Resistance of frog olfactory bulb slow potential and afferent input inhibition to hypoxia and synaptic transmission blockade by manganese, cobalt, and magnesium ions

1983 ◽  
Vol 15 (1) ◽  
pp. 75-82
Author(s):  
A. A. Potapov
Keyword(s):  
Olfactory Bulb ◽  
Synaptic Transmission ◽  
Afferent Input ◽  
Magnesium Ions ◽  
Slow Potential ◽  
Frog Olfactory Bulb

Presynaptic inhibition in the frog olfactory bulb

1968 ◽  
Vol 2 (3) ◽  
pp. 775-777
Author(s):  
G. S. Voronkov ◽  
K. G. Gusel'nikova
Keyword(s):  
Olfactory Bulb ◽  
Presynaptic Inhibition ◽  
Frog Olfactory Bulb

Dopaminergic neuromodulation of synaptic transmission between mitral and granule cells in the teleost olfactory bulb

2012 ◽  
Vol 107 (5) ◽  
pp. 1313-1324 ◽  
Author(s):  
Takafumi Kawai ◽  
Hideki Abe ◽  
Yoshitaka Oka
Keyword(s):  
Olfactory Bulb ◽  
Synaptic Transmission ◽  
Granule Cells ◽  
Glutamate Release ◽  
Field Potential ◽  
Olfactory Nerve ◽  
Oscillatory Activity ◽  
Cellular Mechanisms ◽  
Olfactory Information

A growing body of evidence suggests that teleosts are important models for the study of neural processing of olfactory information, and the functional role of dopamine (DA), which is a potent neuromodulator endogenous to the mammalian olfactory bulb, has been one of the strongest focuses in this field. However, the cellular mechanisms of dopaminergic neuromodulation in olfactory bulbar neural circuits have not been fully understood. We investigated such mechanisms by using the goldfish, which offers several advantages for analyzing olfactory information processing by electrophysiological methods. First, we found in the olfactory bulb that numerous cell bodies of the dopaminergic neurons are mainly distributed in the mitral cell layer and extend fine processes to the glomerular layer. Next, we made in vitro field potential recordings and showed that synaptic transmissions from mitral to granule cells were suppressed by DA application. DA also increased the paired-pulse ratio, suggesting that the suppression of synaptic transmission is caused by a decrease in presynaptic glutamate release from the mitral cells. Furthermore, DA significantly suppressed the oscillatory activity of the olfactory bulb in response to olfactory stimuli. Although DA suppresses the synaptic inputs from the olfactory nerve to the olfactory bulbar neurons in mammals, this phenomenon was not observed in the goldfish. These findings indicate that suppression of the mitral to granule cell synaptic transmission in the reciprocal synapses plays an important role in the negative regulation of olfactory responsiveness in the goldfish olfactory bulb.

Abnormal Synaptic Transmission in the Olfactory Bulb of Fyn-Kinase–Deficient Mice

1998 ◽  
Vol 79 (1) ◽  
pp. 137-142 ◽  
Author(s):  
Hiromasa Kitazawa ◽  
Takeshi Yagi ◽  
Tsuyoshi Miyakawa ◽  
Hiroaki Niki ◽  
Nobufumi Kawai
Keyword(s):  
Olfactory Bulb ◽  
Synaptic Transmission ◽  
Metabotropic Glutamate Receptors ◽  
Granule Cells ◽  
Long Term Potentiation ◽  
Lateral Olfactory Tract ◽  
Metabotropic Glutamate ◽  
Olfactory Tract ◽  
Fyn Kinase ◽  
Deficient Mice

Kitazawa, Hiromasa, Takeshi Yagi, Tsuyoshi Miyakawa, Hiroaki Niki, and Nobufumi Kawai. Abnormal synaptic transmission in the olfactory bulb of Fyn-kinase–deficient mice. J. Neurophysiol. 79: 137–142, 1998. We studied synaptic transmission in the granule cells in the olfactory bulb of the homozygous Fyn (a nonreceptor type tyrosine kinase)-deficient ( fyn z/ fyn z) and heterozygous Fyn-deficient (+/ fyn z) mice by using slice preparations from the olfactory bulb. Stimulation to the lateral olfactory tract and/or centrifugal fibers to the olfactory bulb evoked field excitatory postsynaptic potentials (fEPSPs) in the granule cells. In +/ fyn z mice, fEPSPs were augmented by bicuculline, a γ-aminobutyric acid (GABAA) antagonist and picrotoxin, whereas fEPSPs in fyn z/ fyn z mice were much less sensitive to bicuculline and picrotoxin. Application of d-2-amino-5-phosphonopentanoic acid had no effect but 6-cyano-7-nitroquinoxaline-2,3-dione produced almost complete block of fEPSPs in both +/ fyn z mice and fyn z/ fyn z mice. (1S, 3R)-1-aminocyclo-pentane-1.3-dicarboxylate, an agonist of metabotropic glutamate receptors caused a similar depression of fEPSPs in both +/ fyn z and fyn z/ fyn z mice. In +/ fyn z mice tetanic stimulation to the lateral olfactory tract and/or centrifugal fibers induced N-methyl-d-aspartate (NMDA)-dependent long-term potentiation (LTP) of fEPSPs, whereas LTP was impaired in fyn z/ fyn z mice. Our results demonstrate altered functions of GABAA and NMDA receptors in the olfactory system of Fyn-deficient mice.

Sign in / Sign up

Export Citation Format

Share Document