Nervous System & Muscle Quiz

Neurotransmitter receptors are located on the postsynaptic membrane. This is where the neurotransmitters bind and transmit signals from the presynaptic neuron to the postsynaptic neuron. The postsynaptic membrane is a specialized region of the neuron that contains receptors specific to different neurotransmitters. When a neurotransmitter binds to its corresponding receptor, it triggers a series of biochemical reactions that result in the generation of an electrical signal in the postsynaptic neuron.

If a toxin specifically binds to voltage-gated sodium channels in axons, it would prevent the depolarization phase of the action potential. During the depolarization phase, voltage-gated sodium channels open, allowing sodium ions to enter the axon and causing depolarization. This depolarization leads to the generation of an action potential. By binding to these channels, the toxin would block the entry of sodium ions and prevent depolarization from occurring, thus preventing the initiation of an action potential.

During the contraction of a vertebrate skeletal muscle fiber, calcium ions bind to the troponin complex. This binding causes a conformational change in the troponin-tropomyosin complex, which leads to the exposure of the myosin-binding sites on the actin filaments. This allows the myosin heads to bind to the actin filaments, forming cross-bridges and initiating the sliding filament mechanism of muscle contraction.

Interneurons are a type of neuron that serve as a connection between sensory and motor neurons in the brain. They facilitate communication between different areas of the brain and are responsible for processing and integrating information. While sensory neurons receive information from the environment and motor neurons control muscle movements, interneurons play a crucial role in relaying and interpreting signals within the brain. Therefore, it can be inferred that most of the neurons in the human brain are interneurons.

When several EPSPs arrive at the axon hillock from different dendritic locations, they can add up and reach the threshold for an action potential. This process is known as spatial summation. Temporal summation refers to the addition of EPSPs that arrive at the axon hillock at different times. Tetanus is a sustained contraction of muscles caused by rapid and repetitive stimulation. The refractory state refers to the period after an action potential when the neuron is temporarily unable to generate another action potential. An action potential with an abnormally high peak of depolarization is not mentioned in the explanation.

The cell body, also known as the soma, contains most of the organelles in a neuron. It is responsible for maintaining the cell's metabolic functions and providing energy for the neuron. The dendrites receive signals from other neurons and transmit them to the cell body, where the signals are integrated. The axon hillock is the site where the action potential is initiated, and the axon transmits the electrical impulses away from the cell body. The axon terminals are the end points of the axon where neurotransmitters are released to communicate with other neurons. However, the majority of organelles are located in the cell body.

The sodium-potassium pump is responsible for maintaining the concentration gradient of sodium and potassium ions across the cell membrane. It actively moves three sodium ions out of the cell for every two potassium ions it moves into the cell. This process requires energy in the form of ATP. Therefore, the correct answer is that the sodium-potassium pump moves sodium ions out of the cell and potassium ions into the cell.

The correct answer is I, II, and III. The nervous system has multiple functions, including integration, motor output, and sensory input. Integration refers to the processing and interpretation of sensory information, motor output involves the response of the body to stimuli, and sensory input involves the detection and transmission of sensory information to the brain. Therefore, all three options are correct.

An increase in the movement of potassium ions out of the neuron's cytoplasm would result in hyperpolarization of the neuron. Hyperpolarization occurs when the membrane potential becomes more negative than the resting potential. As potassium ions, which are positively charged, leave the neuron, the net charge inside the neuron becomes more negative, leading to hyperpolarization. This makes it more difficult for the neuron to reach the threshold for firing an action potential.

Myelinated axons have a fatty substance called myelin surrounding them, which acts as an insulating layer. This insulation allows action potentials to jump from one node of Ranvier to another, skipping the sections of the axon covered in myelin. This process, called saltatory conduction, speeds up the transmission of action potentials along the axon. In contrast, non-myelinated axons have a continuous conduction, which is slower. Therefore, action potentials move more rapidly in myelinated axons compared to non-myelinated axons.

Action potentials are usually conducted in only one direction along an axon because of the brief refractory period that prevents the reopening of voltage-gated Na+ channels. During an action potential, the voltage-gated Na+ channels open, allowing Na+ ions to enter the axon and depolarize it. However, after the channels open, they become inactivated for a short period of time, known as the refractory period. This prevents the channels from reopening and allows the action potential to propagate in only one direction along the axon.

When an action potential is initiated in a neuron, it travels in one direction from the axon hillock to the axon terminals. This is due to the refractory period that prevents the backward movement of the action potential. However, if the middle of the axon is experimentally depolarized to threshold using an electronic probe, it can initiate two action potentials. One action potential will travel towards the axon terminal in the normal direction, while the other action potential will travel back towards the axon hillock. This occurs because the depolarization in the middle of the axon creates two regions with different electrical potentials, allowing for the initiation of two separate action potentials.

When a neuron's membrane depolarizes, it means that the voltage across the membrane becomes more positive. This occurs when there is an influx of positively charged ions, such as sodium ions, into the cell. The change in voltage is a result of the opening of ion channels in response to a stimulus, which allows the flow of ions across the membrane. This depolarization is an important step in the generation of an action potential, as it brings the membrane potential closer to the threshold for firing an action potential.

Saltatory conduction refers to the jumping of an action potential from one node of Ranvier to the next in a myelinated neuron. In myelinated neurons, the axon is covered in a fatty substance called myelin, which acts as an insulator. This insulation prevents the leakage of electrical charge and speeds up the conduction of the action potential. As the action potential travels down the axon, it jumps from one node of Ranvier (the small gaps between the myelin sheath) to the next, allowing for faster and more efficient transmission of the electrical signal.

Temporal summation refers to the accumulation of postsynaptic potentials (PSPs) over time from a single presynaptic neuron. In this scenario, multiple IPSPs (inhibitory postsynaptic potentials) are arriving at the axon hillock in rapid succession from a single dendritic location. Each IPSP hyperpolarizes the postsynaptic cell, making it more negative and preventing the generation of an action potential. However, because the IPSPs are arriving rapidly, their effects summate or accumulate, eventually reaching a threshold that prevents an action potential from being generated. Therefore, this situation exemplifies temporal summation.

The correct sequence of events in transmission at a chemical synapse is as follows:
1. An action potential depolarizes the membrane of the axon terminal (3).
2. Calcium ions rush into the neuron's cytoplasm (2).
3. The synaptic vesicles release neurotransmitter into the synaptic cleft (5).
4. Neurotransmitter binds with receptors associated with the postsynaptic membrane (1).
5. Ligand-gated ion channels open (4).

Acetylcholine is a neurotransmitter that transmits signals across synapses. In order for the signal to be terminated, acetylcholine needs to be removed from the synaptic cleft. The correct answer states that its degradation by a hydrolytic enzyme on the postsynaptic membrane is responsible for terminating the activity of acetylcholine. This means that the enzyme breaks down acetylcholine into inactive components, preventing it from continuously stimulating the postsynaptic neuron.

Inhibitory neurotransmitters are responsible for suppressing or reducing the activity of neurons. Hyperpolarizing the membrane refers to an increase in the electrical potential across the cell membrane, making it more negative and less likely to generate an action potential. This inhibitory effect prevents the neuron from firing and transmitting signals to other neurons. Therefore, the correct answer, hyperpolarize the membrane, aligns with the expected action of inhibitory neurotransmitters.

Myosin does not form part of the thin filaments of a muscle cell. Myosin is a thick filament that interacts with actin, a component of the thin filaments, to generate muscle contraction. Troponin, tropomyosin, and actin are all part of the thin filaments and are involved in regulating muscle contraction. The calcium-binding site is also a component of the thin filaments and plays a crucial role in initiating muscle contraction.

During the excitation and contraction of a muscle cell, the correct sequence is as follows: First, an action potential in a motor neuron causes the axon to release acetylcholine, which depolarizes the muscle cell membrane (5). Then, T tubules depolarize the sarcoplasmic reticulum (3), which leads to the release of calcium. The released calcium binds to the troponin complex (2), causing tropomyosin to shift and unblock the cross-bridge binding sites (1). Finally, the thin filaments are ratcheted across the thick filaments by the heads of the myosin molecules using energy from ATP (4).