Block 5 Neuro Embryo and Transmitters MCQ's

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.

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.

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.

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.

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.

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.

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.

Schwann cells are responsible for forming the myelin sheaths surrounding cranial and spinal nerves. These cells are found in the peripheral nervous system and play a crucial role in insulating and protecting nerve fibers. They wrap around the axons of neurons, forming multiple layers of myelin that enhance the speed and efficiency of nerve impulse transmission. In contrast, oligodendrocytes are responsible for forming myelin in the central nervous system. Astrocytes, microglial cells, and neuroglial cells are other types of cells in the nervous system that have different functions and do not contribute to the formation of myelin sheaths.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.