Olfactory Memory Test Research Articles

Development and validation of the Olfactory Memory Test Battery (OMTB) based on odors with high- and low-verbalizability

BackgroundOdor memory is an important field of clinical research for its distinctive characteristics, which differ from those of other sensory systems. To date, several tests have been implemented for the assessment of odor memory. Despite a range of studies demonstrating the importance of verbal mediation in odor memory, few have distinguished odor memory performance in different odor verbalization levels. New methodWe aimed to develop a standardized odor memory test toolbox with one group of odors that are easily verbally identified and the other group of odors that are difficult to identify. The test contained two odor categories (high- and low-verbalizability odors), each consisting of three subtests (short- and long-term memory and working memory). ResultsSatisfactory test-retest reliability and solid validity of the odor recognition and working memory test were shown in both odor categories. Moreover, people scored significantly better with high- than low-verbalizability odors. A negative age effect on odor memory performance was also found. Comparison with existing methodsNo previous odor memory test distinguished odor memory performance in different odor verbalization levels, while the Olfactory Memory Test Battery (OMTB) contains high- and low-verbalizability odors and each category has three subtests. ConclusionsThe present study indicated the OMTB is a comprehensive assessment of odor memory with good reliability and validity. All subtests can be used separately or in combination with each other according to the clinical and research needs.

The Western Australia Olfactory Memory Test: Reliability and Validity in a Sample of Older Adults.

The Western Australia Olfactory Memory Test (WAOMT) is a newly developed test designed to meet a need for a comprehensive measure of olfactory episodic memory (OEM) for clinical and research applications. This study aimed to establish the psychometric properties of the WAOMT in a sample of 209 community-dwelling older adults. An independent sample of 27 test-naïve participants were recruited to assess test retest reliability (between 7 and 28days). Scale psychometric properties were examined using item response theory methods, combined samples (final N = 241). Convergent validity was assessed by comparing performance on the WAOMT with a comprehensive neuropsychological battery of domains (verbal and visual episodic memory, and odor identification), as well as other neuropsychological skills. Based on previous literature, it was predicted that the WAOMT would be positively correlated with conceptually similar cognitive domains. The WAOMT is a psychometrically sound test with adequate reliability properties and demonstrated convergent validity with tests of verbal and episodic memory and smell identification. Patterns of performance highlight learning and memory characteristics unique to OEM (e.g., learning curves, cued and free recall). Clinical and research implications include streamlining future versions of the WAOMT to ease patient and administrative burden, and the potential to reliably detect early neuropathological changes in healthy older adults with nonimpaired OEM abilities.

Neuroprotective Effects of Dexmedetomidine on the Ketamine-Induced Disruption of the Proliferation and Differentiation of Developing Neural Stem Cells in the Subventricular Zone.

Background: Ketamine disrupts the proliferation and differentiation of developing neural stem cells (NSCs). Therefore, the safe use of ketamine in pediatric anesthesia has been an issue of increasing concern among anesthesiologists and children's parents. Dexmedetomidine (DEX) is widely used in sedation as an antianxiety agent and for analgesia. DEX has recently been shown to provide neuroprotection against anesthetic-induced neurotoxicity in the developing brain. The aim of this in vivo study was to investigate whether DEX exerted neuroprotective effects on the proliferation and differentiation of NSCs in the subventricular zone (SVZ) following neonatal ketamine exposure.Methods: Postnatal day 7 (PND-7) male Sprague-Dawley rats were equally divided into the following five groups: control group (n = 8), ketamine group (n = 8), 1 μg/kg DEX+ketamine group (n = 8), 5 μg/kg DEX+ketamine group (n = 8) and 10 μg/kg DEX+ketamine group (n = 8). Immediately after treatment, rats received a single intraperitoneal injection of BrdU, and the proliferation and differentiation of NSCs in the SVZ were assessed using immunostaining at 24 h after the BrdU injection. In the olfactory behavioral tests, rats in each group were raised until 2 months old, and the buried food test and olfactory memory test were performed.Results: The proliferation of NSCs and astrocytic differentiation in the SVZ were significantly inhibited at 24 h after repeated ketamine exposure in the neonatal period, and neuronal differentiation was markedly increased. Furthermore, pretreatment with moderately high (5 μg/kg) or high doses (10 μg/kg) of DEX reversed ketamine-induced disturbances in the proliferation and differentiation of NSCs. In the behavior tests, repeated neonatal ketamine exposure induced olfactory cognitive dysfunction in the adult stage, and moderately high and high doses of DEX reversed the olfactory cognitive dysfunction induced by ketamine.Conclusions: Based on the present findings, pretreatment with a moderately high (5 μg/kg) or high dose (10 μg/kg) of DEX may alleviate the developmental neurogenesis disorder in the SVZ at 24 h after repeated ketamine exposure and improve olfactory cognitive dysfunction in adulthood.

Absence of Both Thyroid Hormone Transporters MCT8 and OATP1C1 Impairs Neural Stem Cell Fate in the Adult Mouse Subventricular Zone.

SummaryAdult neural stem cell (NSC) generation in vertebrate brains requires thyroid hormones (THs). How THs enter the NSC population is unknown, although TH availability determines proliferation and neuronal versus glial progenitor determination in murine subventricular zone (SVZ) NSCs. Mice display neurological signs of the severely disabling human disease, Allan-Herndon-Dudley syndrome, if they lack both MCT8 and OATP1C1 transporters, or MCT8 and deiodinase type 2. We analyzed the distribution of MCT8 and OATP1C1 in adult mouse SVZ. Both are strongly expressed in NSCs and at a lower level in neuronal cell precursors but not in oligodendrocyte progenitors. Next, we analyzed Mct8/Oatp1c1 double-knockout mice, where brain uptake of THs is strongly reduced. NSC proliferation and determination to neuronal fates were severely affected, but not SVZ-oligodendroglial progenitor generation. This work highlights how tight control of TH availability determines NSC function and glial-neuron cell-fate choice in adult brains.

Inducible and conditional activation of ERK5 MAP kinase rescues mice from cadmium-induced olfactory memory deficits

Cadmium (Cd) is a heavy metal that is one of the most toxic environmental pollutants throughout the world. We previously reported that Cd exposure impairs olfactory memory in mice. However, the underlying mechanisms for its neurotoxicity for olfactory function are not well understood. Since adult Subventricular zone (SVZ) and Olfactory Bulb (OB) neurogenesis contributes to olfaction, olfactory memory defects caused by Cd may be due to inhibition of neurogenesis. In this study, using bromodeoxyuridine (BrdU) labeling and immunohistochemistry, we found that 0.6 mg/L Cd exposure through drinking water impaired adult SVZ/OB neurogenesis in C57BL/6 mice. To determine if the inhibition of olfactory memory by Cd can be reversed by stimulating adult neurogenesis, we utilized the transgenic caMEK5 mouse strain to conditional stimulate of adult neurogenesis by activating the endogenous ERK5 MAP kinase signaling pathway. This was accomplished by conditionally induced expression of active MEK5 (caMEK5) in adult neural stem/progenitor cells. The caMEK5 mice were exposed to 0.6 mg/L Cd for 38 weeks, and tamoxifen was administered to induce caMEK5 expression and stimulate adult SVZ/OB neurogenesis during Cd exposure. Short-term olfactory memory test and sand-digging based, odor-cued olfactory learning and memory test were conducted after Cd and tamoxifen treatments to examine their effects on olfaction. Here we report that Cd exposure impaired short-term olfactory memory and odor-cued associative learning and memory in mice. Furthermore, the Cd-impaired olfactory memory deficits were rescued by the tamoxifen-induction of caMEK5 expression. This suggests that Cd exposure impairs olfactory function by affecting adult SVZ/OB neurogenesis in mice.

TOM-32–An extended test for the assessment of olfactory memory

BackgroundOlfactory memory testing is a promising way to explore different aspects of smell-related abilities in healthy subjects as well as to diagnose various diseases associated with disorders of this type of memory. Despite the obvious value of olfactory memory assessments, few available methods enable its diagnosis. New methodThe aim of our study was to create a standardized research tool designed for olfactory memory studies: an extended, 32-item version of an available “Test for Odor Memory”. ResultsThe study involving 222 subjects revealed satisfactory psychometric qualities of TOM-32, and – as hypothesized – subjects with depression scored significantly lower than healthy participants. We additionally showed that TOM-32 scores was associated with sex, age and olfactory awareness. Women performed significantly better than men, young people tended to have lower false alarm rate than older subjects and olfactory awareness was positively associated with olfactory memory. Comparison with existing method(s)TOM-32 could expand the possibilities of testing olfactory memory. It may offer additional information about cognitive and sensory abilities relative to existing research tools, and the large number of included test items may facilitate repeated and longitudinal testing. Wide range of applied odors increases the possibility to detect subtle differences between, as well as changes within, individuals. ConclusionsWe present an extensive olfactory memory test with satisfactory psychometric qualities – a test that is comprehensive enough to show significant inter- and intra-individual differences, but time-efficient enough to be comfortable in daily research and clinical usage.

The Sniffin' Sticks Odor Discrimination Memory Test: A Rapid, Easy-to-Use, Reusable Procedure for Testing Olfactory Memory.

Neurodegenerative diseases can alter odor memory in addition to inducing quantitative impairment, and olfactory memory can be tested using the validated olfactory memory test with encapsulated odors (Odor Discrimination Memory Test [ODMT]). The aim of this study was to investigate the new Sniffin' Sticks ODMT (SSODMT), which is comparable with the ODMT. The SSODMT was administered to 48 subjects (30 women, 18 men; mean age, 34.6 ± 16.3 years). Olfactory function was assessed using the 16-item Sniffin' Sticks Identification Test. The ODMT was administered to a subgroup of 10 subjects to assess the comparability of the SSODMT and the ODMT. Test-retest reliability was studied in another 20 subjects (10 women, 10 men; mean age, 32.9 ± 16.4 years). The mean SSODMT score was 10.7 ± 1.8 (range, 5-12). SSODMT test scores were significantly correlated with Sniffin' Sticks Identification Test scores (r67 = 0.66, P < .001) and were significantly negatively correlated with subject age (r48 = -0.70, P < .001). SSODMT and ODMT scores were highly and significantly correlated, indicating that the test results were comparable (r10 = 0.75, P < .05). Test-retest analysis revealed a significant correlation (r20 = 0.68, P < .001). These results demonstrate the usefulness of the new SSODMT and its comparability with the ODMT. The SSODMT is an easy, rapid, and low-cost tool that is suitable for routine use in evaluating odor memory.

Long-term odor recognition memory in unipolar major depression and Alzheimer׳s disease

Major depression and Alzheimer׳s disease (AD) are often observed in the elderly. The identification of specific markers for these diseases could improve their screening. The aim of this study was to investigate long-term odor recognition memory in depressed and AD patients, with a view to identifying olfactory markers of these diseases. We included 20 patients with unipolar major depressive episodes (MDE), 20 patients with mild to moderate AD and 24 healthy subjects. We investigated the cognitive profile and olfactory memory capacities (ability to recognize familiar and unfamiliar odors) of these subjects. Olfactory memory test results showed that AD and depressed patients were characterized by significantly less correct responses and more wrong responses than healthy controls. Detection index did not differ significantly between patients with major depression and those with AD when the results were analyzed for all odors. However, MDE patients displayed an impairment of olfactory memory for both familiar and unfamiliar odors, whereas AD subjects were impaired only in the recognition of unfamiliar odors, with respect to healthy subjects. If preservation of olfactory memory for familiar stimuli in patients with mild to moderate AD is confirmed, this test could be used in clinical practice as a complementary tool for diagnosis.

Abnormal Social Behavior in Nicotinic Acetylcholine Receptor 4 Subunit-Null Mice

Tobacco addiction has a strong social component. Therefore, nicotinic acetylcholine receptors (nAChR) may influence social behavior. Because the β4 nicotinic receptor subunit is important for possibly related behaviors, such as anxiety-like behavior and the effects of nicotine, we studied the social behavior of mice null for the β4 nAChR subunit. To measure social behavior, we used the intruder test for social memory in wild-type and littermate β4 null mice. In addition, we used a nonsocial olfactory memory test as a control. In the intruder test, β4 null mice showed social amnesia: Wild-type mice spent less time actively interacting with a younger intruder on Day 2 than on Day 1, but β4 null mice interacted for a similar time on both days. In the nonsocial olfactory memory test, control littermates and β4 null mice learnt the associations to a similar extent, showing that the amnesic phenotype in the intruder test is specific for social settings. We conclude that nAChRs that contain the β4 subunit are important for social behaviors. As those receptors are necessary to observe several effects of nicotine including withdrawal, it is tempting to speculate that the social component of tobacco use is related to the same neuronal circuits responsible for continuing tobacco use in smokers.

Gestational stress prevents motherhood-induced improvement of olfactory memory

Event Abstract Back to Event Gestational stress prevents motherhood-induced improvement of olfactory memory Laure Belnoue1*, Nora Djoher Abrous1 and Muriel Koehl1 1 Neurocentre Magendie Inserm U862, France Among mammals ranging from rodents through primates, olfactory cues have been shown to play a ubiquitous role in social recognition. In particular there is an extensive contribution of olfaction in many aspects of maternal care to ensure the coordination of mother-infant interactions. The ability for new mothers to rapidly recognize their own offspring has been proposed as an important component to establish an adaptive maternal behavior, which is disturbed in mothers that have been submitted to gestational stress. These data indicate that motherhood may be associated to enhanced olfactory performances, and that this effect may be abolished by gestational stress.To test this hypothesis, we have analyzed the impact of motherhood under normal conditions or after gestational stress on olfactory memory that we tested two weeks after parturition in: Virgin female (V), mother (M) and Stressed Mother (MS) mice. For this last group, stress was performed during the last week of gestation. The olfactory memory test consisted of two 5 min odor presentations of the same odor with a 6h interval. The time that the animals spent sniffing the odor was recorded. A significant decrease in investigation time during the second presentation indicates that mice were able to recognize an odor presented previously. We found that virgin females did not recognize the odor as familiar after a 6h delay, while mothers did spend less time sniffing it upon the 2nd presentation, indicating an improved olfactory memory. Stressed mothers presented performances similar to those of virgins.Altogether our results indicate that motherhood improves olfactory memory and that this enhancement is abolished by a gestational stress. Since olfactory memories may be formed, in part, by neural circuitry involving neurogenesis in the olfactory bulb, the next step will be to determine the impact of normal and disrupted motherhood on this phenomenon. Conference: 41st European Brain and Behaviour Society Meeting, Rhodes Island, Greece, 13 Sep - 18 Sep, 2009. Presentation Type: Poster Presentation Topic: Poster presentations Citation: Belnoue L, Abrous N and Koehl M (2009). Gestational stress prevents motherhood-induced improvement of olfactory memory. Conference Abstract: 41st European Brain and Behaviour Society Meeting. doi: 10.3389/conf.neuro.08.2009.09.090 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 08 Jun 2009; Published Online: 08 Jun 2009. * Correspondence: Laure Belnoue, Neurocentre Magendie Inserm U862, Bordeaux, France, laure.belnoue@inserm.fr Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Laure Belnoue Nora Djoher Abrous Muriel Koehl Google Laure Belnoue Nora Djoher Abrous Muriel Koehl Google Scholar Laure Belnoue Nora Djoher Abrous Muriel Koehl PubMed Laure Belnoue Nora Djoher Abrous Muriel Koehl Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Social Transmission of Food Preference in Mice

The social transmission of food preference (STFP) is an ethologically relevant test of olfactory memory that can be used in mice. In this test, "observer" mice interact with a "demonstrator" mouse that has recently eaten a novel food. When observer mice are presented with a choice between the food eaten by the demonstrator and some other novel food, observer mice prefer the food eaten by the demonstrator. This phenomenon depends on the observer mice detecting olfactory cues on the breath of the demonstrator mouse during their interaction. The subsequent food preference serves as a measure of memory for those olfactory cues. This unit describes a method for performing STFP in mutant mice. The method explains how to address potential confounding factors and avoid possible pitfalls.

Social transmission of food preference in mice: Methodology and application to galanin-overexpressing transgenic mice.

Social transmission of food preference (STFP) is a test of olfactory memory that can be used in mice. Confounds in STFP that can lead to misinterpretation of an STFP deficit as a memory impairment include changes in social interaction and olfaction. The issue of changes in social interaction was addressed by evaluating an observer-centric and a demonstrator-centric method for scoring the interaction phase of STFP in mice. The demonstrator-centric method was applied to a line of STFP-impaired, galanin-overexpressing transgenic (GAL-tg). GAL-tg mice were impaired in STFP without deficits in social interaction. In tests of olfactory ability, GAL-tg mice were unimpaired on buried-food and habituation-dishabituation tasks. The current studies describe an expanded method for using STFP in mice and confirm a deficit in olfactory memory in GAL-tg mice.

Social transmission of food preference in mice: Methodology and application to galanin-overexpressing transgenic mice.

Social transmission of food preference (STFP) is a test of olfactory memory that can be used in mice. Confounds in STFP that can lead to misinterpretation of an STFP deficit as a memory impairment include changes in social interaction and olfaction. The issue of changes in social interaction was addressed by evaluating an observer-centric and a demonstrator-centric method for scoring the interaction phase of STFP in mice. The demonstrator-centric method was applied to a line of STFP-impaired, galanin-overexpressing transgenic (GAL-tg). GAL-tg mice were impaired in STFP without deficits in social interaction. In tests of olfactory ability, GAL-tg mice were unimpaired on buried-food and habituation-dishabituation tasks. The current studies describe an expanded method for using STFP in mice and confirm a deficit in olfactory memory in GAL-tg mice.

Galanin transgenic mice display cognitive and neurochemical deficits characteristic of Alzheimer's disease.

Galanin is a neuropeptide with multiple inhibitory actions on neurotransmission and memory. In Alzheimer's disease (AD), increased galanin-containing fibers hyperinnervate cholinergic neurons within the basal forebrain in association with a decline in cognition. We generated transgenic mice (GAL-tg) that overexpress galanin under the control of the dopamine beta-hydroxylase promoter to study the neurochemical and behavioral sequelae of a mouse model of galanin overexpression in AD. Overexpression of galanin was associated with a reduction in the number of identifiable neurons producing acetylcholine in the horizontal limb of the diagonal band. Behavioral phenotyping indicated that GAL-tgs displayed normal general health and sensory and motor abilities; however, GAL-tg mice showed selective performance deficits on the Morris spatial navigational task and the social transmission of food preference olfactory memory test. These results suggest that elevated expression of galanin contributes to the neurochemical and cognitive impairments characteristic of AD.

Olfactory memory in unmedicated schizophrenics

Previous studies have indicated that schizophrenic patients have olfactory deficits. The question as to whether olfactory deficits are due to chronic effects of medication has not been addressed. This is the first paper to report that never-medicated schizophrenic patients also have olfactory deficits. Twenty four normal subjects and twenty unmedicated schizophrenic patients were examined with two tests of olfactory function: the University of Pennsylvania Smell Identification Test (UPSIT) and a match-to-sample olfactory memory test. Results indicated that schizophrenics did poorly on both the UPSIT and the olfactory match-to-sample memory test relative to sex and age-matched controls. ANCOVA showed that the deficit in performance on the olfactory match-to-sample test was still present even when the variance due to the UPSIT was taken out of the analysis. Deficits in olfactory identification and olfactory memory are consistent with the concept that schizophrenics have dysfunctional limbic systems.

Rapid, permanent, loss of memory for absolute intensity of taste and smell

Memory formation for the absolute intensity of taste and smell was investigated in a series of experiments. In Experiment 1, 336 subjects tasted 10 ml of 15% sucrose and were asked to remember the strength of the solution. They were retested with 5%, 10%, 15%, or 20% sucrose, at one of four delay intervals (1, 5, or 15 min, or 72 h). They compared the second stimulus with the first stimulus and reported whether the second was “less sweet, ” “the same, ” or “sweeter. ” Subjects reliably reported that 5% sucrose was less sweet and that 20% sucrose was sweeter. However, when the second stimulus was 15% sucrose (i.e., was equal to the standard), approximately 60% of the subjects reported that it was sweeter, regardless of the delay interval between the two stimuli. About 2/3 of those tasting 10% sucrose reported that it was as sweet as or sweeter than the 15% standard. A similar finding from a procedure using magnitude estimation was reported in Experiment 2. The same pattern of results was also found for an olfactory memory test (Experiment 3). When asked to match either a 1.33- or a 5.0-ppm pyridine olfactory stimulus, subjects consistently picked a concentration weaker than the standard. Apparently, olfactory and taste stimuli are remembered as being substantially weaker as soon as the memory for these stimuli can be tested. A memory model that posits a sensory store within which a taste or smell stimulus of a given intensity rapidly fades to a lower level of intensity is suggested. The new memory is then relatively unchanged for at least 3 days.