Synaptic Transmission Study Question Bank

When EPSPs (excitatory postsynaptic potentials) arrive very close together in time, it means that the postsynaptic neuron is receiving a high frequency of excitatory inputs. This leads to a phenomenon called temporal summation, where the EPSPs add up and increase in amplitude, making it more likely for the postsynaptic neuron to reach its threshold and generate an action potential. Therefore, when EPSPs are arriving very close together in time, they are most effective at bringing the postsynaptic neuron to threshold.

γ-aminobutyric acid (GABA) is an inhibitory neurotransmitter in the central nervous system (CNS). It functions to reduce neuronal excitability and inhibit the transmission of signals between nerve cells. This helps to regulate and balance the activity of the CNS. Norepinephrine, glutamate, serotonin, and histamine are all excitatory neurotransmitters that promote neuronal activity and transmission.

An inhibitory post-synaptic potential (IPSP) is a hyperpolarization of the postsynaptic membrane, meaning it increases the membrane potential and makes it more negative. This is achieved by opening Cl- channels, allowing Cl- ions to enter the cell, which leads to an influx of negative charge and hyperpolarization.

Nicotinic ACh receptors are responsible for producing the skeletal muscle end-plate potential. These receptors are located at the neuromuscular junction, where they bind acetylcholine released from motor neurons. This binding triggers the opening of ion channels, allowing the influx of sodium ions into the muscle cell. This influx of sodium ions leads to depolarization of the muscle cell membrane, ultimately causing muscle contraction. Therefore, the activation of nicotinic ACh receptors is crucial for the generation of the end-plate potential and subsequent muscle contraction.

During an EPSP, there is an increased permeability to both K+ and Na+. If there is also an increase in membrane permeability to Cl-, it would lead to an influx of Cl- ions into the cell, which would counteract the depolarizing effect of the K+ and Na+ ions. This would result in a decrease in the amplitude of the EPSP.

Synaptic transmission at the neuromuscular junction is true because it is produced by the release of acetylcholine from the alpha motorneuron. Acetylcholine is a neurotransmitter that is released from the alpha motorneuron and binds to receptors on the muscle membrane, causing muscle contraction. This is the process by which nerve impulses are transmitted from the nervous system to the muscles, allowing for movement and muscle control.

When a person with myasthenia gravis is treated with an acetylcholinesterase (AChE) inhibitor, their muscle strength increases. This is because the AChE inhibitor prevents the breakdown of acetylcholine (ACh) at the muscle end plates, leading to an increase in the level of ACh at the muscle end plates. This allows for more efficient transmission of nerve impulses from the motor nerves to the muscles, resulting in improved muscle strength.

The correct temporal sequence of events at the neuromuscular junction is as follows: first, there is uptake of Ca2+ into the presynaptic terminal. This is followed by the release of acetylcholine (ACh) into the synaptic cleft. Finally, the muscle end plate depolarizes, leading to muscle contraction.

The NMDA receptor is a type of receptor in the brain that is activated by the neurotransmitter glutamate. Glutamate is the primary excitatory neurotransmitter in the central nervous system and plays a crucial role in various brain functions, including learning, memory, and synaptic plasticity. When glutamate binds to the NMDA receptor, it allows the influx of calcium ions into the neuron, leading to the activation of various signaling pathways and ultimately influencing neuronal communication and plasticity.

The refractoriness of the skeletal muscle action potential is due to the continued binding of ACh to receptors in the motor end-plate, which causes an increase in the steady-state level of inactivation of Na+ channels in the muscle membrane adjacent to the endplate. This means that the Na+ channels become less responsive to further stimuli, leading to a decrease in the excitability of the muscle. Additionally, the continued binding of ACh also results in ACh receptor desensitization at the endplate, further contributing to the refractoriness of the muscle action potential.

Dopamine is a catecholamine synthesized from the amino acid tyrosine. This means that dopamine is a type of neurotransmitter that belongs to the catecholamine group and is produced from the amino acid tyrosine. Catecholamines are a class of neurotransmitters that include dopamine, norepinephrine, and epinephrine. This association correctly identifies dopamine as a catecholamine and explains its synthesis process.

During synaptic transmission, the influx of Ca2+ into the presynaptic terminal is primarily due to a voltage-activated increase in membrane gCa. This means that when the membrane potential of the presynaptic terminal depolarizes, it causes an increase in the conductance of Ca2+ channels in the membrane. This allows Ca2+ ions to flow into the terminal, triggering the release of neurotransmitters from synaptic vesicles through exocytosis. Therefore, the voltage-activated increase in membrane gCa is the main mechanism responsible for the influx of Ca2+ during synaptic transmission.

Presynaptic inhibition refers to the regulation of neurotransmitter release from the presynaptic nerve ending. By increasing the Cl- permeability of the presynaptic nerve ending, the membrane potential becomes more negative, resulting in hyperpolarization. This hyperpolarization reduces the likelihood of an action potential being generated, thus decreasing the frequency of action potentials by the presynaptic nerve ending. As a result, the firing rate of alpha motorneurons is affected, leading to a decrease in muscle contraction.

Both the EPSP (excitatory postsynaptic potential) and EPP (endplate potential) are depolarizing because they result from an influx of Na+ ions. This depolarization allows for the propagation of an action potential in the postsynaptic neuron or muscle fiber, respectively. This feature is common to both synaptic transmission in the CNS and at the neuromuscular junction.

At the muscle end plate, acetylcholine (ACh) causes the opening of Na+ and K+ channels. This allows both Na+ and K+ ions to flow across the membrane, resulting in depolarization. The depolarization occurs to a value halfway between the Na+ and K+ equilibrium potentials, which means that the membrane potential becomes less negative. This depolarization is necessary for the generation of an action potential and subsequent muscle contraction.

Inactivation of sodium channels in muscle cells is likely to cause muscle weakness as a result of increased extracellular potassium concentration. Sodium channels are responsible for the depolarization phase of action potentials in muscle cells. When these channels are inactivated, it impairs the ability of muscle cells to generate action potentials and contract properly, leading to muscle weakness.