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Detail of "498-95-3"

  • MSDS Download
  • CAS Number:
  • 498-95-3
  • Name:
  • Nipecotic acid

  • Molecular Structure:
  • Formula:
  • C6H11NO2
  • Molecular Weight:
  • 129.16
  • Synonyms:
  • 3-Piperidinecarboxylicacid;Nipecoticacid (6CI,7CI,8CI);3-Carboxypiperidine;DL-Nipecotic acid;Hexahydronicotinic acid;3-Piperidinecarboxylic Acid;Piperidine-3-carboxylic acid;H-DL-Nip-OH;
  • EINECS:
  • 207-873-9
  • Density:
  • 1.125 g/cm3
  • Melting Point:
  • 261 °C (dec.)(lit.)
  • Boiling Point:
  • 265.8 °C at 760 mmHg
  • Flash Point:
  • 114.5 °C
  • Appearance:
  • off-white to pale yellow-beige powder
  • Hazard Symbols:
  • IrritantXi
  • Risk Codes:
  • 36/37/38
  • Safety:
  • 26-36-37/39 Details

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Chemistry: TOXICITY: SAFETY: Production: Others: Molecular Weight: 129 Melting Point: 259-261

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Reference

Substrate specificity and developmental aspects of a presynaptic GABA receptor regulating glutamate release in the rat cerebellum
Substrate specificity and developmental aspects of a presynaptic GABA receptor regulating glutamate release in the rat cerebellum. Aloisi, F.; Gallo, V.; Levi, Giulio (Ist. Biol. Cell., CNR, Rome 00196, Italy). J. Neurosci. Res. 2763-96-4 and 64603-91-4 which are cas registry numbers are also used here., 10(2), 141-9 (English) 1983. CODEN: JNREDK. ISSN: 0360-4012. DOCUMENT TYPE: Journal CA Section: 2 (Mammalian Hormones) The K+-induced release of the glutamic acid analog, D-aspartic acid [1783-96-6], from rat cerebellar P2 fractions was detd. for the following compds. at 20 mM in the medium (% of control given): muscimol [2763-96-4] (168), 3-aminopropanesulfonic acid [3687-18-1] (161), piperidine-4-sulfonic acid [72450-62-5] (153), isoguvacine [64603-90-3] (123), THIP [64603-91-4] (112), cis-3-aminocyclohexanecarboxylic acid [16636-51-4] (112), nipecotic acid [498-95-3] (104), b-alanine [107-95-9] (106), glycine [56-40-6] (109), and baclofen [1134-47-0] (88%). Although GABA [56-12-2] uptake inhibitors did not enhance K+-evoked D-aspartic acid release from synaptosomes, they were effective in cerebellar slices in which GABA receptor activation can occur indirectly through increased extracellular GABA concns. The substrate specificity of GABA receptors regulating cerebellar glutamic acid [56-86-0] release appears to be similar to that previously reported for GABA receptors in radioligand binding studies. .
Enrichment of differentiated, stellate astrocytes in cerebellar interneuron cultures as studied by GFAP immunofluorescence and autoradiographic uptake patterns with [3H]D-aspartate and [3H]GABA
Enrichment of differentiated, stellate astrocytes in cerebellar interneuron cultures as studied by GFAP immunofluorescence and autoradiographic uptake patterns with [3H]D-aspartate and [3H]GABA. Levi, Giulio; Wilkin, Graham P.; Ciotti, M. Teresa; Johnstone, Stephen (Ist. Biol. Cell. 498-95-3 and 1783-96-6 are also occured in this study., CNR, Rome 00196, Italy). Dev. Brain Res., 10(2), 227-41 (English) 1983. CODEN: DBRRDB. ISSN: 0165-3806. DOCUMENT TYPE: Journal CA Section: 2 (Mammalian Hormones) A study was undertaken to correlate the morphol. expressed by astroglial cells in postnatal cerebellar, interneuron-enriched primary cultures and the ability of these cells to accumulate putative neurotransmitter amino acids. Astroglial cell morphol., as studied by glial fibrillary acidic protein (GFAP) immunofluorescence staining, showed considerable changes during the culture period considered (£12 days in vitro). Whereas the total no. of GFAP-pos. cells decreased with time (cell multiplication was prevented by cytosine arabinoside), a progressive enrichment of stellate astrocytes (cells bearing multiple radially arranged processes) and a striking increase in size of these cells was noted. In 12-day cultures stellate astrocytes accounted for 70-80% of the astrocytes present, and could reach a diam. of >300 mm. The L-glutamate [56-86-0] analog, 3H-labeled D-aspartate [1783-96-6], was avidly taken up by all the astrocytes, independently of their shape and stage of differentiation. Astroglial cell morphol. as delineated by [3H]D-aspartate autoradiog. was identical to that evidenced by GFAP staining. On the other hand, 3H-labeled GABA [56-12-2] was accumulated in substantial amts. only by the stellate astrocytes, i.e. by the cells showing greater morphol. differentiation. Astrocytes of other shapes were only lightly labeled by [3H]GABA in 2- and 15-day cultures, and even less at later stages. Even within the stellate astrocyte population, the extent of [3H]GABA labeling was very variable from one cell to another. Autoradiog. examns. and the detn. of the IC50s for GABA uptake inhibitors consistently indicated that the GABA transport system present in stellate astrocytes did not have the features generally attributed to a glial transport system. In fact, b-alanine [107-95-9] was a very weak inhibitor, whereas nipecotic acid [498-95-3] and cis-1,3-aminocyclohexanecarboxylic acid [65937-28-2] were strongly inhibitory; diaminobutyric acid [305-62-4] inhibitory potency fell somewhere in between. [3H]GABA uptake into the inhibitory interneurons present in the cultures showed similar sensitivity to GABA transport inhibitors. .
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