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Titolo:
GLUTAMATERGIC INHIBITION OF VOLTAGE-OPERATED CALCIUM CHANNELS IN THE AVIAN COCHLEAR NUCLEUS
Autore:
LACHICA EA; RUBSAMEN R; ZIRPEL L; RUBEL EW;
Indirizzi:
UNIV WASHINGTON,VIRGINIA MERRILL BLOEDEL HEARING RES CTR,DEPT OTOLARYNGOL HEAD & NECK SURG SEATTLE WA 98195 UNIV WASHINGTON,VIRGINIA MERRILL BLOEDEL HEARING RES CTR,DEPT OTOLARYNGOL HEAD & NECK SURG SEATTLE WA 98195
Titolo Testata:
The Journal of neuroscience
fascicolo: 3, volume: 15, anno: 1995,
parte:, 1
pagine: 1724 - 1734
SICI:
0270-6474(1995)15:3<1724:GIOVCC>2.0.ZU;2-C
Fonte:
ISI
Lingua:
ENG
Soggetto:
STEM AUDITORY NUCLEI; CYCLIC-AMP FORMATION; PROTEIN-KINASE-C; NEONATAL RAT HIPPOCAMPUS; CEREBELLAR GRANULE CELLS; CHICK SENSORY NEURONS; BRAIN MESSENGER-RNA; SYNAPTIC TRANSMISSION; SIGNAL TRANSDUCTION; PHOSPHOINOSITIDE HYDROLYSIS;
Keywords:
DEAFFERENTATION; EXCITATORY AMINO ACID RECEPTORS; NEUROPROTECTION; CAMP; AUDITORY SYSTEM; METABOTROPIC RECEPTOR;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Physical, Chemical & Earth Sciences
Science Citation Index Expanded
Citazioni:
95
Recensione:
Indirizzi per estratti:
Citazione:
E.A. Lachica et al., "GLUTAMATERGIC INHIBITION OF VOLTAGE-OPERATED CALCIUM CHANNELS IN THE AVIAN COCHLEAR NUCLEUS", The Journal of neuroscience, 15(3), 1995, pp. 1724-1734

Abstract

The auditory nerve serves as the only excitatory input to neurons in the avian cochlear nucleus, nucleus magnocellularis (NM). NM neurons in immature animals are dependent upon auditory nerve signals; when deprived of them, many NM neurons die, and the rest atrophy. Auditory nerve terminals release glutamate, which can stimulate second messenger systems by activating a metabotropic glutamate receptor (mGluR). Therefore, it is possible that the effecters of mGluR-stimulated signal transduction systems are needed for NM neuronal survival. This study showsthat mGluR activation in NM neurons attenuates voltage-dependent changes in [Ca2+](i). Voltage-dependent Ca2+ influx was also attenuated byincreasing cAMP with forskolin, VIP, or 8-bromo-cAMP, indicating thatmGluR activation may stimulate adenylate cyclase. The main results may be summarized as follows. NM neurons possess high voltage-activated Ca2+ channels that were modulated by quisqualate, glutamate, and (+/-)trans-ACPD, in that order of potency. Glutamatergic inhibition of Ca2influx was not blocked by L-AP3 or L-AP4, which antagonize the actions of mGluRs in other neural systems; it was blocked by serine-O-phosphate. Finally, the attenuation of voltage-dependent Ca2+ influx was duplicated by cAMP accumulators. Since NM neurons have high rates of spontaneous activity and higher rates of driven activity, the expression of this mGluR turns out to be very valuable: without it, [Ca2+](i) could reach lethal concentrations. These results provide an important clueas to the identity of an intracellular signal that may play an important role in NM neuronal survival.

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Documento generato il 21/09/20 alle ore 12:27:23