Neurons cell body

Populations of receptors that are excluded from synaptic junctions. These may be distributed over neuronal cell bodies or located around but not directly beneath synapses (perisynaptic). Some receptors have become specialised to setve an extrasynaptic function producing a tonic level of activity in response to ambient levels of neurotransmitter. This tonic current can be used to maintain homeostatic control over neuronal excitation. 

If a substance is to be a NT it should be possible to demonstrate appropriate enzymes for its synthesis from a precursor at its site of action, although peptides are transported to their sites of location and action after synthesis in the axon or distal neuronal cell body. The specificity of any enzyme system must also be established, especially if they are to be modified to manipulate the levels of a particular NT, or used as markers for it. Thus choline acetyltransferase (ChAT) may be taken as indicative of ACh and glutamic acid decarboxylase (GAD) of GABA but some of the synthesising enzymes for the monoamines lack such specificity. 

D2 Mostly in striatum, nucleus accumbens and olfactory tubercle but also on neuron cell bodies in substantia nigra and ventral tegmentum where they are the autoreceptors for locally (dendritic) released DA. The loss of specific D2 antagonist binding in the striatum after lesions of the afferent nigro-striatal tract indicates their presynaptic autoreceptor role on terminals there. Other lesion studies have also established D2 receptors on other inputs such as the cortico striatal tract. 

So far, little is known about this novel 5-HTid receptor but, in the rat and human, its mRNA is found, albeit in low concentrations, in the basal ganglia, nucleus accumbens, hippocampus, frontal cortex and Raphe nuclei. It is negatively coupled to adenylyl cyclase and is possibly located presynaptically, on both the 5-HT neuronal cell body and terminals, but this has yet to be confirmed. 

Block the action of DA on similar inhibitory receptors on the DA neuron cell body itself... 

As with temporal summation, this example has been simplified to illustrate the concept clearly. In actuality, a large number of excitatory inputs from different presynaptic neurons are necessary to depolarize the postsynaptic neuron to threshold. Because a typical neuronal cell body receives thousands of presynaptic inputs, spatial summation also occurs quite readily. The number of presynaptic neurons that are active simultaneously therefore influences the strength of the signal to the postsynaptic neuron. Under normal physiological conditions, temporal summation and spatial summation may occur concurrently. 

Unlike many chemicals in the brain, neurotransmitters are not homogeneously distributed, but concentrated in certain regions. For example, almost two-thirds of the dopamine in the brain is found in the bilateral nigrostriatal (mesostriatal) tract (pathway), where the neuronal cell bodies are located in the substantia nigra and the axons terminate in the corpus striatum. When over 85% of these dopaminergic neurons are lost, the characteristic motor dysfunction of Parkinson s disease is seen. 

Action potential, or nerve impulse The wave of electrical activity that passes from the dendrites of the neuronal cell body, down the axon to the synaptic bouton. 

Dendrite Abundant, short, thread-like extensions of the neuronal cell body. 

Locus coeruleus A collection of noradrenergic neuronal cell bodies located in the pons, from which the axons project to a number of forebrain structures. 

Cav1.2 Otic Cardiac and smooth muscle, endocrine cells, CNS, neuron cell bodies... 

R-type Cav2.3 OllE Neuron cell bodies and presynaptic terminals, heart, pituitary... 

During development, axons extend from the neuronal cell body and grow, frequently over long distances, in order to make very precise connections with a target. Despite the complexity of the nervous system, where over 1012 axons must find their targets, the pattern of axonal outgrowth... 

Details of the mechanisms by which endocytosed material moves from the early to the late and lysosomal compartment are still poorly understood. However, portions of the EEs tubulovesicular structures may be actively transported along microtubules towards the perinuclear region of the cell in both neurons and non-neuronal cells. These endosomes on the move may enclose invaginated membranes and also internally bud off vesicles. For that reason, these complex structures are called multivesicular bodies (MVBs) [76]. Material returning by retrograde axonal transport to the neuronal cell body includes many MVBs [67]. The eventual fate of these structures may vary. Some MVBs may fuse with LEs or they may fuse with each... 

The receptor for NGF is TrkA, a 140 kDa cell surface protein that specifically binds NGF, but not other neurotrophins [5, 6, 9]. TrkA is expressed on the neuronal cell body and on neuronal processes. In its action as a target-derived trophic factor, NGF is secreted within the target organ and it then binds to TrkA receptors present on the growing neuronal process or synapse. The NGF-TrkA complex is then internalized and subsequently translocated to the cell body by retrograde axonal transport. In those cells that respond to NGF through autocrine or paracrine mechanisms, the growth factor can bind to any of the widely distributed TrkA molecules on the neuronal membrane. 

FIGURE BO-2 Wallerian degeneration in the PNS. After an axon is injured, resulting chromatolysis, i.e. stress reaction and increased protein synthesis, occurs in the neuronal cell body, with axonal and myelin degeneration distal to the injury. Growth-permissive Schwann cells secrete growth factors that stimulate axons to regenerate. 

Interruption of the communication between the motor neuron cell body and axon by transection, crush or avulsion induces motor neuron injury 734... 

Whether neurofilament cross-linking is related to the neurofilament accumulation, axonal swellings, and ultimate axonal degeneration observed in -hexane neurotoxicity or is incidental remains to be elucidated (Graham et al. 1995). Since the maintenance of the axon depends on transport of cellular components from the neuronal cell body, the effect of 2,5-hexanedione on axonal transport has been investigated. If... 

A recent study showed THC to be toxic to hippocampal neurons, while sparing cortical neurons in concentrations likely to be reached in normal human doses (0.5 pM) (Chan et al. 1998). Apoptotic changes were noted in the hippocampus such as shrinkage of neuronal cell bodies and nuclei as well as DNA strand breaks. THC stimulates release of arachidonic acid, and it was hypothesized that this neurotoxic effect is mediated by cyclooxygenase pathways and free radical generation. In support of this, the toxicity is inhibited by nonsteroidal anti-inflammatory drugs, such as aspirin, and antioxidants such as vitamin E. 

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