scholarly journals Co-localization of two-color rAAV2-retro confirms the dispersion characteristics of efferent projections of mitral cells in mouse accessory olfactory bulb

2020 ◽  
Vol 41 (2) ◽  
pp. 148-156
Author(s):  
Zheng Ning ◽  
Wang Zhi-Zhong ◽  
Wang Song-Wei ◽  
Yang Fang-Jia ◽  
Zhu Xu-Tao ◽  
...  
Neuroscience ◽  
1991 ◽  
Vol 45 (3) ◽  
pp. 663-670 ◽  
Author(s):  
A.A. Caminero ◽  
S. Segovia ◽  
A. Guillamo´n

1997 ◽  
Vol 42 (3) ◽  
pp. 227-230 ◽  
Author(s):  
Carmen Pérez-Laso ◽  
Santiago Segovia ◽  
Paloma Collado ◽  
Mónica RodrÍguez-Zafra ◽  
Agueda Del Abril ◽  
...  

PLoS Biology ◽  
2015 ◽  
Vol 13 (12) ◽  
pp. e1002319 ◽  
Author(s):  
Asaph Zylbertal ◽  
Anat Kahan ◽  
Yoram Ben-Shaul ◽  
Yosef Yarom ◽  
Shlomo Wagner

1986 ◽  
Vol 24 (1-2) ◽  
pp. 287-290 ◽  
Author(s):  
Azucena Valencia ◽  
Santiago Segovia ◽  
Antonio Guillamón

1999 ◽  
Vol 81 (1) ◽  
pp. 345-355 ◽  
Author(s):  
Changping Jia ◽  
Wei R. Chen ◽  
Gordon M. Shepherd

Jia, Changping, Wei R. Chen, and Gordon M. Shepherd. Synaptic organization and neurotransmitters in the rat accessory olfactory bulb. J. Neurophysiol. 81: 345–355, 1999. The accessory olfactory bulb (AOB) is the first relay station in the vomeronasal system and may play a critical role in processing pheromone signals. The AOB shows similar but less distinct lamination compared with the main olfactory bulb (MOB). In this study, synaptic organization of the AOB was analyzed in slice preparations from adult rats by using both field potential and patch-clamp recordings. Stimulation of the vomeronasal nerve (VN) evoked field potentials that showed characteristic patterns in different layers of the AOB. Current source density (CSD) analysis of the field potentials revealed spatiotemporally separated loci of inward current (sinks) that represented sequential activation of different neuronal components: VN activity (period I), synaptic excitation of mitral cell apical dendrites (period II), and activation of granule cells by mitral cell basal dendrites (period III). Stimulation of the lateral olfactory tract also evoked field potentials in the AOB, which indicated antidromic activation of the mitral cells (period I and II) followed by activation of granule cells (period III). Whole cell patch recordings from mitral and granule cells of the AOB supported that mitral cells are excited by VN terminals and subsequently activate granule cells through dendrodendritic synapses. Both CSD analysis and patch recordings provided evidence that glutamate is the neurotransmitter at the vomeronasal receptor neuron; mitral cell synapses and both NMDA and non-NMDA receptors are involved. We also demonstrated electrophysiologically that reciprocal interaction between mitral and granule cells in the AOB is through the dendrodendritic reciprocal synapses. The neurotransmitter at the mitral-to-granule synapses is glutamate and at the granule-to-mitral synapse is γ-aminobutyric acid. The synaptic interactions among receptor cell terminals, mitral cells, and granule cells in the AOB are therefore similar to those in the MOB, suggesting that processing of chemosensory information in the AOB shares similarities with that in the MOB.


2009 ◽  
Vol 102 (2) ◽  
pp. 1103-1114 ◽  
Author(s):  
Richard S. Smith ◽  
Christopher J. Weitz ◽  
Ricardo C. Araneda

Modulation of dendrodendritic synapses by the noradrenergic system in the accessory olfactory bulb (AOB) plays a key role in the formation of memory in olfactory-mediated behaviors. We have recently shown that noradrenaline (NA) inhibits mitral cells by increasing γ-aminobutyric acid inhibitory input onto mitral cells in the AOB, suggesting an excitatory action of NA on granule cells (GCs). Here, we show that NA (10 μM) elicits a long-lasting depolarization of GCs. This effect is mediated by activation of α1-adrenergic receptors as the depolarization is mimicked by phenylephrine (PE, 30 μM) and completely blocked by the α1-adrenergic receptor antagonist prazosin (300 nM). In addition to this depolarization, application of NA induced the appearance of a slow afterdepolarization (sADP) following a stimulus-elicited train of action potentials. Similarly, the group I metabotropic glutamate receptor (mGluR1) agonist DHPG (10–30 μM) also produced a depolarization of GCs and the appearance of a stimulus-induced sADP. The ionic and voltage dependence and sensitivity to blockers of the sADP suggest that it is mediated by the nonselective cationic conductance ICAN. Thus the excitatory action resulting from the activation of these receptors could be mediated by a common transduction target. Surprisingly, the excitatory effect of PE on GCs was completely blocked by the mGluR1 antagonist LY367385 (100 μM). Conversely, the effect of DHPG was not antagonized by the α1-adrenergic receptor antagonist prazosin (300 nM). These results suggest that most of the noradrenergic effect on GCs in the AOB is mediated by potentiation of a basal activity of mGluR1s.


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