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Paraphrased from the Wikipedia article "Synapse":
There are two fundamentally different kinds of synapses:
Chemical synapses, which convert electrical activity in the presynaptic neuron into the release of neurotransmitters via the activation of voltage-gated calcium channels. The released neurotransmitters, which vary in type by cell, bind to receptors of the postsynaptic cell, giving rise to complex behaviors.
Electrical synapses, in which presynaptic and postsynaptic are connected by "gap junctions" or synaptic clefts capable of passing electrical current, resulting in rapid signal transduction.
Are there certain structures and locations in the nervous system that are mostly or exclusively chemical synapses, and certain ones that are mostly or exclusively electrical? Or, are they mixed throughout the nervous system?
For example, one might suppose that the neurons which transmit signals from brain to limbs might be electrical, due to the apparent advantage of fast transduction times in this scenario. On the other hand, it might be advantageous for the brain to be capable of more the dynamic, albeit slower, signal transmissions made possible by chemical synapses. Are these intuitions accurate?
Synapses are almost all chemical, the electrical synapses are more of a "special case".
The speed of transmission across limbs, etc, has very little to do with the speed of the actual synapse. The signal itself is conducted electrically inside a given cell (this is an "action potential"), aided in many cases by insulating myelination. The synapse is just the endpoint.
Some places where electrical synapses/gap junctions are present are:
- Between cardiomyocytes, to synchronize heart contraction
- Between certain networks of inhibitory interneurons in the CNS
- In some (but not nearly all) reflex circuits
Synapse is a term pioneered by Charles S. Sherrington in 1897. It is derived from the Greek word “Synapsis”, which means to conjugate or clasp. The communication between the neurons is through synapses only, which facilitate nerve signal transmission from one to the next cell.
A scientist named Sanford Palay observed the ultrastructure of neural tissue to prove the subsistence of synapse. Synapses function as a key junction in the nervous system, without which a signal cannot reach the brain directly.
Electrical synapses can directly pass the nerve impulse to neighbouring cells during the time of fast defence responses. On the other hand, chemical synapses involve the excitation of a nerve impulse that causes the release of neurotransmitters, which can carry the signal further via binding with specific cell receptors.
In this post, we will learn the definition, types (based on neuron attachment and presence of neuroreceptors and neurotransmitters) and function of the synapses. Also, the mechanism and diagram of electrical and chemical synapses have been explained.
Synapses are functional connections between neurons, or between neurons and other types of cells.   A typical neuron gives rise to several thousand synapses, although there are some types that make far fewer.  Most synapses connect axons to dendrites,   but there are also other types of connections, including axon-to-cell-body,   axon-to-axon,   and dendrite-to-dendrite.  Synapses are generally too small to be recognizable using a light microscope except as points where the membranes of two cells appear to touch, but their cellular elements can be visualized clearly using an electron microscope.
Chemical synapses pass information directionally from a presynaptic cell to a postsynaptic cell and are therefore asymmetric in structure and function. The presynaptic axon terminal, or synaptic bouton, is a specialized area within the axon of the presynaptic cell that contains neurotransmitters enclosed in small membrane-bound spheres called synaptic vesicles (as well as a number of other supporting structures and organelles, such as mitochondria and endoplasmic reticulum). Synaptic vesicles are docked at the presynaptic plasma membrane at regions called active zones.
Immediately opposite is a region of the postsynaptic cell containing neurotransmitter receptors for synapses between two neurons the postsynaptic region may be found on the dendrites or cell body. Immediately behind the postsynaptic membrane is an elaborate complex of interlinked proteins called the postsynaptic density (PSD).
Proteins in the PSD are involved in anchoring and trafficking neurotransmitter receptors and modulating the activity of these receptors. The receptors and PSDs are often found in specialized protrusions from the main dendritic shaft called dendritic spines.
Synapses may be described as symmetric or asymmetric. When examined under an electron microscope, asymmetric synapses are characterized by rounded vesicles in the presynaptic cell, and a prominent postsynaptic density. Asymmetric synapses are typically excitatory. Symmetric synapses in contrast have flattened or elongated vesicles, and do not contain a prominent postsynaptic density. Symmetric synapses are typically inhibitory.
The synaptic cleft —also called synaptic gap— is a gap between the pre- and postsynaptic cells that is about 20 nm (0.02 μ) wide.  The small volume of the cleft allows neurotransmitter concentration to be raised and lowered rapidly. 
An autapse is a chemical (or electrical) synapse formed when the axon of one neuron synapses with its own dendrites.
Here is a summary of the sequence of events that take place in synaptic transmission from a presynaptic neuron to a postsynaptic cell. Each step is explained in more detail below. Note that with the exception of the final step, the entire process may run only a few hundred microseconds, in the fastest synapses. 
- The process begins with a wave of electrochemical excitation called an action potential traveling along the membrane of the presynaptic cell, until it reaches the synapse.
- The electrical depolarization of the membrane at the synapse causes channels to open that are permeable to calcium ions.
- Calcium ions flow through the presynaptic membrane, rapidly increasing the calcium concentration in the interior.
- The high calcium concentration activates a set of calcium-sensitive proteins attached to vesicles that contain a neurotransmitter chemical.
- These proteins change shape, causing the membranes of some "docked" vesicles to fuse with the membrane of the presynaptic cell, thereby opening the vesicles and dumping their neurotransmitter contents into the synaptic cleft, the narrow space between the membranes of the pre- and postsynaptic cells.
- The neurotransmitter diffuses within the cleft. Some of it escapes, but some of it binds to chemical receptor molecules located on the membrane of the postsynaptic cell.
- The binding of neurotransmitter causes the receptor molecule to be activated in some way. Several types of activation are possible, as described in more detail below. In any case, this is the key step by which the synaptic process affects the behavior of the postsynaptic cell.
- Due to thermal vibration, the motion of atoms, vibrating about their equilibrium positions in a crystalline solid, neurotransmitter molecules eventually break loose from the receptors and drift away.
- The neurotransmitter is either reabsorbed by the presynaptic cell, and then repackaged for future release, or else it is broken down metabolically.
Neurotransmitter release Edit
The release of a neurotransmitter is triggered by the arrival of a nerve impulse (or action potential) and occurs through an unusually rapid process of cellular secretion (exocytosis). Within the presynaptic nerve terminal, vesicles containing neurotransmitter are localized near the synaptic membrane. The arriving action potential produces an influx of calcium ions through voltage-dependent, calcium-selective ion channels at the down stroke of the action potential (tail current).  Calcium ions then bind to synaptotagmin proteins found within the membranes of the synaptic vesicles, allowing the vesicles to fuse with the presynaptic membrane.  The fusion of a vesicle is a stochastic process, leading to frequent failure of synaptic transmission at the very small synapses that are typical for the central nervous system. Large chemical synapses (e.g. the neuromuscular junction), on the other hand, have a synaptic release probability of 1. Vesicle fusion is driven by the action of a set of proteins in the presynaptic terminal known as SNAREs. As a whole, the protein complex or structure that mediates the docking and fusion of presynaptic vesicles is called the active zone.  The membrane added by the fusion process is later retrieved by endocytosis and recycled for the formation of fresh neurotransmitter-filled vesicles.
An exception to the general trend of neurotransmitter release by vesicular fusion is found in the type II receptor cells of mammalian taste buds. Here the neurotransmitter ATP is released directly from the cytoplasm into the synaptic cleft via voltage gated channels. 
Receptor binding Edit
Receptors on the opposite side of the synaptic gap bind neurotransmitter molecules. Receptors can respond in either of two general ways. First, the receptors may directly open ligand-gated ion channels in the postsynaptic cell membrane, causing ions to enter or exit the cell and changing the local transmembrane potential.  The resulting change in voltage is called a postsynaptic potential. In general, the result is excitatory in the case of depolarizing currents, and inhibitory in the case of hyperpolarizing currents. Whether a synapse is excitatory or inhibitory depends on what type(s) of ion channel conduct the postsynaptic current(s), which in turn is a function of the type of receptors and neurotransmitter employed at the synapse. The second way a receptor can affect membrane potential is by modulating the production of chemical messengers inside the postsynaptic neuron. These second messengers can then amplify the inhibitory or excitatory response to neurotransmitters. 
After a neurotransmitter molecule binds to a receptor molecule, it must be removed to allow for the postsynaptic membrane to continue to relay subsequent EPSPs and/or IPSPs. This removal can happen through one or more processes:
- The neurotransmitter may diffuse away due to thermally-induced oscillations of both it and the receptor, making it available to be broken down metabolically outside the neuron or to be reabsorbed. 
- Enzymes within the subsynaptic membrane may inactivate/metabolize the neurotransmitter. pumps may actively pump the neurotransmitter back into the presynaptic axon terminal for reprocessing and re-release following a later action potential. 
The strength of a synapse has been defined by Sir Bernard Katz as the product of (presynaptic) release probability pr, quantal size q (the postsynaptic response to the release of a single neurotransmitter vesicle, a 'quantum'), and n, the number of release sites. "Unitary connection" usually refers to an unknown number of individual synapses connecting a presynaptic neuron to a postsynaptic neuron. The amplitude of postsynaptic potentials (PSPs) can be as low as 0.4 mV to as high as 20 mV.  The amplitude of a PSP can be modulated by neuromodulators or can change as a result of previous activity. Changes in the synaptic strength can be short-term, lasting seconds to minutes, or long-term (long-term potentiation, or LTP), lasting hours. Learning and memory are believed to result from long-term changes in synaptic strength, via a mechanism known as synaptic plasticity.
Desensitization of the postsynaptic receptors is a decrease in response to the same neurotransmitter stimulus. It means that the strength of a synapse may in effect diminish as a train of action potentials arrive in rapid succession – a phenomenon that gives rise to the so-called frequency dependence of synapses. The nervous system exploits this property for computational purposes, and can tune its synapses through such means as phosphorylation of the proteins involved.
Synaptic transmission can be changed by previous activity. These changes are called synaptic plasticity and may result in either a decrease in the efficacy of the synapse, called depression, or an increase in efficacy, called potentiation. These changes can either be long-term or short-term. Forms of short-term plasticity include synaptic fatigue or depression and synaptic augmentation. Forms of long-term plasticity include long-term depression and long-term potentiation. Synaptic plasticity can be either homosynaptic (occurring at a single synapse) or heterosynaptic (occurring at multiple synapses).
Homosynaptic plasticity Edit
Homosynaptic Plasticity (or also homotropic modulation) is a change in the synaptic strength that results from the history of activity at a particular synapse. This can result from changes in presynaptic calcium as well as feedback onto presynaptic receptors, i.e. a form of autocrine signaling. Homosynaptic plasticity can affect the number and replenishment rate of vesicles or it can affect the relationship between calcium and vesicle release. Homosynaptic plasticity can also be postsynaptic in nature. It can result in either an increase or decrease in synaptic strength.
One example is neurons of the sympathetic nervous system (SNS), which release noradrenaline, which, besides affecting postsynaptic receptors, also affects presynaptic α2-adrenergic receptors, inhibiting further release of noradrenaline.  This effect is utilized with clonidine to perform inhibitory effects on the SNS.
Heterosynaptic plasticity Edit
Heterosynaptic Plasticity (or also heterotropic modulation) is a change in synaptic strength that results from the activity of other neurons. Again, the plasticity can alter the number of vesicles or their replenishment rate or the relationship between calcium and vesicle release. Additionally, it could directly affect calcium influx. Heterosynaptic plasticity can also be postsynaptic in nature, affecting receptor sensitivity.
One example is again neurons of the sympathetic nervous system, which release noradrenaline, which, in addition, generates an inhibitory effect on presynaptic terminals of neurons of the parasympathetic nervous system. 
In general, if an excitatory synapse is strong enough, an action potential in the presynaptic neuron will trigger an action potential in the postsynaptic cell. In many cases the excitatory postsynaptic potential (EPSP) will not reach the threshold for eliciting an action potential. When action potentials from multiple presynaptic neurons fire simultaneously, or if a single presynaptic neuron fires at a high enough frequency, the EPSPs can overlap and summate. If enough EPSPs overlap, the summated EPSP can reach the threshold for initiating an action potential. This process is known as summation, and can serve as a high pass filter for neurons. 
On the other hand, a presynaptic neuron releasing an inhibitory neurotransmitter, such as GABA, can cause an inhibitory postsynaptic potential (IPSP) in the postsynaptic neuron, bringing the membrane potential farther away from the threshold, decreasing its excitability and making it more difficult for the neuron to initiate an action potential. If an IPSP overlaps with an EPSP, the IPSP can in many cases prevent the neuron from firing an action potential. In this way, the output of a neuron may depend on the input of many different neurons, each of which may have a different degree of influence, depending on the strength and type of synapse with that neuron. John Carew Eccles performed some of the important early experiments on synaptic integration, for which he received the Nobel Prize for Physiology or Medicine in 1963.
When a neurotransmitter is released at a synapse, it reaches its highest concentration inside the narrow space of the synaptic cleft, but some of it is certain to diffuse away before being reabsorbed or broken down. If it diffuses away, it has the potential to activate receptors that are located either at other synapses or on the membrane away from any synapse. The extrasynaptic activity of a neurotransmitter is known as volume transmission.  It is well established that such effects occur to some degree, but their functional importance has long been a matter of controversy. 
Recent work indicates that volume transmission may be the predominant mode of interaction for some special types of neurons. In the mammalian cerebral cortex, a class of neurons called neurogliaform cells can inhibit other nearby cortical neurons by releasing the neurotransmitter GABA into the extracellular space.  Along the same vein, GABA released from neurogliaform cells into the extracellular space also acts on surrounding astrocytes, assigning a role for volume transmission in the control of ionic and neurotransmitter homeostasis.  Approximately 78% of neurogliaform cell boutons do not form classical synapses. This may be the first definitive example of neurons communicating chemically where classical synapses are not present. 
An electrical synapse is an electrically conductive link between two abutting neurons that is formed at a narrow gap between the pre- and postsynaptic cells, known as a gap junction. At gap junctions, cells approach within about 3.5 nm of each other, rather than the 20 to 40 nm distance that separates cells at chemical synapses.   As opposed to chemical synapses, the postsynaptic potential in electrical synapses is not caused by the opening of ion channels by chemical transmitters, but rather by direct electrical coupling between both neurons. Electrical synapses are faster than chemical synapses.  Electrical synapses are found throughout the nervous system, including in the retina, the reticular nucleus of the thalamus, the neocortex, and in the hippocampus.  While chemical synapses are found between both excitatory and inhibitory neurons, electrical synapses are most commonly found between smaller local inhibitory neurons. Electrical synapses can exist between two axons, two dendrites, or between an axon and a dendrite.   In some fish and amphibians, electrical synapses can be found within the same terminal of a chemical synapse, as in Mauthner cells. 
One of the most important features of chemical synapses is that they are the site of action for the majority of psychoactive drugs. Synapses are affected by drugs such as curare, strychnine, cocaine, morphine, alcohol, LSD, and countless others. These drugs have different effects on synaptic function, and often are restricted to synapses that use a specific neurotransmitter. For example, curare is a poison that stops acetylcholine from depolarizing the postsynaptic membrane, causing paralysis. Strychnine blocks the inhibitory effects of the neurotransmitter glycine, which causes the body to pick up and react to weaker and previously ignored stimuli, resulting in uncontrollable muscle spasms. Morphine acts on synapses that use endorphin neurotransmitters, and alcohol increases the inhibitory effects of the neurotransmitter GABA. LSD interferes with synapses that use the neurotransmitter serotonin. Cocaine blocks reuptake of dopamine and therefore increases its effects.
During the 1950s, Bernard Katz and Paul Fatt observed spontaneous miniature synaptic currents at the frog neuromuscular junction. [ citation needed ] Based on these observations, they developed the 'quantal hypothesis' that is the basis for our current understanding of neurotransmitter release as exocytosis and for which Katz received the Nobel Prize in Physiology or Medicine in 1970. [ citation needed ] In the late 1960s, Ricardo Miledi and Katz advanced the hypothesis that depolarization-induced influx of calcium ions triggers exocytosis.
Sir Charles Scott Sherringtonin coined the word 'synapse' and the history of the word was given by Sherrington in a letter he wrote to John Fulton:
'I felt the need of some name to call the junction between nerve-cell and nerve-cell. I suggested using "syndesm". He [ Sir Michael Foster ] consulted his Trinity friend Verrall, the Euripidean scholar, about it, and Verrall suggested "synapse" (from the Greek "clasp").'–Charles Scott Sherrington 
- all motor neurons activating skeletal muscle. [Discussion]
- all preganglionic neurons of the autonomic nervous system [Discussion]
- the postganglionic neurons of the parasympathetic branch of the autonomic nervous system.
Nicotinic vs. Muscarinic Acetylcholine Receptors
- Nicotinic receptors are
- found at the neuromuscular junction of skeletal (only) muscles,
- on the post-ganglionic neurons of the parasympathetic nervous system, and
- on many neurons in the brain (e.g. neurons in the hypothalamus whose activation by nicotine suppresses appetite).
- Nicotine is an agonist (hence the name).
- Curare is an antagonist (hence its ability to paralyze skeletal muscles).
- found at the neuromuscular junctions of cardiac and smooth muscle as well as on
- glands, and on
- the post-ganglionic neurons of the sympathetic nervous system.
- Muscarine (a toxin produced by certain mushrooms) is an agonist.
- Atropine is an antagonist (hence its use in acetylcholinesterase poisoning).
- Glutamic acid (Glu) used at excitatory synapses in the central nervous system (CNS). Essential for long term potentiation (LTP), a form of memory.
Like GABA, Glu acts on two types of CNS synapses:
- FAST (
- Noradrenaline (also called norepinephrine). Released by postganglionic neurons of the sympathetic branch of the autonomic nervous system. Also used at certain synapses in the CNS.
- Dopamine. Used at certain synapses in the CNS.
- Serotonin (also known as 5-hydroxytryptamine or 5HT). Synthesized from tryptophan (Trp).
Both of these neurotransmitters are confined to synapses in the brain. (However, serotonin is also secreted from the duodenum, where it acts in a paracrine manner to stimulate intestinal peristalsis, and as a circulating hormone, where it is taken up by platelets and also suppresses bone formation.)
Nerve Cells and Synapses: Grade 9 Understanding for IGCSE Biology 2.88 2.89
There is very little in the iGCSE specification about nerve cells and synapses. This is a shame since neuroscience is going to be one of the massive growth areas in Biology in the 21st century. There is a syllabus point about reflex acs and I draw your attention to this blog post about that: https://pmgbiology.wordpress.com/2014/04/22/a-simple-reflex-arc/
But in this new post I am going to give you a tiny bit more detail about the types of nerve cells (neurones) that you might encounter, together with an explanation about the most important component of the nervous systems: the chemical synapse.
Neurones are the cells in the nervous system that are adapted to send nerve impulses. You won’t fully understand what the nerve impulse is until year 13 but it is correct so that it is a temporary electrical event that can be transmitted over large distances within a cell with no loss of signal strength. The upshot of this is that neurones can be very long indeed…..
There are three basic types of neurone that are grouped according to their function:
Motor neurones (efferent neurones) take nerve impulses from the CNS to skeletal muscle causing it to contract
Sensory neurones (afferent neurones) take nerve impulses from sensory receptors into the CNS
Relay (or sometimes Inter) neurones are found within the CNS and basically link sensory to motor neurones.
These three types of neurone also have different structures although many features are shared….
This is a diagram of a generalised motor neurone: I know it is a motor neurone since the cell body is at one end of the cell. The cell body contains the nucleus, most of the cytoplasm and many organelles. Structures that carry a nerve impulse towards the cell body are called dendrites (if there are lots of them) and a dendron if there is only one. The axon is the long thin projection of the cell that takes the nerve impulse away from the cell body. The axon will finish with a collection of nerve endings or synapses.
Neurones can only send nerve impulses in one direction. In the diagram above these two cells can only send impulses from left to right as shown. This is due to the nature of the junction between the cells, the synapse (see later on….)
The diagram above shows a sensory neurone. You can tell this because it has receptors at one end collecting sensory information to take to the CNS. The position of the cell body is also different in sensory neurones: in all sensory neurones the cell body is off at right angles to the axon/dendron.
You can see from the diagrams that motor and sensory neurones tend to be surrounded by a myelin sheath. Myelin is a type of lipid that acts as an insulator, speeding up the nerve impulse from around 0.5m/s in unmyelinated neurones to about 100 m/s in the fastest myelinated ones. The myelin sheath is made from a whole load of cells (glial cells) but there are gaps between glial cells called nodes of Ranvier. These will become important in Y12/13 when you study how the impulse manages to travel so fast in a myelinated neurone.
Relay neurones, also known as interneurones, have a much simpler structure. They are only found in the CNS, almost always unmyelinated and have their cell body in the centre of the cell.
The diagram above shows the three types of neurone and indeed how they are linked up in a simple reflex arc. The artist hasn’t really shown the interneurone structure very well, but it was the best I could find just now…..
Nerve cells are linked together (and indeed linked to muscle cells) by structures known as synapses. There are a lot of synapses in your nervous system. The human brain contains around 100 billion neurones and each neurone is linked by synapses to around 1000 other cells: a grand total of 100 trillion synapses. 100 000 000 000 000 is a big number.
The big idea with synapses is that the two neurones do not actually touch. There is a tiny gap called the synaptic cleft between the cells. The nerve impulse does not cross this tiny gap as an electrical event but instead there are chemicals called neurotransmitters that diffuse across the synaptic cleft.
The nerve impulse arrives at the axon terminal of the presynaptic neurone. Inside this swelling are thousands of tiny membrane packets called vesicles, each one packed with a million or so molecules of neurotransmitter. When the impulse arrives at the terminal, a few hundred of these vesicles are stimulated to move towards and then fuse with the cell membrane, releasing the neurotransmitter into the synaptic cleft. The neurotransmitter will diffuse rapidly across the gap and when it reaches the post-synaptic membrane, it binds to specific receptor molecules embedded in the post-synaptic membrane. The binding of the neurotransmitter to the receptor often causes a new nerve impulse to form in the post-synaptic cell.
These chemical synapses are really beautiful things. They ensure the nerve impulse can only cross the synapse in one direction (can you see why?) and also they are infinitely flexible. They can be strengthened and weakened, their effects can be added together and when this is all put together, complex behaviour can emerge. I am going to exhibit some complex behaviour now by choosing to take my dogs for a walk… And it all happened due to synapses in my brain!
What is an Electrical Synapse
An electrical synapse refers to cell junctions between nerve cells through which the transmission of nerve impulses occur by means of ions. The synaptic cleft of an electrical synapse is small, and the two plasma membranes of the neurons are connected together via a gap junction. One gap junction contains precisely aligned channel protein pairs in both pre-synaptic and post-synaptic membranes. Each channel pair forms a pore, which is much larger than the pore of a typical ion channel. Therefore, large molecules can be transported through these gap junctions in addition to the ions. Hence, intracellular metabolites and second messengers can pass through two neurons. However, electrical synapses allow the passive transmission of the action potential through the pores of the gap junctions from one neuron to the second neuron. The structure of the electrical synapses is shown in figure 2.
Figure 2: Electrical Synapses
The transmission of the action potentials can occur in both directions through an electrical synapse. Moreover, the speed of transmission of the action potentials is very high. The electrical synapses are mainly involved in synchronizing the activity of a group of neurons. The neurons in the hypothalamus contain electrical synapses, firing the action potentials of many neurons at the same time.
Chapter Review Questions
Neurons contain_____________ , which can receive signals from other neurons.
A(n)_____________ neuron has one axon and multiple dendrites.
How are neurons similar to other cells? How are they unique?
Multiple sclerosis causes demyelination of axons in the brain and spinal cord. Why is this prob- lematic?
The part of the brain that is responsible for coordination during movement is the________ _.
Which part of the nervous system directly controls the digestive system?
- parasympathetic nervous system
- central nervous system
- spinal cord
- sensory-somatic nervous system
What are the main functions of the spinal cord?
What are the main differences between the sympathetic and parasympathetic branches of the autonomic nervous system?
What are the main functions of the sensory-somatic nervous system?
For a neuron to fire an action potential, its membrane must reach___________ _.
- the threshold of excitation
- the refractory period
- inhibitory postsynaptic potential
After an action potential, the opening of additional voltage-gated_____________ channels and the
inactivation of sodium channels, cause the membrane to return to its resting membrane potential.
How does myelin aid propagation of an action potential along an axon? How do the nodes of Ranvier help this process?
What are the main steps in chemical neurotransmission?
Neurons contain organelles common to all cells, such as a nucleus and mitochondria. They are unique because they contain dendrites, which can receive signals from other neurons, and axons that can send these signals to other cells.
Myelin provides insulation for signals traveling along axons. Without myelin, signal transmission can slow down and degrade over time. This would slow down neuronal communication across the nervous system and affect all downstream functions.
Figure 17.8 Potassium channel blockers slow the repolarization phase, but have no effect on depolarization. to Exercise 17.3.2 (p. 367)
Myelin prevents the leak of current from the axon. Nodes of Ranvier allow the action potential to be regenerated at specific points along the axon. They also save energy for the cell since voltage-gated ion channels and sodium-potassium transporters are not needed along myelinated portions of the axon.
An action potential travels along an axon until it depolarizes the membrane at an axon terminal. Depo- larization of the membrane causes voltage-gated Ca + channels to open and Ca + to enter the cell. The intracellular calcium influx causes synaptic vesicles containing neurotransmitter to fuse with the presynaptic membrane. The neurotransmitter diffuses across the synaptic cleft and binds to receptors on the postsynap- tic membrane. Depending on the specific neurotransmitter and postsynaptic receptor, this action can cause positive (excitatory postsynaptic potential) or negative (inhibitory postsynaptic potential) ions to enter the cell.
The spinal cord transmits sensory information from the body to the brain and motor commands from the brain to the body through its connections with peripheral nerves. It also controls motor reflexes.
The sympathetic nervous system prepares the body for “fight or flight,” whereas the parasympathetic nervous system allows the body to “rest and digest.” Sympathetic neurons release norepinephrine onto target organs parasympathetic neurons release acetylcholine. Sympathetic neuron cell bodies are located in sympathetic ganglia. Parasympathetic neuron cell bodies are located in the brainstem and sacral spinal cord. Activation of the sympathetic nervous system increases heart rate and blood pressure and decreases digestion and blood flow to the skin. Activation of the parasympathetic nervous system decreases heart rate and blood pressure and increases digestion and blood flow to the skin.
The sensory-somatic nervous system transmits sensory information from the skin, muscles, and sensory organs to the CNS. It also sends motor commands from the CNS to the muscles, causing them to contract.
The Uncertainty Principle: Electronic Synapses
- Contributed by Ed Vitz, John W. Moore, Justin Shorb, Xavier Prat-Resina, Tim Wendorff, & Adam Hahn
- ChemPRIME at Chemical Education Digital Library (ChemEd DL)
The Heisenberg Uncertainty Principle is easily stated, but it obviously has had a huge impact our science. Here we'll look at the implications for neural conduction through lesser known electronic synapes. Electronic synapses are found throughout the nervous system, but they are less common than chemical synapses, through which neural transmitters like serotonin carry the signal. In electronic synapses, electrons carry the signal, so they can be faster, and possibly more reliable than chemical synapses.
The uncertainty principle states that the product of the uncertainty in momentum (P) and the position of a particle cannot be less than a constant expressed in terms of Planck's Constant, h:
Here &Delta can be taken as the standard deviation, or random uncertainty in measurement. Planck's constant is h = 6.626 x 10 -34 J s, but the uncertainty principle is sometimes expressed in terms of : (hbar) , which is h/2&pi:
The Uncertainty Principle can be stated in terms of other complementary variables, like energy and time:
Example (PageIndex<1>): Uncertainty of the Position of an Electron
Suppose we have an electrical synapse rather than a chemical synapse. Electrical synapses are not as common as chemical synapses, but are found throughout the nervous system. They provide a narrow gap between the pre- and postsynaptic cells of about 3.5 nm rather than the 20 to 40 nm distance of chemical synapses  . If the electron is transmitted from one neuron to the other with a velocity of 5 x 10 6 m/s (its speed in a hydrogen atom) and the speed is known to within 10% due to variable properties of the synapse, what is the uncertainty in the position of the electron?
The uncertainty in momentum is &Deltamv, and if the mass (9.11 x 10 -31 kg) is known with good precision, this is m&Deltav = 9.11 × 10 -31 kg x 0.10 x 5 x 10 6 m/s = 4.6 x 10 -25 kg m s -1
(Delta X ge ext <1.2> imes ext<10>^ <-10> ext
We're told that the entire synapse is 3.5 nm (3.5 x 10 -9 m), so the electron's position is localized in some 10% of the synaptic cleft. If no other factors (like chemical forces that direct the electron more precisely by decreasing the uncertainty in its motion) improve this localization, what do you conclude about the precision of neural transmission through electrical synapses?
Suppose that the electron in the example above were not in a synapse, but rather in a hydrogen atom, in one of the orbitals around the nucleus. We know that the hydrogen atom has a diameter of about 1 x 10 -10 m (100 pm), so the electron could be anywhere in that space if we assume the 10% uncertainty in speed (it would be delocalized over 10 atoms if we specified the velocity to 1%).
Our inability to locate an electron exactly may seem rather strange, but it arises whether we think in terms of waves or of particles. Suppose an experiment is to be done to locate a billiard ball moving across a pool table whose surface is hidden under a black cloth.
Figure (PageIndex<1>) Determining the location and speed of a particle. (a) Locating a billiard ball (X)by bouncing a second billiard ball (Y) off it (b) locating a billiard ball by bouncing a table-tennis ball off it (c) locating a billiard ball by bouncing photons of visible off it (d) locating an electron by bouncing a photon off it.
One way to do this would be to try to bounce a second billiard ball off the first one (Fig. (PageIndex<1>). When a hit was made and the second ball emerged from under the cloth, we would have a pretty good idea of where the first ball was. The only trouble with the experiment is that the position and speed of the first ball would almost certainly be changed by the collision. To lessen this effect, a table-tennis ball could be substituted for the second billiard ball&mdashits smaller mass would produce a much smaller change in the motion of the first ball. Clearly, the lighter and more delicate the &ldquoprobe&rdquo we use to try to locate the first ball, the less our measurement will affect it. The best way to locate the first billiard ball and determine its speed would be to remove the cover from the table so it could be seen. In this case, however, something is still &ldquobouncing&rdquo off the first billiard ball (Fig. (PageIndex<1>)c). If we are to see the ball, particles of visible light, or photons, must strike the ball and be reflected to our eyes. Since each photon is very small and has very little energy by comparison with that needed to change the motion of the billiard ball, looking at a ball is an excellent means of observing it without changing its position or speed.
But to observe an electron is quite another story, since the mass of an electron is far smaller than that of a billiard ball. Anything (such as a photon of light) which can be bounced off an electron in such a way as to locate it precisely would have far more energy than would be required to change the path of the electron. Hence it would be impossible to predict the electron&rsquos future speed or position from the experiment. The idea that it is impossible to determine accurately both the location and the speed of any particle as small as an electron is called the uncertainty principle. It was first proposed in 1927 by Werner Heisenberg (1901 to 1976).
According to the uncertainty principle, even if we draw an analogy between the electron in a box and a billiard ball (Fig. 1a in Wave Mechanics), it will be impossible to determine both the electron&rsquos exact position in the box and its exact speed. Since kinetic energy depends on speed (½ mu 2 ) and Eq. (4) in Wave Mechanics assigns exact values of kinetic energy to the electron in the box, the speed can be calculated accurately. This means that determination of the electron&rsquos position will be very inexact. It will be possible to talk about the probability that the electron is at a specific location, but there will also be some probability of finding it somewhere else in the box. Since it is impossible to know precisely where the electron is at a given instant, the question, &ldquoHow does it get from one place to another?&rdquo is pointless. There is a finite probability that it was at the other place to begin with!
It is possible to be quantitative about the probability of finding a &ldquobilliard-ball&rdquo electron at a given location, however. Shortly after the uncertainty principle was proposed, the German physicist Max Born (1882 to 1969) suggested that the intensity of the electron wave at any position in the box was proportional to the probability of finding the electron (as a particle) at that same position. Thus if we can determine the shapes of the waves to be associated with an electron, we can also determine the relative probability of its being located at one point as opposed to another. The wave and particle models for the electron are thus connected to and reinforce each other. Niels Bohr suggested the term complementary to describe their relationship. It does no good to ask, &ldquoIs the electron a wave or a particle?&rdquo Both are ways of drawing an analogy between the microscopic world and macroscopic things whose behavior we understand. Both are useful in our thinking, and they are complementary rather than mutually exclusive.
A graphic way of indicating the probability of finding the electron at a particular location is by the density of shading or stippling along the length of the box. This has been done in Fig. (PageIndex<2>) for the same three electron waves previously illustrated in Fig. 1 from Wave Mechanics. Notice that the density of dots is large wherever the electron wave is large.(This would correspond in the guitar-string analogy to places where the string was vibrating quite far from its rest position.)
Figure (PageIndex<2>) Indicating electron density or electron probability by the density of dots for the electron in a box. Nodes. where the probability of finding the electron is zero, are indicated. In the guitar-string analogy a node corresponds to a point on the string which is not vibrating up and down.
Where the electron wave is small (near the ends of the box in all three cases and at the nodes indicated in the figure), there are only a small number of dots. (A node is a place where the intensity of the wave is zero, that is, in the guitar-string analogy, where the string has not moved from its rest position.)
If the electron is thought of as a wave occupying all parts of the box at once, we can speak of an electron cloud which has greater or lesser density in various parts of the box. There will be a greater quantity of negative charge in a region of high density (a region where there is a greater concentration of dots) than in one of low density. In an atom or molecule, according to the uncertainty principle, the best we can do is indicate electron density in various regions&mdashwe cannot locate the precise position of the electron. Therefore electron dot-density diagrams, such as the ones shown in Fig. (PageIndex<2>), give a realistic and useful picture of the behavior of electrons in atoms. In such a diagram the electron density or probability of finding the electron is indicated by the number of dots per unit area. We will encounter electron dot-density diagrams quite often throughout this book. These have all been generated by a computer from accurate mathematical descriptions of the atom or molecule under discussion.
David C. Spray , . Eliana Scemes , in Encyclopedia of the Neurological Sciences , 2003
Gap Junctions between Neurons
The concept that electrical synapses might play a major role in neural transmission has been supported by recent identification of frequent, although tiny, gap junctions between neurons in the central nervous system and by the discovery that at least one connexin [connexin36 (Cx36)] is almost exclusive in its neuronal expression and leads to loss of coupling among neurons when its gene is silenced (Cx36 knockout mice). Electrotonic synapses between GABAergic interneurons formed of Cx36 are believed to facilitate neuronal synchrony and contribute to large-range oscillatory rhythms in cerebral cortex, striatum, hippocampus, and cerebellum. Gap junctions between neurons also appear to play an important role in development, coordinating activity of afferents so as to optimize the formation of chemical synaptic inputs onto appropriate targets, as in the case of tectal projection of retinal ganglion neurons.
Nervous system is a term used to refer to a network of nerve cells and fibres which transmits nerve impulses between parts of the body. It can also be defined as a highly complex part of the body of an animal that coordinates its actions and sensory information by transmitting signals to and from different parts of the body.It is a group of specialised cells for the conduction of electrochemical stimuli from sensory receptors through a network to the site at which a response occurs. What is a stimuli? * It is a change in external environment of an organism for example changes in light, sound, temperature, motion and odour. The function of the nervous system on a general basis is stimulus response coordination.
Types of the nervous system
Central Nervous System
Peripheral Nervous System
✴The central nervous system os made up of the brain and spinal cord thus it is referred to as central because it combines information from the entire body. ✴The peripheral nervous system is composed of the somatic nervous system and autonomic nervous system. The specialised cells that make up a nervous system are called neurons. Neurons are specialised nerve cells that come in many different shapes and sizes. They are like ordinary cells but they have a few differentiated cellular organelles. These organelles are dendrites and axons. Dendrites bring electrical signals to the cell body while axons take information away from the cell body. Neurons communicate with each other through an electrochemical process. They also contain specialised features besides axons and dendrites which are organs(synapses) and chemicals(neurotransmitters). A synapse is a structure that permits a neuron to pass an electrical chemical signal to another neuron to the target effector cell.
Classification of Neurons
1.) According to the number of extensions that extend from the neuron’s cell to the cell body ✴according to the above classification there results three types of neurons.
- Bipolar neurons -these neurones have two extensions for example retinal cells.
- Pseudounipolar neurons -these have two axons from example the dorsal root ganglion cells.
- Multipolar neurons -these have many extensions for example spinal motor neurons.
2.) According to the direction in which they send information
✴according to this classification there results three types of neurons.
- Sensory neurons(afferent neurons) *these neurons send information through sensory receptors towards the central nervous system.
Sensory neurons are nerve cells within the nervous system responsible for converting external stimuli from the organism’s environment into internal electrical impulses. Fro example some sensory neurons respond to tactile stimuli and can activate motor neurons in order to achieve muscle contraction. Sensory neurons are unipolar with cell bodies in spinal or cranial nerve ganglia. Cell bodies of the sensory neurons leading to the spinal cord are located in clusters, the dorsal root ganglia, next to the spinal cord. The axon extends in both directions .
- Motor neurones(efferent neurons) -these send information away from the central nervous system to muscles or glands.
Motor neurons are nerve cells forming part of a pathway along which impulses pass from the brain or spinal cord to a muscle or gland. Motor neurons are responsible for transmitting signals from the spinal cord to muscles, enabling muscle contraction. Motor neurons function by injecting into muscle groups visible tracers that are transported by axons of the lower motor neurons back to their cell bodies, the lower motor neurons that innervate the body’s skeletal muscles can be seen in histological sections of the ventral horns of the spinal cord.
- Relay neurons(interneurones) -these send information between sensory neurons and motor neurones. They are mostly located in the central nervou system..
Relay neurons are nerve cells responsible for sending information between sensory neurons and motor neurons.
Some general differences between the three types of neurons
(*CNS means central nervous system for the table above)
For information to be transmitted it is in the form of a chemical called a neurotransmitter. A neurotransmitter is released by the axon terminal when the vesicles fuse with the membrane of the axon terminal spilling the neurotransmitter into the synaptic cleft. Neurotransmitters by definition are endogenous chemicals that enable neurotransmission. It is a type of chemical messenger which transmits signals across a chemical synapse such as a neuromuscular junction from one neuron to another”target” neuron, muscle cell or gland cell.