Neuronal cell bodies and

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. 

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... 

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. 

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

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. 

Fig. 2. Hypostome (mouth) of a Hydra oligactis whole mount labeled with monoclonal antibody DB5. (A) Nonconfocal image of sensory neurons and processes (B) confocal optical section of the same field as (A) illustrating details of neuronal cell bodies and processes. Scale bar = 25 pm.

The mechanism of the neurological symptoms in Parkinson s disease was discovered from the ability of reserpine to cause akinesia in humans by the depletion of central catecholamine stores. The dopamine levels in patients who died from parkinsonism were found to be extremely low because of deterioration of the dopaminergic neuronal cell bodies and the pathways connecting the substantia nigra with the corpus striatum. 

Anandamide can be hydrolyzed to arachidonic acid and ethanolamine by fatty acid amide hydrolase (FAAH) (Cravatt et al., 1996 Wei et al., 2006) (Fig. 1). FAAH is highly expressed in the brain, where it is expressed at high concentrations in neuronal cell bodies and dendrites that are juxtaposed to axon terminals containing CB receptors. This suggests that anandamide hydrolysis occurs post-synaptically (Piomelli, 2003). 

The immunoreactive processes intermingled in the neuropil represent dendrites. Scale bar 50 pm. In (D), the immunogold labeling of part of an NRD immunoreactive neuronal cell body and of nearby dendrites (d) predominates on their plasma membrane. (E) Immunogold labeling of 5-HT1A immunoreactive dendrites (d) in NRD. The silver-intensified immunogold particles are mostly associated with the plasma membrane of these processes. Note the absence of particles in areas of synaptic differentiation on these dendrites (between small arrows). Scale bars in (D) and (E) 1 pm. (Reproduced with permission from ref. 25.)... 

Detection of mRNA of each cloned DA receptor by means of in situ hybridization is a sensitive and specific methodology. mRNA, however, is almost exclusively contained in the neuronal cell body and, therefore, this technique does not allow the identification of receptors within dendritic arborizations or axon terminals. In addition, the presence of RNA transcript does not allow to determine to what extent the mRNA is translated into protein, and does not always correlate with the presence of active receptor protein or ligand binding sites. 

The clinical signs of EPM are the result of both direct damage to neurons, by protozoal proliferation within the neuronal cell bodies, and indirect damage to neural elements, produced by edema and inflammation in response to the merozoites and meronts in the CNS. Deposition of the parasite... 

As we saw in Chapter 9, sodium channels (Nay channels) consist of a pore-forming a subunit, which is sufficient for functional expression, associated with auxiliary p subunits which modify both the kinebcs and the voltage dependence of channel gabng of the channel. Nine mammalian Nay channel isoforms are known, of which Nayl. 1 and Nayl.3 are predominantly locabsed in neuronal cell bodies and proximal dendrites, where they conbol... 

Like Glu, Asp plays an important role in general cell metabolism and in the synthesis of proteins. Thus, it can be difficult to identify the transmitter pool of Asp and Glu in the brain. By immunocytochemical methods it is possible to visualize the Asp and Glu content separately in different neuronal compartments. One would expect that a substance that has a transmitter role in the brain is localized in nerve endings, which is the site of transmitter release, rather than in neuronal cell bodies and dendrites. 

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