore, the correct sequence of formation is DOPA --> DA --> Norepi --> Epi.Rate this question:
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- 20.
A patient with Parkinson's disease tells you that he learned from an Internet patient blog that cocaine can relieve the symptoms of Parkinson's disease. You can tell him that this might well be true because cocaine
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Acts as a growth factor that prevents apoptosis of dopamine neurons
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Is a muscarinic agonist that stimulates acetylcholine receptors in the brain, therefore compensating for the shortage of dopamine
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Inhibits the uptake of dopamine into nerve terminals
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Enhances dopamine action by inhibiting MAO-A
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Is a dopamine agonist that stimulates dopamine receptors directly
Correct Answer
A. Inhibits the uptake of dopamine into nerve terminalsExplanation
Cocaine inhibits the uptake of dopamine into nerve terminals, which means it prevents the reuptake of dopamine by the neurons. This leads to an increased concentration of dopamine in the synaptic cleft, resulting in enhanced dopamine action. In Parkinson's disease, there is a shortage of dopamine, so inhibiting its uptake can potentially alleviate the symptoms. However, it is important to note that the use of cocaine for this purpose is not recommended or safe, as it is a highly addictive and illegal substance.Rate this question:
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Mar 22, 2023Quiz Edited by
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Jan 15, 2012Quiz Created by
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