Action Potentials and Synapse Biology - MCAT Biological and Biochemical Foundations of Living Systems

Voltage-gated calcium channels do not cause depolarization in neurons, but are integral to depolarization in muscle. Voltage-gated sodium channels are responsible for neural depolarization; there are no sodium leaky channels in neurons, as these would disrupt the resting potential. Voltage-gated potassium channels actively import potassium, whereas the sodium-potassium pump actively exports potassium. There is no such thing a potassium-calcium pump.

During depolarization, voltage-gated sodium channels open and allow a rapid influx of sodium ions. The membrane voltage rises from its resting potential of -70 mV to 35 mV. Depolarization is not associated with endocytosis of neurotransmitters.

The answer is saltatory conduction. Saltatory conduction is the term used to define the process of action potential jumping described in the question. The other possbilities, while involved in the nervous system and its function, do not adaquately describe the process in question.

Sodium channels have an inactivation gate, as well as a voltage gate. This allows the sodium channels to be turned off, even while voltage changes persist, thereby facilitating repolarization. This dual gate structure also causes the refractory period.

Potassium is the major species that repolarizes a neuron following depolarization. After sodium has entered the cell to create depolarization, repolarization is driven by potassium ion efflux.

A chemical synapse is a type of synapse that uses neurotransmitters to transmit signals. A presynaptic neuron receives an action potential, which prompts neurotransmitters to be released into the synaptic cleft. These neurotransmitters traverse across the synaptic cleft and bind to receptors on the postsynaptic neuron. Binding of neurotransmitters initiates a signal pathway in the postsynaptic neuron.

One of the characteristics of a chemical synapse is that it is unidirectional. This means that the signal can only be propagated in one direction. The signal is always transmitted from the presynaptic to the postsynaptic neuron, never the other way around.

Chemical synapses are indeed more common than electrical synapses. Most nerves, neuromuscular junctions, and major organs in the body use chemical synapses to transmit action potentials. The only major exception is the heart; cardiac cells in the heart use electrical synapses to transmit signal from one cell to the other.

In a chemical synapse, the presynaptic neuron transmits a signal to the adjacent postsynaptic neuron. The postsynaptic neuron receives this signal via neurotransmitters. Recall that a neuron has directionality, with dendrites on one end and an axon on the other end. Dendrites receive an outside signal (signal enters neuron), whereas an axon transmits the signal to an adjacent neuron or muscle (signal exits neuron). This means that the axon end of the presynaptic neuron transmits the signal to the dendrite end of the postsynaptic neuron via a chemical synapse.

During normal impulse conduction, 3 Na+ ions move out of a neuron while 2 K+ ions move in. This results in a high concentration of Na+ outside the cell and low K+ outside the cell. TXX will disrupt the electrochemical gradient by blocking the Na+/K+ voltage-gated channel. A patient suffering from TXX intoxication usually dies from respiratory paralysis brought on by the disruption of neural conduction along nerve fibers and axons. The most appropriate response to the question is the disrupted conduction of nerve impulses.

Depolarization occurs as the Na+ ions rush into the neuron. During depolarization, 3 Na+ ions move in and 2 K+ ions move out of the cell via the Na+/K+ pump. Repolarization returns the cell potential to its resting value by rushing K+ ions out of the cell. Hyperpolarization further decreases the cell potential after repolarization.

For an action potential to occur, voltage-gated sodium channels must open to cause a sharp depolarization (increase) in the membrane potential. Pairing that information with knowledge that action potentials originate at the axon hillock, no other answer choice makes sense. It is only logical, then, that a high density of voltage-gated channels be present at the location where action potentials are first initiated.

Saltatory conduction is a process that propagates an action potential more quickly down the length of an axon in a "leapfrog" manner. This propagation occurs in the gaps between myelin on an axon, called nodes of Ranvier. Without myelin, these nodes would not exist, and the rate at which an action potential is transmitted would decrease. People suffering with multiple sclerosis (MS) have myelin degradation, and thus have decreased motor and other neurological processes.

Electrical synapses transmit signals faster than chemical synapses due to the physical connection of neural cells through gap junctions. Chemical synapses are slower due to the action potential needing to arrive in the terminal bud, causing calcium channels to open. This causes neurotransmitter vesicles to fuse to the presynaptic membrane, releasing neurotransmitters to diffuse across the synaptic cleft.

Electrical synapses can allow bi-directional transmission of signals, but chemical synapses cannot. Saltatory conduction involves action potential propagation along the axon via the nodes of Ranvier, and is not involved in the synapse.

During the docking and fusion of synaptic vesicles, the increased levels of calcium in the synaptic terminal will lead to calcium ions binding to synaptotagmin, which facilitates the binding of V- and T-snares to initiate fusion. None of the other answer choices make sense with respect to vesicle fusion at the presynaptic terminal.

Metabotropic receptors involve the reception of a neurotransmitter via a G-protein signaling cascade. Muscarinic receptors are an example of metabotropic receptors.

Ionotropic receptors involve the binding of a neurotransmitter directly to an ion channel, and the ion channel subsequently opening and allowing its respective ion into or out of a cell.

As a result, ionotropic receptors elicit effects more quickly, as they do not involve intermediate steps.

The presence of potassium leak channels in the membrane allows potassium to drive the resting cell membrane potential nearer to its equilibrium potential than to sodium's.

The equilibrium potential is the electric potential that would exaclty balance the competing forces of concentration and electrical gradients. High potassium concentration in the cytosol drives potassium out of leak channels in the membrane, toward the extracellular space, but the inside develops a negative charge as a result. When this negative charge pulling positive potassium ions back in is enough to exactly cancel the concentration forces pushing potassium out, the equilibrium potential has been reached.

The sodium-potassium pump, or Na/K ATPase, is what restores ionic concentrations back to normal after an action potential. This pump is electrogenic, and active, using ATP to pump three sodium out of the cell, and two potassium into the cell. Along wtih the potassium leak channels, this keeps the potassium concentration in a cell high, and sodium concentration low.

Post-synaptic potentials are graded, while action potentials are "all-or-nothing". This means that the farther from the point of integration in a nerve cell an electrical input enters, the weaker its corresponding post-synaptic potential will be when it reaches the distant integration site.

In this way, post-synaptic potentials can be summed as a function of intensity and distance, while action potentials are always the same amplitude no matter from how far they travel.

The sodium channel being inactivated, via its inactivation gate, prevents a stimulus from initiating an action potential immediately after a previous stimulus.

During the absolute refractory period, this is a fact regardless of how strong the stimulus is. During the relative refractory period the neuron can be stimulated, but only by a very large stimulus.

The proteins responsible for allowing ionic flow into and out of axons are most likely to be found at Nodes of Ranvier, where there is no myelin and ions can move freely. Action potentials travel via saltatory conduction, meaning that the ion channels are only stimulated a certain points on the membrane. The majority of the impulse is conducted through the interior of the axon without further external stimulation.