I am currently reviewing my base of knowledge. Although, I found such content to be tedious and hard-understanding, it has come to my senses that such knowledge is not quite difficult to grasp and quite interesting in fact.
The tropical cone snail is known for both its colourfully vibrant shell and dangerous venom. This carnivore (marine snail) hunts, kills and dines on fish through the injection of venom with a hollow, harpoon-like part of its mouth. This results in immediate paralysis. The injection is so potent that with just a single injection, unaware scuba divers have been known to die due to its potent venom. What makes this cone snail venom so fast acting and lethal?
The answer to this question is a mixture of molecules that disable neurons, which are nerve cells that transfer information within the body. Since the venom virtually disrupts neuronal control of vital functions, such as locomotion and respiration, an animal that’s attacked y the cone snail can neither defend itself nor escape.
Communication by neurons mainly consist of two distinct types of signals: long-distance electrical signals and short-distance chemical signals. The specialized structure of neurons allows them to use pulses of electrical current to receive, transmit, and regulate the flow of information over long distances within the body. In transferring information from one cell to another, neurons often rely on chemical signals that act over very short distances. The venom’s potency is to due to the interference with which it causes with respect to both electrical and chemical signaling by neurons.
Neurons convey many different types of information such as the transmission of sensory information, which include heart rate, coordinate hand and eye movement, memories, dreams and much more. All this information is transmitted within neurons as an electrical current, consisting of the movement of ions. The connections made by a neuron specify what information is transmitted. Interpreting signals in the nervous system therefore involves sorting a complex set of neuronal paths and connections. In more complex animals, this higher-order processing is carried out largely in groups of neurons organized into a brain or into simpler clusters ganglia.
Before delving into the activity of an individual neuron, let’s take an overall look at how neurons function in the flow of information throughout the animal body. We’ll use as our example the squid, an organism that has some extraordinarily large nerve cells that are suited for physiological studies.
The squid uses its brain to process information captured by its image-forming eyes while the squid surveys it environment. When the squid spots prey, signals travelling from its brain to neurons in its mantle causes muscle contractions that propel the squid forward.
The squid’s hunting activity illustrates three important stages in its information processing: sensory input, integration, and motor output. In all but the simplest animals, specialized populations of neurons handle each stage. Sensory neurons transmit information from eyes and other sensors that detect external stimuli (light, sound, touch, heat, smell, and taste) or internal conditions (such as blood pressure, blood carbon dioxide and muscle tension). This information is sent to processing centers in the brain or in ganglia. Neurons in the brain or ganglia integrate (analyze and interpret) the sensory input, taking into account the immediate context and the animal’s past experience.
The vast majority of neurons in the brain are interneurons, which make only local connections. Motor output relies on neurons that exit the processing centers in bundles called nerves and generate output by triggering muscle or gland activity. For example, motor neurons transmit signals to muscle cells, causing them to contract.
In many animals, the neurons that carry out integration are organized in a central nervous system (CNS), which includes the brain and a longitudinal nerve cord. The neurons that carry information into and out of the CNS constitute the peripheral nervous system (PNS).
A neuron’s ability to receive and transmit information is based on a highly specialized cellular organization. Most of a neuron’s organelles, including its nucleus, are located in the cell body. A typical neuron has numerous dendrites, highly branches extensions that receive signals from other neurons. A neuron also has a single axon, an extension that transmits signals to other cells. Axons are often much longer than dendrites, and some, such as those that reach from the spinal cord of a giraffe to the muscle cells in its feet, are over a meter long. The cone-shaped region of an axon where it joins the cell body is called the axon hillock; as we will see, this is typically the region where the signals that travel down the axon are generated. Near its other end, the axon usually divides into several branches.
Each branched end of an axon transmits information to another cell at a junction called a synapse. The part of each axon branch that forms this specialized junction is a synaptic terminal. At most synapses, chemical messengers called neurotransmitters pass information from the transmitting neuron to the receiving cell. In describing a synapse, we refer to the transmitting neuron as the presynaptic cell and the neuron, muscle, gland cell that receives he signal as the postsynaptic cell. Depending ont he number of synapses, a neuron has with other cells, its shape can vary from simple to quite complex. Some interneurons have highly branches dendrites that take part in about 100,000 synapses in contrast, neurons with simpler dendrites have far fewer synapses.
To function normally, the neurons of vertebrates and most invertebrates require supporting cells called glial cells, or glia . Depending on the type, glia may nourish neurons, insulate the axons of neurons , or regulate the extracellular fluid surrounding neurons. Overall, glia outnumber neurons in the mammalian brain 10- to 50-fold.
All cells have a membrane potential, a voltage (difference in electrical charge) across their plasma membrane. In neurons, inputs from other neurons or specific stimuli cause changes in this membrane potential that act as signals, transmitting and processing information. Rapid changes in membrane potential are what enable us to see a flower, read a book or climb a tree. Thus, to understand how neurons function, we first need to examine how membrane potentials are formed, maintained and altered.
The membrane potential of a resting neuron- one that is not sending signals is its resting potential and is typically -60 and -80mV (millivolts). The minus sign indicates that the inside of a neuron at rest is negative relative to the outside.
Potassium ions (K+) and sodium ions (Na+) play critical roles in the formation of the resting potential. For each, there is a concentration gradient across the plasma membrane of a neuron. In the case of mammalian neurons, the concentrations of k+ is 140 millimolar (mM) inside the cell, but only 5mM outside. The Na+ concentration gradient is nearly the opposite: 150nM outside and only 15mM inside. These Na+ and K+ gradients are determined by sodium-potassium pumps in the plasma membrane. These ion pumps use the energy of ATP hydrolysis to actively transport Na+ out of the cell and k+ into the cell.
The concentration gradients of K+ and Na+ across the plasma membrane represent a chemical form of potential energy. Converting this chemical potential to an electrical potential involves ion channels, pores formed by clusers of specialized proteins that span the membrane. Ion channels allow ions to diffuse back and forth across the membrane. As ions diffuse through channels, they carry with them units of electrical charge. Any resulting net movement of positive or negative charge will generate a voltage, or potential, across the membrane.
The ion channels that establish the membrane potential have selective permeability, meaning that they only allow certain ions to pass. For example, a potassium channel allows K+ to diffuse freely across the membrane, but not other ions such as Na+. A resting neuron has many open potassium channels but very few open sodium channels.
The diffusion of potassium through open potassium channels is critical for the formation of the resting potential. In the resting mammalian neuron, these channels allow K+ to pass in either direction across the membrane. Because the higher concentration of k+ is much higehr inside the cell, the chemical concentration favors a net outflow k+. However since potassium channels allow only K+ to pass, Cl- and other anions inside the cell cannot accompany the k+ across the membrane. As a result, the outflow of K+ leads to an excess of negative charge inside the cell. This buildup of negative charge within the neuron is the source of the membrane potential.
What prevents the buildup of negative from increasing indefinitely? The answer lies in the electrical potential itself. The excess negative cells inside the cell exert an attractive force that opposes the flow of additional positively charged potassium ions out of the cell. The separation of charge (voltage) thus results in an electrical gradient that counterbalances the chemical concentration gradient of K+.
The net flow of K+ out of a neuron proceeds until the chemical and electrical forces are in balance. How well do just these two forces account for the resting potential in a mammalian neuron? To answer this question, let’s consider a simple model consisting of two chambers separated by an artifical membrane. To begin, imagine taht the membrane contain many open ion channels, all of which allow only K+ to diffuse across. To produce a concentration gradient for k+ like that of a mammalian neuron, we place a solution of 140mM potassium chloride in the inner chamber and 5mM KCl in the outer chamber. The potassium ions will diffuse down their concentration gradient into the outer chamber. But because the chloride ions lack a mean of crossing the membrane, there will be an excess of negative charge in the inner chamber.
When out model neuron reaches equilibrium, the electrical gradient will exactly balance the chemical gradient, such that no further net diffusion of K+ occurs across the membrane. The magnitude of the membrane voltage at equilibrium for a particular ion is called that ion’s equilibrium potential (Eion). For a membrane permeable toa single type of ion, Eion can be calculated using a formula called the Nernst equation. At human body temperature (37 celsius) and for an ion witha net charge of 1+, such as K+ or Na+, the Nernst equation is
Eion = 62mV(log[Ion]outside/[Ion]inside)
Plugging the K+ concentrations into the Nernst equation reveals that the equilibrium potential for K+ (Ek) is -90mV. The minus sign indicates that k+ is at equilibrium when the inside of the membrane is 90mV more negative than the outside. Although the equilibrium potential for k+ is -90mV, the resting potential of a mammalian neuron is somewhat less negative. This difference reflects the small but steady movement of Na+ across the few open sodium channels in a resting neuron. Because the concentration gradient of Na+ has a direction opposite to that of K+, Na+ diffuses into the cell and thus makes the inside of the cell less negative. If we model a membrane in which the only open channels are selectively permeable to Na+, we find that a tenfold higher concentration of Na+ in the outer chamber results in an equilibrium potential (ENa) of +62mV. The resting potential of an actual neuron is -60 to 80mV. The resting potential is much closer to Ek than to Ena in a neuron because there are many open potassium channels but only a small number of open sodium channels.
Because neither K+ nor Na+ is at equilibrium in a resting neuron, each ion has a net flow (a current) across the membrane. The resting potential remains steady, which means that the K+ and Na+ currents are equal and opposite. Ion concentrations on either side of the membrane also remain steady because the charge separation needed to generate the resting potential is extremely small (about 10^-12mole/cm^2 of membrane). This represents the movement of far fewer ions than would be required to alter the chemical concentration gradent.
Under conditions that allow Na+ to cross the membrane more readily the membrane potential will move towards ENa and away from EK.
We saw in the previous section that the resting potential results form the fact the plasma membrane of a resting neuron contains man open potassium channels but only a few open sodium channels. However, when neurons are active, membrane permeability and membrane potential change. The changes occur because neurons contain gated ion channels, ion channels that open or close in response to stimuli. This gating of ion channels forms the basis of nearly all electrical signaling in the nervous system. The opening or closing of an ion channel alters the membrane’s permeability to particular ions, which in turns alters the membrane potential. How have scientists studied these changes? The technique of intracellular recording provides a readout of the state of a single neuron in real time.
To begin exploring gated channels, let’s consider what happens when gated potassium channels that are closed in a resting neuron open. Opening more potassium channels increases the membrane’s permeability to K+, increasing the net diffusion of k+ out of the neurons. In other words, the inside of the membrane becomes more negative. As the membrane potential approaches Ek (-90mV at 37 celsius), the separation of charge or polarity increases. Thus the increase int he magnitude of the membrane potential is called a hyperpolarization. In general hyperpolarization results from any stimulus that increases either the outflow of positive ions or the inflow of negative ions.
Although opening potassium channels causes hyperpolarization, opening some other types of ion channels has an opposite effect, making the inside of the membrane less negative. This reduction in the magnitude of the membrane potential is called a depolarization. Depolarization in neurons often involves gated sodium channels. If the gated sodium channels open,the membrane’s permeability of Na+ increases, causing a depolarization as the membrane potential shifts towards ENa (+62mV at 37 celsius).
The types of hyperpolarization and depolarization we have considered so far are graded potentials because the magnitude of the change in membrane potential varies with the strength of the stimulus.
A larger stimulus causes a greater change in permeability (gated ion channels FTW!) and thus a greater change in the membrane potential. Graded potentials are not the actual nerve signals that travel along axons, but they have a major effect on the generation of nerve signals.
Many of the gated ion channels in neurons are voltage-gated ion channels; that is, they open or close in response to a change in the membrane potential. If a depolarization opens voltage-gated sodium channels, the resulting flow of Na+ into the neuron results in further depolarization. Because the sodium channels are voltage gated, an increased depolarization in turn causes more sodium channels to open, leading to an even greater flow of current. The result is a very rapid opening of all the voltage-gated sodium channels. Such a series of events triggers a massive change in membrane voltage called an action potential.
Action potentials are the nerve impulses, or signals, that carry information along an axon. Before we can discuss how these signals move, or propagate, along an axon, we must first understand more about the changes in membrane voltage that accompany an action potential.
Action potentials occur whenever a depolarization increases the membrane voltage to a particular value, called the threshold. For mammalian neurons, the threshold is a membrane of about -55mV. Once initiated, the action potential has a magnitude that is independent of the strength of the triggering stimulus. Because action potentials occur fully or not at all, they represent an all-or-none response to stimuli. This all-or-none property reflects the fact that depolarization opens voltage-gated sodium channels, and the opening of sodium channel causes further depolarization. This positive-feedback loop of depolarization and channel opening triggers an action potential whenever the membrane potential reaches the threshold.
In most neurons, an action potential lasts only 1-2 milliseconds. Because action potentials are so brief, a neuron can produce hundreds of them per second. Furthermore the frequency with which a neuron generates action potentials can vary in response to input. Such differences in action potential frequency convey information about signal strength. In hearing, for example, louder sounds are reflected by more frequent action potentials in neurons connecting the ear to the brain.