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  • Neuroregulators  (1)
  • Rabbit  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Colocalization of amino acid signal molecules in neurons and endocrine cells (1996)
    Springer
    Anatomy and embryology 194 (1996), S. 1-12 
    Details
    ISSN: 1432-0568
    Keywords: Neuroregulators ; Hormones ; GABA ; Glutamates ; Glycine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract During the last 20 to 30 years, numerous examples have been provided of neurons and endocrine cells that are able to produce, store, and in many cases release more than one type of signal molecule. Recent models propose that neurons often employ an amino acid, an amine, and one or more neuroactive peptides, and that endocrine cells may release more than one peptide hormone. In neurons, the different classes of transmitter convey fast, intermediate, and slow signalling respectively. However, a series of studies demonstrates that neurons may colocalize more than one neuroactive amino acid, and that endocrine cells may contain an amino acid along with their peptide hormone. These forms of colocalization seem to add new levels of complexity to the role of amino acids in cell signalling, suggesting that, in neurons, amino acids may interact at the receptor level, modifying the effect of each other, and that, in endocrine cells, amino acids may act together with or parallel to a peptide hormone in a paracrine or autocrine manner.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00196310
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Distribution of GABA immunoreactivity in kainic acid-treated rabbit retina (1994)
    Springer
    Experimental brain research 100 (1994), S. 227-238 
    Details
    ISSN: 1432-1106
    Keywords: Neurotoxicity ; Kainic acid ; Retina GABA ; Rabbit
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Ischaemic retinal cell degeneration seems to involve both NMDA and non-NMDA receptor over stimulation. However, different retinal cell types differ largely in their susceptibility to excitatory amino acid induced neurotoxicity. We have investigated the vulnerability of GABAergic cells in the rabbit retina to the non-NMDA receptor agonist kainic acid (KA). The distribution of GABA immunoreactivity (GABA-IR) was examined in the central inferior retina at different survival times (5 h–6 days) following an intra-ocular injection of 140 nmol KA and compared to that of control and untreated retinas. In the normal retina, the majority of GABA-positive cells (79%) were located in the inner nuclear layer (INL), in one to four cell rows next to the inner plexiform layer (IPL), and in one cell row next to the outer plexiform layer (OPL). The remainder (21%) were found in the ganglion cell layer (GCL). Dense immunoreactivity was seen throughout the IPL. In the OPL, stained dots and occasional immunoreactive large processes could be seen. KA-exposed retinas processed for GABA immunocytochemistry 5 and 24 h after the injection showed an 85% reduction in the number of GABA immunoreactive cells. About the same degree of depletion was seen among GABA-IR cells located at different retinal levels. However, at these survival times, immunostaining was observed in three distinct bands in the IPL, indicating that the vulnerability to KA is not uniformly distributed among all GABAergic cells. At 48 h, an additional decrease in the number of labelled cells was noted, but immunoreactive cells were still found both in the INL and GCL. Even 6 days after KA treatment, a few stained cell bodies were seen in the INL next to the IPL, as well as a few processes in the IPL. The study shows that KA receptor overstimulation induces a marked depletion of the endogenous cellular GABA pools of the central rabbit retina, most likely as a result of GABAergic cell loss. However, a small population of GABAergic cells located in the INL appears to be less vulnerable to the toxic effects of 140 nmol KA.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00227193
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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