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  • Articles: DFG German National Licenses  (2)
  • Cerebellar ontogeny  (1)
  • alpha-ketoglutarate  (1)
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  • Articles: DFG German National Licenses  (2)
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Years
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Experimental brain research 107 (1996), S. 361-366 
    ISSN: 1432-1106
    Keywords: Metabotropic glutamate receptors ; Cerebellar ontogeny ; Methylazoxymethanol ; Mouse
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract [3H]-l-glutamate binding site distribution corresponding to metabotropic receptors was studied by autoradiography during normal and altered cerebellar ontogeny in mice treated on postnatal days (PND) 5 and 6 with the antimitotic methylazoxy-methanol (MAM). Quisqualate (QA)-induced and (2S, 3S, 4S)-α-(carboxycyclopropyl)-glycine (L-CCG-I)-induced [3H]-l-glutamate binding inhibition allowed us to distinguish between group I and group II metabotropic receptor binding sites. In control cerebellar cortex, the QA-sensitive binding site density increases during development, while the L-CCG-I-sensitive binding site density decreases. In the deep cerebellar nuclei (DCN), both populations of binding sites decrease during ontogeny. The antimitotic treatment induces: (1) a slight but significant increase in the QA-sensitive binding sites in the DCN at PND 10 and in the cerebellar cortex beginning from PND 20; (2) a retarded decrease in the L-CCG-I-sensitive metabotropic receptor binding site density. These differences could be due to a retarded cell maturation and/or an over-expression of some postsynaptic receptors in the adult cerebellum in response to the afference deficiency.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1573-6903
    Keywords: Glutamate ; alpha-ketoglutarate ; glutamine ; release
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Depolarization-elicited release of neurotransmitter glutamate was studied in rat cerebellar slices previously loaded with either [3H]l-glutamate or [3H]l-glutamine. Both depolarization conditions used (e.g. long-lasting tonic depolarization elicited by veratridine, or short repetive electrical pulses) increased 6 to 8 folds the release of labelled glutamate and of another compound, presumably alpha-ketoglutarate, without modifying the release of labeled glutamine. Because of the position of the label in the precursor radioactive molecules, GABA was weakly labeled and aspartate was unlabeled. The properties of the evoked glutamate release from cerebellar slices were those of a neurotransmitter since it was inhibited by tetrodotoxin and was Ca2+-dependent. Alpha-ketoglutarate is either coreleased from nerve terminals or is released from astrocytes and could participate in glutamate recycling. The data confirm the generally accepted model implying the presence of two neurotransmitter glutamate pools, a neuronal pool of newly synthesized glutamate and an astrocytic storage pool, but in addition indicate that the former is in rapid isotopic equilibrium with the extracellular compartment. Our present results also indicate that the glutamate/glutamine cycle is not activated in depolarizing conditions.
    Type of Medium: Electronic Resource
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