What Is the Synaptic Cleft?

B. Synapses, 1896 S. Sherrington names the functional contacts between neurons and neurons as synapses. There are two types of synapses: electrical synapses and chemical synapses.

Synapses

C. 1896 S. Sherrington named the functional contacts between neurons and neurons as synapses (

Furshpan and Potter first pointed out that

In many animals (including coelenterates, arthropods, arthropods, molluscs, lower and

There are still many difficulties in studying the chemical properties of neurotransmitters, especially central transmitters. Many synaptic neurotransmitters have not been identified. To determine that a substance is a transmitter of an organization, certain criteria must be met, such as the following:
(1) When applied to the post-synaptic membrane, it causes the same physiological effects as those induced by pre-synaptic cells.
(2) This substance must be released when presynaptic neurons are active.
(3) Its effect must be blocked by a blocking agent capable of blocking normal transmission.
Table 1 lists some neurotransmitters and their sites of action.

Acetylcholine is currently the most familiar neurotransmitter. Acetylcholine is released from vertebrate motor axonal ends, vertebrate vegetative nervous system preganglionic ends, parasympathetic postganglionic ends, and some neurons of the vertebrate central nervous system. The transmitter of certain invertebrate neurons is also acetylcholine. Acetylcholine is released from the axon to bind to the receptor, and is then hydrolyzed by cholinesterase to choline and acetic acid on the post-synaptic membrane, terminating the effect of acetylcholine on the post-synaptic membrane. Choline is absorbed by the presynaptic terminals to resynthesize acetylcholine (see figure).

(Acetylcholine receptors can also be divided into two types: one is muscarinic receptor (M-type receptor); the other is nicotinic receptor (N-type receptor) ). M-type receptors are present on all the parasympathetic ganglion-fiber-dominated effectors, and also on the post-sympathetic ganglion-fiber-dominated sweat glands, and on sympathetic vasculature-dominated skeletal muscle vessels. Acetylcholine and M-type Receptor binding can produce a similar effect to muscarinic binding, including cardiac arrest, contraction of bronchial gastrointestinal smooth muscle and pupil sphincter, digestive gland secretion, sweat gland secretion, skeletal muscle vasodilation, etc. Atropine can interact with M N-type receptors block the action of acetylcholine. N-type receptors are present on the post-synaptic membrane of neuromuscular junctions and on the post-synaptic membrane of splanchnic ganglia (sympathetic, parasympathetic ganglia). Acetylcholine can bind to N-type receptors. Produces a similar effect to that of a small amount of nicotine binding to it, that is, the excitation of skeletal muscle and postganglionic neurons. Arrow poison can bind to N-type receptors on the post-synaptic membrane of neuromuscular junctions. Acetylcholine; hexamethonium diamines may, parasympathetic ganglia N postsynaptic membrane receptor binding action and sympathetic blocking acetylcholine.

Norepinephrine, dopamine and serotonin are similar compounds. These compounds are found in neurons of certain vertebrates and invertebrates. Most of them are concentrated in nerve endings. Norepinephrine is an excitatory transmitter of cells in the sympathetic nervous system. The figure above shows the biosynthetic pathways of norepinephrine and epinephrine.

The figure above shows the chemical changes in the adrenergic synapse. After norepinephrine is released from the presynaptic terminals, it combines with the adrenergic receptors on the postsynaptic membrane to exert physiological effects. Most of them are reabsorbed and used by the terminals. Shift enzyme inactivation. The effect of stopping acetylcholine depends on the hydrolysis of acetylcholine by cholinesterase, and the effect of stopping norepinephrine mainly depends on the reabsorption of transmitters by the peripheral. Adrenaline receptors can also be divided into alpha-type adrenaline receptors (referred to as alpha receptors) and beta-type adrenaline receptors (referred to as beta receptors). The combination of norepinephrine and epinephrine with alpha receptors causes excitement of the effector, but there are also cases of inhibition, such as smooth muscle of the small intestine; binding with beta receptors causes inhibition of the effector, but the effect on the heart is excitement, and some adrenal The distribution and effect of the receptors are shown in the table.
Certain amino acids, such as glutamic acid, are transmitters released from excitatory synapses in the central nervous system of vertebrates and excitatory neuromuscular junctions in insects and crustaceans. Gamma aminobutyric acid (GABA), NH2-CH2-CH2-CH2-COOH, is an inhibitory transmitter of the vertebrate central nervous system (cerebral cortex, cerebellum) and plays a very important role. Crustacean inhibitory motor synaptic transmitters are also gamma-aminobutyric acid.
Neuropeptides are a group of polypeptide molecules other than the few "classic" transmitters mentioned above. They are produced and released in the nervous system and function as transmitters or synaptic modulators that affect synaptic transmission. The first neuropeptide was U. S. von Euler and J. H. Gaddum was discovered in 1931. When they tested acetylcholine in rabbit brain and small intestine extracts, they found that this extract caused a contraction of the free intestine similar to acetylcholine, but this contraction could not be blocked by acetylcholine antagonists. They found that the contraction was caused by a polypeptide, named substance P. Since then a series of neuropeptides have been found in the central nervous system, peripheral nervous system, autonomic nervous system and invertebrate nervous system in vertebrates. Interestingly, some neuropeptides were originally found in the internal organs, such as glucagon and cholecystokinin in gastrointestinal hormones. In recent years, fluorescent peptides can be used to locate neuropeptides in tissue sections. There are dozens of neuropeptides currently known, including substance P, enkephalin, vasoactive intestinal polypeptide (VIP), antidiuretic, oxytocin, adrenocorticotropic hormone-releasing factor and the like. Some neuropeptides act as both neurotransmitters and neurohormones, just like norepinephrine. In recent years, it has also been found that some neuropeptides can coexist in the nerve endings with classic transmitters such as acetylcholine and norepinephrine, and are released as cotransmitter of classic transmitters.

Enkephalins and endorphins are two interesting types of neuropeptides because they have analgesic and opioid euphoria. Unlike other neuropeptides, the first thing found in the body is the opioid receptor. In 1973, three laboratories independently discovered the presence of opioid receptors in mammalian brains, which bind to opioids and initiate their effects. The presence of opioid receptors indicates that there are also endogenous opioids in the body, because the natural role of opioid receptors is not to interact with extracts of plants such as poppy, but to interact with certain opioids in the body. A few years later, peptides with opioid activity, opioid peptides, were found in mammalian brains. Opioid peptides vary widely in size from enkephalins of 5 amino acids to -endorphins of 31 amino acids, but they all share 5 common amino acid sequences, namely tyrosine-glycine-glycine-phenylalanine Acid-methionine (or leucine). This sequence is a hallmark of opioid peptides and is necessary for them to bind to opioid receptors and to exhibit opioid pharmacological activity.
Dale proposed in 1935 that the neuron is a unified whole, and the transmitters released by its peripherals should be the same. In 1957 J. Eccles is further summarized as a neuron releasing only one transmitter, known as the Dale principle. Therefore, neurons are named after the released transmitters, such as acetylcholine neurons, epinephrine neurons, and so on. Recent studies have shown that a neuron can contain more than one transmitter, such as neuropeptides in addition to classic transmitters. In some cells of the submandibular ganglia that dominate the salivary glands of cats, vasoactive intestinal peptide (VIP) and acetylcholine coexist. Stimulation of the parasympathetic nerve that innervates the submandibular gland can detect acetylcholine and vasoactive intestinal peptide from the venous blood of the submandibular gland, indicating that two neurotransmitters are released from nerve endings. Low-frequency electrical stimulation (2 Hz) causes vasodilation and saliva secretion. These effects can be enhanced with physostigmine and blocked by atropine, suggesting the effects of acetylcholine. However, vasodilation caused by high-frequency electrical stimulation (15 Hz) is not blocked by atropine, which is the effect of vasoactive peptides.
Recent studies have shown that in addition to the role of neurotransmitters in neuromodulation, neuromodulators are also playing a role. Neuromodulators are substances released by nerve cells and certain endocrine cells. They do not directly cause changes in the function of the dominated cells, but rather modulate the activity of classic transmitters released by presynaptic terminals and the effects of post-synaptic cells on transmitters. reaction.