Neurons and Action Potential - MCAT Biological and Biochemical Foundations of Living Systems

Electrical synapses have two main characteristics. First, they transmit signals through specialized tunnels between cells called gap junctions. Gap junctions facilitate movement of molecules and ions between cells. This movement enables transmission of signals between adjacent cells. Second, electrical synapses have a much higher speed of signal transmission than chemical synapses. This occurs because the signals in electrical synapses are transmitted directly from one cell to the next via gap junctions. In chemical synapses, however, signals are transmitted indirectly via neurotransmitters, which decreases the speed of signal transmission.

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.

The axon ends in a terminal bud, which transmits signals to target cells by releasing neurotransmitters across the synapse. The soma is the body of the cell and contains the nucleus. This is where the majority of protein synthesis occurs. The dendrites receive electrochemical stimuli from other neurons and cells and transmit the signal to the soma and axon.

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 enteric nervous system (ENS) is a component of the autonomic nervous system, which is a component of the peripheral nervous system. The ENS is responsible for innervating the digestive organs and, thus, regulating digestion.

The central nervous system is composed of the brain and spinal cord, while the peripheral nervous system prolifertates the body. The somatic nervous system is under voluntary control, while the autonomic is involuntary. The cranial nerves are a set of specialized nerves that branch directly off of the spinal cord.

The relative refractory period is the moment directly after an action potential when the neuron can only be stimulated to fire another action potential if there is a larger than normal stimulus. During an action potential, voltage-gated sodium channels open. After the action potential, the channels are gated and cannot be re-stimulated. This period is the absolute refractory period. The secondary gating is released, making the sodium-channels functional again, but the neuron has not been fully restored to resting potential. Release of potassium through voltage-gated potassium channels leads to hyperpolarization until the sodium-potassium pump is able to restore ion balance. This restoration takes longer than the un-gating of sodium channels, creating a period when the cell is hyperpolarized, but the voltage-gated sodium channels are capable of stimulation. If a large enough stimulus overcomes the cell hyperpolarization and reaches threshold, and action potential can still occur. This period is the relative refractory period.

It is important to recognize that sodium is flowing into the neuron during depolarization. The area outside of the neuron is electrically positive relative to the area inside of the neuron, resulting in the negative resting membrane potential of the cell. This potential allows positively charged sodium ions to flow from a high concentration of positive charge, towards the negative charge in the cell interior. Because the sodium travels from a region of relatively positive charge to a region of relatively negative charge, it is flowing down its electrical gradient.

Due to action by the sodium-potassium pump, there is also a large concentration of sodium ions outside of the cell, relative to the small sodium ion concentration inside the cell. This imbalance creates a chemical gradient across the axon membrane. The opening of the voltage-gated sodium channels during depolarization allows sodium to flow down chemical gradient from high ion concentration to low ion concentration.

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.

While sodium and potassium maintain important functions in the conduction of action potentials along the axon of the neuron, it is calcium that is responsible for the binding of vesicles containing neurotransmitters to the pre-synaptic membrane. A severe lack of calcium would inhibit the release of neurotransmitters into the synaptic cleft. When the action potential reaches the axon terminal, it stimulates the opening of voltage-gated calcium channels. The resulting influx of calcium binds to synaptic vesicles, initiating the process to release their neurotransmitter contents into the synaptic cleft.

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.

Saltatory conduction is the property that allows an action potential to jump from one node to the next along a neural axon. This is accomplished by the presence of myelin, a non-conducting sheath around the axon. Myelin interrupts the flow of current down the membrane, forcing it to skip from one region of membrane to the next, rather than fluidly traveling down the entire axon length.

Depolarization is the stage of action potential transmission in which sodium channels are opened, and sodium rushes into the cell down its concentration gradient. The resting potential of the neural membrane is roughly . The rapid influx of positive sodium ions causes this potential in increase to at the action potential peak.

Repolarization is the stage of action potential transmission in which potassium channels of a cell are opened, and potassium moves out of the cell. This event re-establishes the negative resting membrane potential.

The refractory period is the obligatory temporal gap between action potentials. After an action potential, the primary gating mechanism of the voltage-gated sodium channels causes the channels to close and deactivate. This constitutes the absolute refractory period, during which no stimulus is capable of producing an action potential. The relative refractory period follows, during the cell repolarization, when potassium efflux causes the membrane potential to drop below the resting potential. This state of hyperpolarization means that a greater stimulus is required to reach threshold, and constitutes the relative refractory period.

There are two types of synapses: the chemical synapse and the electrical synapse. Chemical synapses are more common than electrical synapses, and use neurotransmitters (chemicals) to propagate action potentials. Electrical synapses have tunnels between cells, called gap junctions, that quickly transmit signals from one cell to the other. Electrical synapses are found extensively in the heart, since it is essential to have quick signal transmission between cardiac cells.

In chemical synapses an action potential reaches the end of a presynaptic neuron, which causes neurotransmitters to be released from the presynaptic neuron. These neurotransmitters bind to receptors on the postsynaptic neuron and initiate a signal transduction pathway in the postsynaptic neuron. The space between the presynaptic and postsynaptic neuron is called the synaptic cleft. Synaptic clefts are important regions where neurotransmitters are released and regulated.

Calcium ions play an important role in chemical synapses. Once an action potential arrives at the presynaptic neuron terminal, calcium ion channels on the presynaptic neuron become permeable to calcium ions. This facilitates the movement of calcium ions into the presynaptic neuron. Influx of calcium ions signals the presynaptic neuron to release neurotransmitters into the synaptic cleft, which eventually bind to receptors on the postsynaptic neuron. The calcium ions do not enter the postsynaptic neuron at the synapse.