Immunocytochemical localization of the mGluR1? metabotropic glutamate receptor in the dorsal cochlear nucleus

1996 ◽  
Vol 364 (4) ◽  
pp. 729-745 ◽  
Author(s):  
Debora D. Wright ◽  
Craig D. Blackstone ◽  
Richard L. Huganir ◽  
David K. Ryugo
Keyword(s):  
Glutamate Receptor ◽  
Cochlear Nucleus ◽  
Metabotropic Glutamate Receptor ◽  
Dorsal Cochlear Nucleus ◽  
Immunocytochemical Localization ◽  
Metabotropic Glutamate

Immunocytochemical localization of the metabotropic glutamate receptor mGluR4a in the piriform cortex of the rat

2000 ◽  
Vol 417 (3) ◽  
pp. 263-274 ◽  
Author(s):  
Roc�o Ben�tez ◽  
Oscar Fern�ndez-Capetillo ◽  
Esther L�zaro ◽  
Jos� Mar�a Mateos ◽  
Alexandra Osorio ◽  
...  
Keyword(s):  
Glutamate Receptor ◽  
Metabotropic Glutamate Receptor ◽  
Piriform Cortex ◽  
Immunocytochemical Localization ◽  
Metabotropic Glutamate

Eighth nerve activity regulates intracellular calcium concentration of avian cochlear nucleus neurons via a metabotropic glutamate receptor

1996 ◽  
Vol 76 (6) ◽  
pp. 4127-4139 ◽  
Author(s):  
L. Zirpel ◽  
E. W. Rubel
Keyword(s):  
Intracellular Calcium ◽  
Glutamate Receptor ◽  
Cochlear Nucleus ◽  
Calcium Concentration ◽  
Metabotropic Glutamate Receptor ◽  
Intracellular Calcium Concentration ◽  
Field Potentials ◽  
Nerve Activity ◽  
Eighth Nerve ◽  
Metabotropic Glutamate

1. Neurons in the cochlear nucleus, nucleus magnocellularis (NM), of embryonic and neonatal chicks are dependent on eighth nerve activity for their maintenance and survival. Removing this input results in the death of 20–40% of the NM neurons and profound changes in the morphology and metabolism of surviving neurons. 2. One of the first changes in NM neurons after an in vivo cochlea removal is an increase in intracellular calcium concentration ([Ca2+]i). Increased [Ca2+]i has been implicated in a number of neuropathologic conditions. 3. In this study, we orthodromically and antidromically stimulated NM neurons in an in vitro brain stem slice preparation and monitored NM field potentials while simultaneously assessing the [Ca2+]i of NM neurons using fura-2. 4. During continuous orthodromic stimulation, [Ca2+]i of NM neurons remained constant at 80 nM. In the absence of stimulation, NM neuron [Ca2+]i increased steadily to 230 nM by 90 min. Antidromic and contralateral stimulation produced a [Ca2+]i increase in NM neurons that was similar in magnitude but slightly more rapid than that observed in the absence of stimulation. 5. Addition of the metabotropic glutamate receptor (mGluR) antagonists (R,S)-alpha-methyl-4-carboxyphenylglycine or 2-amino-3-phosphonopropionic acid to the superfusate during continued orthodromic stimulation resulted in a dose-dependent, rapid, and dramatic increase in NM neuron [Ca2+]i without affecting the postsynaptic field potentials recorded from NM. 6. The ionotropic glutamate receptor antagonists 6-cyano-7-nitroquinoxaline-2,3-dione and 2-amino-5-phosphonovalerate eliminated NM field potentials during continued orthodromic stimulation but did not result in an increase in [Ca2+]i. 7. Continuous superfusion of trans-(+/-)-aminocyclopentane dicarboxylate, but not glutamate, prevented the increase in [Ca2+]i in the absence of stimulation. 8. These results suggest that NM neurons rely on eighth nerve activity-dependent activation of a mGluR to maintain physiological [Ca2+]i. Removal of this mGluR activation results in an increase in [Ca2+]i that may contribute to the early stages of degeneration and eventual death of these neurons.

Metabotropic Glutamate Receptor Activation Modulates Sound Level Processing in the Cochlear Nucleus

1998 ◽  
Vol 80 (1) ◽  
pp. 209-217 ◽  
Author(s):  
Dan H. Sanes ◽  
JoAnn McGee ◽  
Edward J. Walsh
Keyword(s):  
Glutamate Receptors ◽  
Glutamate Receptor ◽  
Cochlear Nucleus ◽  
Metabotropic Glutamate Receptors ◽  
Metabotropic Glutamate Receptor ◽  
Long Term Potentiation ◽  
Receptor Activation ◽  
Sound Level ◽  
Metabotropic Glutamate

Sanes, Dan H., JoAnn McGee, and Edward J. Walsh. Metabotropic glutamate receptor activation modulates sound level processing in the cochlear nucleus. J. Neurophysiol. 80: 209–217, 1998. The principal role of ionotropic glutamate receptors in the transmission and processing of information in the auditory pathway has been investigated extensively. In contrast, little is known about the functional contribution of the G-protein–coupled metabotropic glutamate receptors (mGluRs), although their anatomic location suggests that they exercise a significant influence on auditory processing. To investigate this issue, sound-evoked responses were obtained from single auditory neurons in the cochlear nuclear complex of anesthetized cats and gerbils, and metabotropic ligands were administered locally through microionophoretic pipettes. In general, microionophoresis of the mGluR agonists, (1 S,3 R)-1-aminocyclopentane-1,3-dicarboxylic acid or (2 S,1′ S,2′ S)-2-(carboxycyclopropyl)glycine, initially produced a gradual increase in spontaneous and sound-evoked discharge rates. However, activation and recovery times were significantly longer than those observed for ionotropic agonists, such as N-methyl-d-aspartate or α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid, consistent with the recruitment of a second-messenger system. The efficacy of mGluR agonists was diminished after administration of the mGluR antagonist, (+)-α-methyl-4-carboxyphenylglycine, consistent with a selective action at metabotropic recognition sites. In contrast, two distinct changes were observed after the mGluR agonist had been discontinued for several minutes. Approximately 50% of neurons exhibited a chronic depression of sound-evoked discharge rate reminiscent of long-term depression, a cellular property observed in other systems. Approximately 30% of neurons exhibited a long-lasting enhancement of the sound-evoked response similar to the cellular phenomenon of long-term potentiation. These findings suggest that mGluR activation has a profound influence on the gain of primary afferent driven activity in the caudal cochlear nucleus.

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