Neuronal perikarya

In contrast to the small transmitter molecules, the neuropeptides are synthesized in the rough endoplasmic reticulum of the neuronal perikarya. They are enclosed in vesicles in the Golgi apparatus. The vesicles travel down to the terminals by axonal transport. 

The concentration of catecholamines within nerve terminals remains relatively constant. Despite the marked fluctuations in the activity of catecholamine-containing neurons, efficient regulatory mechanisms modulate the rate of synthesis of catecholamines [ 11 ]. A long-term process affecting catecholamine synthesis involves alterations in the amounts of TH and DBH present in nerve terminals. When sympathetic neuronal activity is increased for a prolonged period of time, the amounts of mRNA coding for TH and DBH are increased in the neuronal perikarya. DDC does not appear to be modulated by this process. The newly synthesized enzyme molecules are then transported down the axon to the nerve terminals. 

The pathological hallmark of the disease is the presence in the brain of Lafora bodies round, basophilic, PAS-positive intracellular inclusions varying in size from small, dust-like bodies less than 3 nm in diameter to large bodies up to 30 nm in diameter. Lafora bodies are typically seen in neuronal perikarya and processes, not in glial cells, and are more abundant in cerebral cortex, substantia nigra, thalamus, globus pallidus and dentate nucleus. Ultrastructural studies have shown that Lafora bodies consist of two components amorphous electron-dense... 

Aghajanian. G. K... Kuhar, M. J., and Roth, R. H. (1973) Serotonin-containing neuronal perikarya and terminals differential effects of p-chlorophenylalanine. Brain Res., 54 85-101. 

IHC shows CYP19 in neuronal perikarya of quail, rat, monkey, human (Naftolin et al., 1996). 

DA control of anterior pituitary hormone secretion also mediated through transynaptic regulation of hypothalamic neurosecretory neurons. This occurs via axonal-somatic/ dendritic interactions in hypothalamic regions containing neurosecretory neuron perikarya and/or through axonal-axonal interactions on their terminals in the median eminence. Diencephalic DA neurons may regulate neuropeptide release directly via stimulatory Di or inhibitory D2 receptors located on hypothalamic neurosecretory neurons, or they may act indirectly through stimulatory and/or inhibitory interneurons. 

A variety of chemically-identified neurons within the ARC receive both indirect (extrinsic) and direct (intrinsic) enkephalinergic neuronal input (Magoul et al., 1993) suggesting a role for enkephalin in the neuroendocrine regulation of pituitary hormone secretion. Enkephalin-IR perikarya in the bed nucleus of the stria terminalis, medial preoptic nucleus, periventricular nucleus and dorsomedial nucleus all provide extrinsic input to the rostral ARC, whereas intrinsic enkephalin neurons connect the rostral and caudal portions of the ARC (Magoul et al., 1993). Enkephalin-IR neurons innervate TH-IR neurons (perikarya and dendrites) in the DM-ARC (but not in the VL-ARC), (5-endorphin neurons in the VL-ARC, and NPY neurons in the ventromedial ARC (Magoul et al., 1994). There are symmetrical synaptic connections between enkephalin axon terminals and POMC perikarya in the ARC (Zhang et al., 1987), and reciprocal synaptic associations with NPY neurons in the ventromedial ARC (Li et al., 1993). 

The sites of production (neuronal perikarya) and release (axon terminals) of the respective, selectively stained messenger substances could be ascertained by tracing their disposition throughout... 

Karmy G, Carr PA, Yamamoto T, Chan SHP, Nagy JI (1991) Cytochrome oxidase immunohistochemistry in rat brain and dorsal root ganglia visualization of enzyme in neuronal perikarya and in parvalbumin-positive neurons. Neuroscience, 40, 825-839. 

There is evidence tliat PrP " in neurons is concenttated in die synaptic region. The protein is axonally transported to nerve terminals (Borchelt et al, 1994) and is enriched in presynaptic membranes obtained by subcellular fractionation (Herms et al, 1999). It has also been localized to synaptic profiles by immunoelectron microscopy (Fournier et al, 1995 Sales et al, 1998). By light microscopic immuno-cytochemistry, PrP " is found primarily in synaptic fields of the olfactory bulb, limbic structures, striatonigral complex, and cerebellar molecular layer, with little staining of neuronal perikarya or fiber pathways (Sales etal, 1998 Herms etal, 1999). These data would suggest a role for PrP in synaptic function, although additional studies are clearly necessary. 

Because of its extreme potency and commercial availability, kainic acid has been the excitotoxin most widely used for producing localized lesions in the mammalian central nervous system. While most studies indicate that in situ injection of kainic acid is an effective means of selectively destroying most neuronal perikarya in the vicinity of the injection site, it has become increasingly apparent that the effects of this agent are complex, variable, and often indirect. In order to appreciate the specificity, selectivity, and variability of neuronal vulnerability to locally injected kainic acid, the effects of this agent in two well-characterized brain regions will be reviewed. 

The extensive studies carried out in vivo and in vitro on kainic acid have laid the groundwork for understanding its neurotoxic effects. Although neurons vary in their sensitivity to kainic acid, the acute neurotoxic effects appear highly specific for neuronal perikarya, but usually spare axons of passage and of termination as well as nonneuronal elements within the lesioned area under most circumstances. Some neurons are remarkably resistant to its neurotoxic effects, such as the neurons in the... 

In comparative studies of the neurotoxic effects of NMDA and kainic acid in the hippocampal formation, we have found that NMDA is approximately 100-fold less potent as a neurotoxin than kainic acid on a molar basis (Zaczek et aL, 1981). The lesion associated with local injection of NMDA is limited to the injection site in the hippocampal formation and appears to uniformly affect all neuronal perikarya within its circumference. However, doses of NMDA effective in causing significant lesions in the dentate gyrus precipitated a severe electroencephalographic and behavioral seizure disturbance punctuated by frequent tonic-clonic convulsions occasionally resulting in death. Thus, the superiority of NMDA over kainic acid and ibotenic acid for intracerebral injection remains to be established. 

Sharp, F. R., 1976a, Relative cerebral glucose uptake of neuronal perikarya and neuropil determined with 2-deoxyglucose in resting and swimming rat. Brain Res. 110 127-139. 

In rats microinjected unilaterally with kainic acid (0.75 [xg) in the globus pallidus, loss of neuronal perikarya and reactive gliosis occurred (Di Chi-ARA et al. 1980). 

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