Cell body, of neuron

Impulse-evoked release of 5-HT, like that of noradrenaline, is subject to fine control by a system of autoreceptors, in particular 5-HTia receptors on the cell bodies of neurons in the Raphe nuclei and 5-HTib/id receptors on their terminals. Because these are all G /o protein-coupled receptors, their activation reduces the synthesis of cAMP so that 5-HTia agonists (or 5-HT itself) decrease neuronal excitability and the firing of Raphe neurons whereas activation of 5-HTib/id receptors seems to disrupt the molecular cascade that links the receptor with transmitter release (see Chapter 4). 

The gray matter, which contains the cell bodies of neurons, is on the outer surface of the cerebrum and forms the cerebral cortex. The white matter, composed of the myelinated axons of neurons, is found underlying the cortex in the core of the cerebrum. These axons are bundled together according to function and organized into units referred to as tracts. The three types of tracts in the cerebrum are ... 

The postsynaptic receptors on any given neuron receive information from transmitters released from another neuron. Typically, postsynaptic receptors are located on dendrites or cell bodies of neurons, but may also occur on axons or nerve terminals in the latter case, an axoaxonic synaptic relationship may cause increases or decreases in transmitter release. In contrast, autoreceptors are found on certain neurons and respond to transmitter molecules released from the same neuron. Autoreceptors may be widely distributed on the surface of the neuron. At the nerve terminal, they respond to transmitter molecules released into the synaptic cleft on the cell body, they may respond to transmitter molecules released by dendrites. Functionally, most autoreceptors appear to decrease further transmitter release in a kind of negative feedback loop. Autoreceptors have been identified for all the catecholamines, as well as for several other neurotransmitters. a2-adrenergic receptors are often found on noradrenergic nerve terminals of postganglionic sympathetic nerves, as well as on noradrenergic neurons in the CNS [36], and activation of these receptors decreases further norepinephrine release. Dopamine autoreceptors,... 

Some substances, such as carbon monoxide and barbiturates, can deprive brain cells of oxygen or glucose - they produce anoxia - with potentially serious consequences for gray matter. Other substances, such as lead, hexachlorophene, and the antitubercular drug isoniazid, are capable of causing loss of myelin, a coating or sheath for the axon and dendrites that extend from the central unit (cell body) of neurons. Demyelination can occur in either the CNS or PNS. 

Many experimental results have confirmed the chemical basis of memory. For example, learning is facilitated by administration to animals of small doses of strychnine.1015 Puromycin and other inhibitors of protein synthesis disrupt the transfer of information into long-term memory. They are especially effective during the first hour after the initial learning event.1016 Increased synthesis both of mRNA and of proteins within the cell bodies of neurons is observed. 

The neuronopathic symptoms described above are caused by substances that attack and destroy the cell bodies of neurons. Another class of toxic effects occurs as the result of deterioration of nerve axons and its surrounding myelin. Symptoms resulting from this effect are called axonopa-thies. A classic toxicant cause of axonopathies is that of y-diketones, most commonly 2,5-hex-anedione ... 

Various organomercury compounds (e.g. ethylmercuric chloride, methyl mercury, dimethyl mercury), found as environmental contaminants or used as fungicides, are irreversible neurotoxins. Damage cell bodies of neurones in the dorsal root ganglia and brain. See also mercury. 

EXPERIMENTAL FIGURE 20-17 The rate of axonal transport in vivo can be determined by radiolabeling and gel electrophoresis. The cell bodies of neurons In the sciatic nerve are located In dorsal-root ganglia. Radioactive amino acids Injected Into these ganglia In experimental animals are Incorporated Into newly synthesized proteins, which are then transported down the axon to the synapse. Animals are sacrificed at various times after Injection and the dissected sciatic nerve Is cut Into small segments for analysis with the use of gel electrophoresis. The red, blue, and purple dots represent groups of proteins that are transported down the axon at different rates, red most rapidly, purple least rapidly. 

Small and large punctate deposits are found, which disappear when the brain matures. Two other forms, sheath laminin and somal laminin, reduce in intensity but persist throughout adult life. Each has a unique spatial and temporal distribution. Small puncta appear first in development and disappear after fibre pathways have formed sheath laminin is associated with the microvasculature, the ependyma, the choroid plexus and the surface of the brain. Somal laminin, the last appearing, is found associated mainly with the cell body of neurons and is correlated with the appearance of compacting brain nuclei. 

The cell bodies of neurons that involve NE are located in the brain stem, with projections to the thalamus, cortex,hippocampus, and cerebellum. Other neurotransmitters, such as ACh and some neuropeptides, are broken down while still in the synaptic cleft. In the synapses connecting neurons and muscle cells, the enzyme acetyl cholinesterase performs this task. Excitatory ACh receptors that activate skeletal musdes at the neuromuscular juncture are called nicotinic receptors because they are stimulated by nicotine. 

HT,d receptors have at least two further possible cellular localisations. They are located on the terminals of non-serotonergic neurons where they may act as presynaptic heteroreceptors i.e. in the superficial grey layer of the superior colliculus and in the substantia nigra and they are postsynaptically located on the dendrites or cell bodies of neurons in other brain areas i.e. the caudate-putamen and globus pallidus. 

FIGURE 30.1 Structure of the central nervous system (CNS). (a) The CNS includes the brain and the spinal cord, (b) The gray matter of the CNS contains the cell bodies of neurons as well as dendritic and axonal processes, (c) When an electrode is placed within the heterogeneous cellular environment of the CNS it is unclear which neuronal elements are effected by stimulation. 

NissI granules (NissI bodies) Particles seen within the cell bodies of neurons. They are rich in RNA and stain strongly with basic dyes. They are named after F. NissI (1860-1919), the German neurologist who discovered them. 

Two related questions of high intrinsic interest are whether the dendrites and cell body of neurons differ in their membrane properties, and whether the formal neuronal model developed initially by Rail to describe the motoneuron (Jacks et aL, 1975 Redman, 1976 Rail, 1962,... 

Somatostatin applied to the cell bodies of neurones in the pyramidal layer of the CAl and CA2 regions of the rat hippocampus resulted in a strong excitation which was fast in onset and thus resembled that evoked by glutamate (Dodd and Kelly 1978). 

Ganglion cells are foe cell bodies of neurons. The axons of the ganglion cells form the optic nerve, which synapses in the lateral geniculate body of the mitl-brain. 

Several substances, once injected in a given central structure, are taken up by axon terminals and transported retrogradely over long distances, to the cell bodies of neurons projecting to the injection area. They are then visualized by means of histochemical (or immunohistochemical) reactions, making it possible to trace neural pathways. 

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