Glutamate modulates intracellular Ca2+ stores in brain stem auditory neurons

Abstract

1. Fura-2 imaging was used to measure the effects of glutamate on caffeine-sensitive Ca2+ stores in neurons of the avian cochlear nucleus, n. magnocellularis (NM). 2. On average, 100-mM caffeine stimulated a 250-nM increase in intracellular calcium ion concentration {[Ca2+]i} in Ca(2+)-free media; 1-mM glutamate significantly attenuated caffeine-stimulated Ca2+ responses. 3. The metabotropic glutamate receptor agonist, ACPD, also inhibited the caffeine-stimulated rise in [Ca2+]i. 4. Glutamate has an important role in regulating Ca2+ stores in NM neurons. Glutamate-deprivation (viz. cochlear removal) results in a rise in [Ca2+]i that may, in part, be the result of release from Ca2+ stores. We hypothesize that Ca(2+)-induced Ca2+ release stores (CICRs) may be involved in deprivation-induced cell death.

Plasticity of the auditory brainstem: Cochleotomy-induced changes of calbindin-D28k expression in the rat

“…Correspondingly, the concentration of intracellular calcium increases in the deafferented neurons of the nucleus magnocellularis, the avian cochlear nucleus, after unilateral cochlea removal in embryonal or neonatal chicken (Zirpel et al, 1995). Moreover, the application of glutamate in concentrations estimated to be present at glutamatergic synapses, but not at higher concentrations, suppresses the caffeine-mediated release of calcium from intracellular calcium stores in the avian cochlear nucleus (Kato et al, 1996). It therefore appears that both increase and decrease of an excitatory input induces extended calcium buffering capacities in the postsynaptic cell.…”

Metabotropic glutamate receptors in auditory processing

“…In the following years, mGluR-mediated regulation of Ca 2+ signaling in NM neurons was extensively studied, primarily by the same research group (Lachica et al, 1995; 1998; Kato et al, 1996; Zirpel and Rubel 1996; Zirpel et al, 1995, 1998; Kato and Rubel, 1999; Zirpel and Parks, 2001). The key conclusion from these studies is that mGluRs, especially group I mGluRs, play critical roles in regulating Ca 2+ signaling and maintaining Ca 2+ homeostasis and cell survival in NM neurons.…”

Blood Glutamate Scavenging: Insight into Neuroprotection

“…Excessive activation of ionotropic receptors leads to the opening of receptor-coupled ionophores, including calcium channels, which are of particular importance. Efflux of calcium into neurons, which activates plasmatic proteolytic enzymes, results in neuronal death via apoptosis or necrosis [7–11]. Animal models and human clinical studies reveal the association of pathologically elevated ECF glutamate levels and several acute and chronic neurodegenerative disorders, including stroke [12], traumatic brain injury (TBI) [13], intracerebral hemorrhage [14], meningitis, brain hypoxia [15], amyotrophic lateral sclerosis (ALS) [16], glaucoma [17], HIV dementia [18], glioma [19] and many others.…”