No Influence of Scopolamine Hydrobromide on Odor Detection Performance of Rats

Doty, Richard L.; Bagla, Ritu; Misra, Robert; Mueller, Eric; Kerr, Kara-Lynne

doi:10.1093/chemse/bjg067

Cited by 17 publications

(16 citation statements)

References 24 publications

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“…In our research, odor-detection performance was not affected by infusions of scopolamine, as shown in the olfactory perception test. Such data agree with a recent study reporting that systemic administration of different doses of scopolamine, which are known to influence odor memory and learning, did not cause alterations in the odor-detection performance of rats (Doty et al 2003). Secondly, the duration of the scopolamine action in the brain is an aspect to consider in the explanation of our findings.…”

Section: Discussionsupporting

confidence: 93%

Differential effects of muscarinic receptor blockade in prelimbic cortex on acquisition and memory formation of an odor-reward task

Carballo-Márquez¹,

Vale-Martínez²,

Guillazo-Blanch³

et al. 2007

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The present experiments determined the consequences of blocking muscarinic cholinergic receptors of the prelimbic (PL) cortex in the acquisition and retention of an odor-reward associative task. Rats underwent a training test (five trials) and a 24-h retention test (two retention trials and two relearning trials). In the first experiment, rats were bilaterally infused with scopolamine (20 or 5 µg/site) prior to training. Although scopolamine rats showed acquisition equivalent to PBS-injected controls, they exhibited weakened performance in the 24-h retention test measured by number of errors. In the second experiment, rats were injected with scopolamine (20 µg/site) immediately or 1 h after training and tested 24 h later. Scopolamine rats injected immediately showed severe amnesia detected in two performance measures (errors and latencies), demonstrating deficits in retention and relearning, whereas those injected 1 h later showed good 24-h test performance, similar to controls. These results suggest that muscarinic transmission in the PL cortex is essential for early memory formation, but not for acquisition, of a rapidly learned odor discrimination task. Findings corroborate the role of acetylcholine in consolidation processes and the participation of muscarinic receptors in olfactory associative tasks.

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Section: Discussionsupporting

confidence: 93%

Differential effects of muscarinic receptor blockade in prelimbic cortex on acquisition and memory formation of an odor-reward task

Carballo-Márquez¹,

Vale-Martínez²,

Guillazo-Blanch³

et al. 2007

Learn. Mem.

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“…For example, the blockade of mAChRs may attenuate olfactory sensitivity, alter sensitivity to the foot shock, and/or alter the odor-shock associative plasticity. Our odor investigation experiment along with another report (Doty et al 2003) suggests that scopolamine does not significantly affect olfactory processing, at least with the odorant concentrations used here. A prior study has also demonstrated that systemic scopolamine does not affect foot-shock sensitivity in mice (Anagnostaras et al 1999).…”

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confidence: 64%

Cholinergic modulation during acquisition of olfactory fear conditioning alters learning and stimulus generalization in mice

et al. 2012

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We investigated the role of cholinergic neurotransmission in olfactory fear learning. Mice receiving pairings of odor and foot shock displayed fear to the trained odor the following day. Pretraining injections of the nicotinic antagonist mecamylamine had no effect on subsequent freezing, while the muscarinic antagonist scopolamine significantly reduced freezing. To test whether cholinergic manipulation affected fear generalization, mice were presented with odors similar to the trained odor. Generalization was increased following pretraining scopolamine, while the muscarinic agonist oxotremorine decreased generalization. These results suggest that muscarinic neurotransmission during the acquisition of olfactory association modulates both the strength and specificity of learning.The olfactory system receives cholinergic input from the horizontal limb of the diagonal band of Broca (HDB) (Zaborszky et al. 1986). Blocking olfactory system cholinergic receptors disrupts several aspects of olfactory processing including olfactory shortterm memory (Hunter and Murray 1989;Paolini and McKenzie 1993;Miranda et al. 2009), perceptual learning, and discrimination (Ravel et al. 1992;Fletcher and Wilson 2002;Linster and Cleland 2002;Mandairon et al. 2006). Despite this, relatively little is known about the role of cholinergic activation during acquisition of olfactory aversive learning. While a recent study has demonstrated that cholinergic blockade during acquisition reduces odor-evoked displays of defensive responses to the learned odor (Kroon and Carobrez 2009), the cholinergic contribution to the magnitude and specificity of olfactory fear learning is currently unknown.Sensory cue-evoked fear conditioning has long been used in the study of the neural mechanisms underlying associative memory. In the standard fear-conditioning paradigm, a neutral stimulus is associated with an aversive foot shock, allowing the conditioned stimulus to acquire an aversive valence and induce fear responses, such as freezing (LeDoux 2003). Olfactory cues have been used as an effective conditioned stimulus in promoting fear-conditioned responses (Otto et al. 2000;Jones et al. 2005;Kroon and Carobrez 2009) and studies in other sensory systems have shown that cholinergic neurotransmission is involved in fear learning (Tinsley et al. 2004). For example, in auditory-cued fear conditioning, blockade of muscarinic receptors disrupts the acquisition of the tone-fear conditioning (Young et al. 1995;Anagnostaras et al. 1999;Feiro and Gould 2005), while blocking nicotinic activation does not affect this learning (Feiro and Gould 2005). Despite this, it remains to be seen whether nicotinic and muscarinic receptors can also mediate conditioned freezing responses to olfactory stimuli.In this study, we found that pretraining injections of the nicotinic receptor antagonist (nAChR) mecamylamine had no effect on olfactory fear learning. However, pretraining injections of the muscarinic antagonist scopolamine (mAChR) significantly reduced freezing to the trained od...

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“…To assess olfactory capabilities, Csf1 op/op and WT littermates were subjected to classic buried food challenges [73], [74], [75]. On the first evening of the tests, each mouse was placed in an arena (86 cm×63 cm×18 cm) for a habituation period.…”

Section: Methodsmentioning

confidence: 99%

Absence of Colony Stimulation Factor-1 Receptor Results in Loss of Microglia, Disrupted Brain Development and Olfactory Deficits

et al. 2011

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The brain contains numerous mononuclear phagocytes called microglia. These cells express the transmembrane tyrosine kinase receptor for the macrophage growth factor colony stimulating factor-1 (CSF-1R). Using a CSF-1R-GFP reporter mouse strain combined with lineage defining antibody staining we show in the postnatal mouse brain that CSF-1R is expressed only in microglia and not neurons, astrocytes or glial cells. To study CSF-1R function we used mice homozygous for a null mutation in the Csflr gene. In these mice microglia are >99% depleted at embryonic day 16 and day 1 post-partum brain. At three weeks of age this microglial depletion continues in most regions of the brain although some contain clusters of rounded microglia. Despite the loss of microglia, embryonic brain development appears normal but during the post-natal period the brain architecture becomes perturbed with enlarged ventricles and regionally compressed parenchyma, phenotypes most prominent in the olfactory bulb and cortex. In the cortex there is increased neuronal density, elevated numbers of astrocytes but reduced numbers of oligodendrocytes. Csf1r nulls rarely survive to adulthood and therefore to study the role of CSF-1R in olfaction we used the viable null mutants in the Csf1 (Csf1op) gene that encodes one of the two known CSF-1R ligands. Food-finding experiments indicate that olfactory capacity is significantly impaired in the absence of CSF-1. CSF-1R is therefore required for the development of microglia, for a fully functional olfactory system and the maintenance of normal brain structure.

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No Influence of Scopolamine Hydrobromide on Odor Detection Performance of Rats

Cited by 17 publications

References 24 publications

Differential effects of muscarinic receptor blockade in prelimbic cortex on acquisition and memory formation of an odor-reward task

Differential effects of muscarinic receptor blockade in prelimbic cortex on acquisition and memory formation of an odor-reward task

Cholinergic modulation during acquisition of olfactory fear conditioning alters learning and stimulus generalization in mice

Absence of Colony Stimulation Factor-1 Receptor Results in Loss of Microglia, Disrupted Brain Development and Olfactory Deficits

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