Glutamate decarboxylase activity in brain regions of differentially-housed mice; a difference in the olfactory bulb

1980 ◽  
Vol 36 (7) ◽  
pp. 853-854 ◽  
Author(s):  
J. M. Blindermann ◽  
F. V. DeFeudis ◽  
M. Maitre ◽  
R. Misslin ◽  
P. Mandel
Keyword(s):  
Olfactory Bulb ◽  
Glutamate Decarboxylase ◽  
Brain Regions ◽  
Decarboxylase Activity

scholarly journals Transient Activity Induces a Long-Lasting Increase in the Excitability of Olfactory Bulb Interneurons

2008 ◽  
Vol 99 (1) ◽  
pp. 187-199 ◽  
Author(s):  
Tsuyoshi Inoue ◽  
Ben W. Strowbridge
Keyword(s):  
Olfactory Bulb ◽  
Granule Cells ◽  
Receptor Activation ◽  
Brain Regions ◽  
Persistent Activity ◽  
Cellular Mechanisms ◽  
Calcium Dependent ◽  
Transient Activity ◽  
Olfactory Bulb Slices ◽  
Processing And Storage

Little is known about the cellular mechanisms that underlie the processing and storage of sensory in the mammalian olfactory system. Here we show that persistent spiking, an activity pattern associated with working memory in other brain regions, can be evoked in the olfactory bulb by stimuli that mimic physiological patterns of synaptic input. We find that brief discharges trigger persistent activity in individual interneurons that receive slow, subthreshold oscillatory input in acute rat olfactory bulb slices. A 2- to 5-Hz oscillatory input, which resembles the synaptic drive that the olfactory bulb receives during sniffing, is required to maintain persistent firing. Persistent activity depends on muscarinic receptor activation and results from interactions between calcium-dependent afterdepolarizations and low-threshold Ca spikes in granule cells. Computer simulations suggest that intrinsically generated persistent activity in granule cells can evoke correlated spiking in reciprocally connected mitral cells. The interaction between the intrinsic currents present in reciprocally connected olfactory bulb neurons constitutes a novel mechanism for synchronized firing in subpopulations of neurons during olfactory processing.

scholarly journals Effect of undernutrition in early life on glutamate decarboxylase activity in the adult brain

1972 ◽  
Vol 130 (1) ◽  
pp. 12P-12P ◽  
Author(s):  
B P F Adlard ◽  
J Dobbing ◽  
A Lynch ◽  
R Balázs ◽  
A P Reynolds
Keyword(s):  
Glutamate Decarboxylase ◽  
Early Life ◽  
Adult Brain ◽  
Decarboxylase Activity

scholarly journals The dominant functional nicotinic receptor in progenitor cells in the rostral migratory stream is the α3β4 subtype

2013 ◽  
Vol 109 (3) ◽  
pp. 867-872 ◽  
Author(s):  
Geeta Sharma
Keyword(s):  
Olfactory Bulb ◽  
Perceptual Learning ◽  
Progenitor Cells ◽  
Glutamate Release ◽  
Brain Regions ◽  
Odor Discrimination ◽  
Rostral Migratory Stream ◽  
Receptor Expression ◽  
Granule Cell Layer ◽  
Migratory Stream

Addition of newly generated neurons into mature neural circuits in the adult CNS responds to changes in neurotransmitter levels and is tightly coupled to the activity of specific brain regions. This postnatal neurogenesis contributes to plasticity of the olfactory bulb and hippocampus and is thought to play a role in learning and memory, context and odor discrimination, as well as perceptual learning. While acetylcholine plays an important role in odor discrimination and perceptual learning, its role in adult neurogenesis in the olfactory bulb has not been elucidated. In this study, I have examined the functional expression of nAChRs in progenitor cells of the rostral migratory stream (RMS) in the adult olfactory bulb of mice. I show that most of these cells in the RMS exhibit large nAChR-mediated calcium transients upon application of acetylcholine (ACh). Unlike in the hippocampus, the predominant functional nAChRs on progenitor cells are of α3β4 subtype. Interestingly, functional receptor expression is lost once progenitor cells mature, and are incorporated into the granule cell layer. Instead, nAChRs are now expressed on some presynaptic terminals and modulate glutamate release onto granule cells. My results imply that ACh is a part of the permissive niche and likely plays a role in development of progenitor cells.

scholarly journals Environmental Enrichment Attenuates Oxidative Stress and Alters Detoxifying Enzymes in an A53T α-Synuclein Transgenic Mouse Model of Parkinson’s Disease

Antioxidants ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 928
Author(s):  
Jung Hwa Seo ◽  
Seong-Woong Kang ◽  
Kyungri Kim ◽  
Soohyun Wi ◽  
Jang Woo Lee ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Olfactory Bulb ◽  
Frontal Cortex ◽  
Brain Stem ◽  
Environmental Enrichment ◽  
Brain Regions ◽  
Wild Type ◽  
Detoxifying Enzymes

Although environmental enrichment (EE) is known to reduce oxidative stress in Parkinson’s disease (PD), the metabolic alternations for detoxifying endogenous and xenobiotic compounds according to various brain regions are not fully elucidated yet. This study aimed to further understand the role of EE on detoxifying enzymes, especially those participating in phase I of metabolism, by investigating the levels of enzymes in various brain regions such as the olfactory bulb, brain stem, frontal cortex, and striatum. Eight-month-old transgenic PD mice with the overexpression of human A53T α-synuclein and wild-type mice were randomly allocated to either standard cage condition or EE for 2 months. At 10 months of age, the expression of detoxifying enzymes was evaluated and compared with wild-type of the same age raised in standard cages. EE improved neurobehavioral outcomes such as olfactory and motor function in PD mice. EE-treated mice showed that oxidative stress was attenuated in the olfactory bulb, brain stem, and frontal cortex. EE also reduced apoptosis and induced cell proliferation in the subventricular zone of PD mice. The overexpression of detoxifying enzymes was observed in the olfactory bulb and brain stem of PD mice, which was ameliorated by EE. These findings were not apparent in the other experimental regions. These results suggest the stage of PD pathogenesis may differ according to brain region, and that EE has a protective effect on the PD pathogenesis by decreasing oxidative stress.

Two approaches to the determination of glutamate decarboxylase activity in vivo

1979 ◽  
Vol 4 (5) ◽  
pp. 702
Author(s):  
L.P. Miller ◽  
J.R. Walters ◽  
D.L. Martin ◽  
N. Eng
Keyword(s):  
Glutamate Decarboxylase ◽  
Decarboxylase Activity
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