scholarly journals Noradrenergic plasticity of olfactory sensory neuron inputs to the main olfactory bulb

2014 ◽  
Author(s):  
Dennis Eckmeier ◽  
Stephen David Shea
Keyword(s):  
Olfactory Bulb ◽  
Locus Coeruleus ◽  
Sensory Neuron ◽  
Receptor Activation ◽  
Olfactory Sensory Neuron ◽  
Brain State ◽  
Wide Field ◽  
Main Olfactory Bulb ◽  
Glomerular Layer

Sensory responses are modulated throughout the nervous system by internal factors including attention, experience, and brain state. This is partly due to fluctuations in neuromodulatory input from regions such as the noradrenergic locus coeruleus (LC) in the brainstem. LC activity changes with arousal and modulates sensory processing, cognition and memory. The main olfactory bulb (MOB) is richly targeted by LC fibers and noradrenaline profoundly influences MOB circuitry and odor-guided behavior. Noradrenaline-dependent plasticity affects the output of the MOB. However, it is unclear whether noradrenergic plasticity includes modulation in the glomerular layer, the site of input to the MOB. Noradrenergic terminals are found in the glomerular layer, but noradrenaline receptor activation does not seem to acutely modulate olfactory sensory neuron terminals in vitro. We investigated whether noradrenaline induces plasticity at the glomerulus. We used wide-field optical imaging to measure changes in odor responses following electrical stimulation of locus coeruleus in anesthetized mice. Surprisingly, the odor-evoked intrinsic optical signals at the glomerulus were persistently weakened after LC activation. Calcium imaging selectively from olfactory sensory neurons confirmed that this effect was due to a uniform gain suppression of presynaptic input, and did not require exposure to a stimulus during the LC activation. Finally, noradrenaline antagonists prevented glomerular suppression. We conclude that noradrenaline release from LC has persistent effects on odor processing already at the first synapse of the main olfactory system. This mechanism could contribute to arousal-dependent memories.

scholarly journals Requirement for Slit-1 and Robo-2 in Zonal Segregation of Olfactory Sensory Neuron Axons in the Main Olfactory Bulb

2007 ◽  
Vol 27 (34) ◽  
pp. 9094-9104 ◽  
Author(s):  
J. H. Cho ◽  
M. Lepine ◽  
W. Andrews ◽  
J. Parnavelas ◽  
J.-F. Cloutier
Keyword(s):  
Olfactory Bulb ◽  
Sensory Neuron ◽  
Olfactory Sensory Neuron ◽  
Main Olfactory Bulb ◽  
Zonal Segregation

Direct Excitation of Mitral Cells Via Activation of α1-Noradrenergic Receptors in Rat Olfactory Bulb Slices

2001 ◽  
Vol 86 (5) ◽  
pp. 2173-2182 ◽  
Author(s):  
Abdallah Hayar ◽  
Phillip M. Heyward ◽  
Thomas Heinbockel ◽  
Michael T. Shipley ◽  
Matthew Ennis
Keyword(s):  
Olfactory Bulb ◽  
Locus Coeruleus ◽  
Equilibrium Potential ◽  
Channel Blockers ◽  
Mitral Cells ◽  
Patch Clamp Recording ◽  
Whole Cell ◽  
Inward Current

The main olfactory bulb receives a significant modulatory noradrenergic input from the locus coeruleus. Previous in vivo and in vitro studies showed that norepinephrine (NE) inputs increase the sensitivity of mitral cells to weak olfactory inputs. The cellular basis for this action of NE is not understood. The goal of this study was to investigate the effect of NE and noradrenergic agonists on the excitability of mitral cells, the main output cells of the olfactory bulb, using whole cell patch-clamp recording in vitro. The noradrenergic agonists, phenylephrine (PE, 10 μM), isoproterenol (Isop, 10 μM), and clonidine (3 μM), were used to test for the functional presence of α1-, β-, and α2-receptors, respectively, on mitral cells. None of these agonists affected olfactory nerve (ON)–evoked field potentials recorded in the glomerular layer, or ON-evoked postsynaptic currents recorded in mitral cells. In whole cell voltage-clamp recordings, NE (30 μM) induced an inward current (54 ± 7 pA, n= 16) with an EC50 of 4.7 μM. Both PE and Isop also produced inward currents (22 ± 4 pA, n = 19, and 29 ± 9 pA, n = 8, respectively), while clonidine produced no effect ( n = 6). In the presence of TTX (1 μM), and blockers of excitatory and inhibitory fast synaptic transmission [gabazine 5 μM, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) 10 μM, and (±)-2-amino-5-phosphonopentanoic acid (APV) 50 μM], the inward current induced by PE persisted (EC50 = 9 μM), whereas that of Isop was absent. The effect of PE was also observed in the presence of the Ca2+ channel blockers, cadmium (100 μM) and nickel (100 μM). The inward current caused by PE was blocked when the interior of the cell was perfused with the nonhydrolyzable GDP analogue, GDPβS, indicating that the α1 effect is mediated by G-protein coupling. The current-voltage relationship in the absence and presence of PE indicated that the current induced by PE decreased near the equilibrium potential for potassium ions. In current-clamp recordings from bistable mitral cells, PE shifted the membrane potential from the downstate (−52 mV) toward the upstate (−40 mV), and significantly increased spike generation in response to perithreshold ON input. These findings indicate that NE excites mitral cells directly via α1 receptors, an effect that may underlie, at least in part, increased mitral cell responses to weak ON input during locus coeruleus activation in vivo.

Chemically defined neuron groups and their subpopulations in the glomerular layer of the rat main olfactory bulb

1995 ◽  
Vol 23 (1) ◽  
pp. 73-88 ◽  
Author(s):  
Katsuko Kosaka ◽  
Yusuke Aika ◽  
Kazunori Toida ◽  
Claus W. Heizmann ◽  
Willi Hunziker ◽  
...  
Keyword(s):  
Olfactory Bulb ◽  
Main Olfactory Bulb ◽  
Glomerular Layer

Very delayed neuronal loss occurs in the glomerular layer of the main olfactory bulb following transient ischemia in gerbils

2004 ◽  
Vol 366 (3) ◽  
pp. 272-276 ◽  
Author(s):  
In Koo Hwang ◽  
Jae Chul Lee ◽  
Jun Hwi Cho ◽  
Ki-Yeon Yoo ◽  
Duk Soo Kim ◽  
...  
Keyword(s):  
Olfactory Bulb ◽  
Neuronal Loss ◽  
Main Olfactory Bulb ◽  
Transient Ischemia ◽  
Glomerular Layer

scholarly journals Postnatal Developmental Expression of Calbindin, Calretinin and Parvalbumin in Mouse Main Olfactory Bulb

2005 ◽  
Vol 37 (4) ◽  
pp. 276-282 ◽  
Author(s):  
Zhao-Ping Qin ◽  
Shu-Ming Ye ◽  
Ji-Zeng Du ◽  
Gong-Yu Shen
Keyword(s):  
Olfactory Bulb ◽  
Cell Layer ◽  
Plexiform Layer ◽  
Olfactory Nerve ◽  
Mitral Cell ◽  
Granule Cell Layer ◽  
Developmental Expression ◽  
Main Olfactory Bulb ◽  
Glomerular Layer ◽  
Layer 4

Abstract The distribution of calbindin, calretinin and parvalbumin during the development of the mouse main olfactory bulb (MOB) was studied using immunohistochemistry techniques. The results are as follows: (1) calbindin-immunoreactive profiles were mainly located in the glomerular layer, and few large calbindin-immunoreactive cells were found in the subependymal layer of postnatal day 10 (P1 0) to postnatal day 40 (P40) mice; (2) no calbindin was detected in the mitral cell layer at any stage; (3) calretinin-immunoreactive profiles were present in all layers of the main olfactory bulb at all stages, especially in the olfactory nerve layer, glomerular layer and granule cell layer; (4) parvalbumin-immunoreactive profiles were mainly located in the external plexiform layer (except for P10 mice); (5) weakly stained parvalbumin-immunoreactive profiles were present in the glomerular layer at all stages; and (6) no parvalbumin was detected in the mitral cell layer at any stage.

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