scholarly journals Noradrenergic but not cholinergic modulation of olfactory bulb during processing of near threshold concentration stimuli.

2012 ◽  
Vol 126 (5) ◽  
pp. 720-728 ◽  
Author(s):  
Olga Escanilla ◽  
Sam Alperin ◽  
Monica Youssef ◽  
Matthew Ennis ◽  
Christiane Linster
2008 ◽  
Vol 33 (4) ◽  
pp. 331-338 ◽  
Author(s):  
Angela Pignatelli ◽  
Ottorino Belluzzi

2002 ◽  
Vol 15 (4-6) ◽  
pp. 709-717 ◽  
Author(s):  
Christiane Linster ◽  
Thomas A Cleland

2006 ◽  
Vol 24 (11) ◽  
pp. 3234-3244 ◽  
Author(s):  
Nathalie Mandairon ◽  
Casara Jean Ferretti ◽  
Conor M. Stack ◽  
Daniel B. Rubin ◽  
Thomas A. Cleland ◽  
...  

2021 ◽  
pp. 1-19
Author(s):  
Abdallah Ahnaou ◽  
Lucile Chave ◽  
Nikolay V. Manyakov ◽  
Wilhelmus H.I.M. Drinkenburg

<b><i>Background/Aims:</i></b> Olfactory dysfunction can provide valuable insight into early pathophysiological processes of brain disorders. Olfactory processing of chemosensory and odour sensitivity relies on segregating salient odours from background odours cues. Odour-evoked fast oscillations in the olfactory bulb (OB) are hypothesized to be an important index of odour quality coding. The present preclinical work aimed at better understanding connectivity associated with odour coding and behavioural odour discrimination. <b><i>Methods:</i></b> Network oscillations and functional connectivity (FC) were measured in C57BL/6 mice performing the olfactory associative odour learning (OL) test, using multichannel local field potential recordings in key olfactory networks. Cholinergic modulation of odour processing was investigated using the muscarinic antagonist scopolamine. <b><i>Results:</i></b> At the behavioural level, olfactory memory, which refers to the acquisition and recollection of a reference odour by reduced exploration time, was observed in animals that correctly learned the task. Significant decrease in mean investigation and retrieval time of the associated odour-food reward was observed between trials. At the network level, the associated odour during sniffing behaviour was associated with enhanced coherence in the β and γ frequency oscillations across the olfactory pathway, with marked changes observed between the OB and anterior piriform cortex (PC). The enhanced phase-amplitude cross-frequency coupling in the OB and the weak coupling index in the hippocampal CA1 suggests a role of the OB network in olfaction encoding and processing. Scopolamine impaired behavioural and FC underlying recall and retrieval of the associated odour. <b><i>Conclusion:</i></b> The results suggest that the acquisition and formation of odour reference memory rely primarily on FC at the OB-PC network and confirm the role of muscarinic receptors in olfactory retrieval processing.


2001 ◽  
Vol 201 (2) ◽  
pp. 276-277 ◽  
Author(s):  
Benjamin Hall ◽  
Kerry Delaney

1979 ◽  
Vol 42 (04) ◽  
pp. 1187-1192 ◽  
Author(s):  
Iren B Kovács ◽  
P Görög

SummaryAddition of N-acetyl neuraminic acid (sialic acid, NANA) to citrated rat platelet-rich plasma significantly inhibited aggregation induced by near-threshold concentration of ADP, collagen or thrombin. In heparinized rat platelet-rich plasma aggregation of platelets induced by endotoxin or tumour cells of various origins was also inhibited by sialic acid.It is suggested that exogenous or endogenous sialic acid may act against various aggregating stimuli on the platelet membrane by masking a common factor through which various aggregating agents exert their effect.


2010 ◽  
Vol 104 (6) ◽  
pp. 2963-2974 ◽  
Author(s):  
Richard S. Smith ◽  
Ricardo C. Araneda

The accessory olfactory bulb (AOB), the first relay of chemosensory information in the Vomeronasal system, receives extensive cholinergic innervation from the basal forebrain. Cholinergic modulation of neuronal activity in the olfactory bulb has been hypothesized to play an important role in olfactory processing; however, little is known about the cellular actions of acetylcholine (ACh) within the AOB. Here using in vitro slice preparation, we show that muscarinic acetylcholine receptor (mAChR) activation increases neuronal excitability of granule and mitral/tufted cells (GCs and MCs) in the AOB. Activation of mAChRs increased excitability of GCs by three distinct mechanisms: induction of a long-lasting depolarization, activation of a slow afterdepolarization (sADP), and an increase in excitatory glutamatergic input due to MC depolarization. The depolarization and sADP were elicited by the selective agonist 4-[[[(3-chlorophenyl)amino]carbonyl]oxy]- N,N,N-trimethyl-2-butyn-1-aminium chloride (100 μM) and blocked by low concentrations of pirenzepine (300 nM), indicating that they result from activation of M1-like mAChRs. In contrast, cholinergic stimulation increased the excitability of MCs via recruitment of nicotinic AChRs (nAChRs) and M1-like mAChRs. Submaximal activation of these receptors, however, decreased the excitability of MCs. Surprisingly, we found that unlike GCs in the main olfactory bulb, GCs in the AOB are excited by mAChR activation in young postnatal neurons, suggesting marked differences in cholinergic regulation of development between these two regions of the olfactory bulb.


2013 ◽  
Vol 109 (5) ◽  
pp. 1360-1377 ◽  
Author(s):  
Licurgo de Almeida ◽  
Marco Idiart ◽  
Christiane Linster

In this work we investigate in a computational model how cholinergic inputs to the olfactory bulb (OB) and piriform cortex (PC) modulate odor representations. We use experimental data derived from different physiological studies of ACh modulation of the bulbar and cortical circuitry and the interaction between these two areas. The results presented here indicate that cholinergic modulation in the OB significantly increases contrast and synchronization in mitral cell output. Each of these effects is derived from distinct neuronal interactions, with different groups of interneurons playing different roles. Both bulbar modulation effects contribute to more stable learned representations in PC, with pyramidal networks trained with cholinergic-modulated inputs from the bulb exhibiting more robust learning than those trained with unmodulated bulbar inputs. This increased robustness is evidenced as better recovery of memories from corrupted patterns and lower-concentration inputs as well as increased memory capacity.


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