Showing papers on "Olfaction published in 2017"
TL;DR: Genetic and neurobiological data that reveal features unique to the human olfactory system are regularly misinterpreted to underlie the putative microsmaty, and the impact of human Olfactory dysfunction is underappreciated in medical practice.
Abstract: BACKGROUND It is widely believed that the human sense of smell is inferior to that of
other mammals, especially rodents and dogs. This Review traces the
scientific history of this idea to 19th-century neuroanatomist Paul Broca.
He classified humans as “nonsmellers” not owing to any sensory
testing but because he believed that the evolutionary enlargement of the
human frontal lobe gave human beings free will at the expense of the
olfactory system. He especially emphasized the small size of the human
brain’s olfactory bulb relative to the size of the brain overall, and
noted that other mammals have olfactory bulbs that are proportionately much
larger. Broca’s claim that humans have an impoverished olfactory
system (later labeled “microsmaty,” or tiny smell) influenced
Sigmund Freud, who argued that olfactory atrophy rendered humans susceptible
to mental illness. Humans’ supposed microsmaty led to the scientific
neglect of the human olfactory system for much of the 20th century, and even
today many biologists, anthropologists, and psychologists persist in the
erroneous belief that humans have a poor sense of smell. Genetic and
neurobiological data that reveal features unique to the human olfactory
system are regularly misinterpreted to underlie the putative microsmaty, and
the impact of human olfactory dysfunction is underappreciated in medical
practice. ADVANCES Although the human olfactory system has turned out to have some biological
differences from that of other mammalian species, it is generally similar in
its neurobiology and sensory capabilities. The human olfactory system has
fewer functional olfactory receptor genes than rodents, for instance, but
the human brain has more complex olfactory bulbs and orbitofrontal cortices
with which to interpret information from the roughly 400 receptor types that
are expressed. The olfactory bulb is proportionately smaller in humans than
in rodents, but is comparable in the number of neurons it contains and is
actually much larger in absolute terms. Thus, although the rest of the brain
became larger as humans evolved, the olfactory bulb did not become smaller.
When olfactory performance is compared experimentally between humans and
other animals, a key insight has been that the results are strongly
influenced by the selection of odors tested, presumably because different
odor receptors are expressed in each species. When an appropriate range of
odors is tested, humans outperform laboratory rodents and dogs in detecting
some odors while being less sensitive to other odors. Like other mammals,
humans can distinguish among an incredible number of odors and can even
follow outdoor scent trails. Human behaviors and affective states are also
strongly influenced by the olfactory environment, which can evoke strong
emotional and behavioral reactions as well as prompting distinct memories.
Odor-mediated communication between individuals, once thought to be limited
to “lower animals,” is now understood to carry information
about familial relationships, stress and anxiety levels, and reproductive
status in humans as well, although this information is not always
consciously accessible. OUTLOOK The human olfactory system is increasingly understood to be highly dynamic.
Olfactory sensitivity and discrimination abilities can be changed by
experiences like environmental odor exposure or even just learning to
associate odors with other stimuli in the laboratory. The neurobiological
underpinnings of this plasticity, including “bottom-up”
factors like regulation of peripheral odor receptors and
“top-down” factors like the sensory consequences of emotional
and cognitive states, are just beginning to be understood. The role of
olfactory communication in shaping social interactions is also actively
being explored, including the social spread of emotion through olfactory
cues. Finally, impaired olfaction can be a leading indicator of certain
neurodegenerative diseases, notably Parkinson’s disease and
Alzheimer’s disease. New experimentation will be required to
understand how olfactory sequelae might also reflect problems elsewhere in
the nervous system, including mental disorders with sensory symptomatology.
The idea that human smell is impoverished compared to other mammals is a
19th-century myth.
480 citations
TL;DR: Whether damage to such a substrate is the basis for the perceptual differences in olfaction or whether disease-specific or other entities, such as respiratory infections or pollution, are responsible might provide crucial insight into the cause of disease pathology at its earliest stages of development.
Abstract: Summary In patients with neurodegenerative diseases, there is a spectrum of smell dysfunction ranging from severe loss, as seen in Alzheimer's disease and Parkinson's disease, to relatively little loss, as seen in progressive supranuclear palsy. Given the ubiquitous but varying degrees of olfactory dysfunction among such diseases, it is conceivable that differential disruption of a common primordial neuropathological substrate causes these differences in olfactory function. For example, the amount of damage to forebrain neurotransmitter and neuromodulator circuits, most notably those involving cholinergic transmission, appears to be correlated with quantitative smell test scores across a wide range of neurodegenerative diseases. Thus, a key question is whether damage to such a substrate is the basis for the perceptual differences in olfaction or whether disease-specific or other entities, such as respiratory infections or pollution, are responsible. In light of the early preclinical onset of smell deficits in many neurodegenerative diseases, the answer to this question might provide crucial insight into the cause of disease pathology at its earliest stages of development.
325 citations
Rockefeller University1, Arizona State University2, University of Michigan3, IBM4, Semmelweis University5, Monell Chemical Senses Center6, University of Pennsylvania7, Ajinomoto8, SAS Institute9, Katholieke Universiteit Leuven10, University of Copenhagen Faculty of Science11, Icahn School of Medicine at Mount Sinai12, Howard Hughes Medical Institute13
TL;DR: Results of a crowdsourcing competition show that it is possible to accurately predict and reverse-engineer the smell of a molecule, with a predictive accuracy that closely approaches a key theoretical limit.
Abstract: It is still not possible to predict whether a given molecule will have a perceived odor or what olfactory percept it will produce. We therefore organized the crowd-sourced DREAM Olfaction Prediction Challenge. Using a large olfactory psychophysical data set, teams developed machine-learning algorithms to predict sensory attributes of molecules based on their chemoinformatic features. The resulting models accurately predicted odor intensity and pleasantness and also successfully predicted 8 among 19 rated semantic descriptors (“garlic,” “fish,” “sweet,” “fruit,” “burnt,” “spices,” “flower,” and “sour”). Regularized linear models performed nearly as well as random forest–based ones, with a predictive accuracy that closely approaches a key theoretical limit. These models help to predict the perceptual qualities of virtually any molecule with high accuracy and also reverse-engineer the smell of a molecule.
293 citations
TL;DR: The existing literature on olfactory function in Parkinson’s disease is summarized, focusing on the potential for olfaction as a biomarker for early or differential diagnosis and prognosis.
Abstract: Olfactory dysfunction is common in Parkinson’s disease (PD) and often predates the diagnosis by years, reflecting early deposition of Lewy pathology, the histologic hallmark of PD, in the olfactory bulb. Clinical tests are available that allow for the rapid characterization of olfactory dysfunction, including tests of odor identification, discrimination, detection, and recognition thresholds, memory, and tests assessing the build-up of odor intensity across increasing suprathreshold stimulus concentrations. The high prevalence of olfactory impairment, along with the ease and low cost of assessment, has fostered great interest in olfaction as a potential biomarker for PD. Hyposmia may help differentiate PD from other causes of parkinsonism, and may also aid in the identification of “pre-motor” PD due to the early pathologic involvement of olfactory pathways. Olfactory function is also correlated with other non-motor features of PD and may serve as a predictor of cognitive decline. In this article, we summarize the existing literature on olfaction in PD, focusing on the potential for olfaction as a biomarker for early or differential diagnosis and prognosis.
260 citations
TL;DR: A significant, positive effect of olfactory training is found for all Olfactory abilities, with large effects of training on identification, discrimination and TDI-score and small-to-moderate effect in the case of threshold for odor detection.
Abstract: The neural plasticity of the olfactory system offers possibilities of treatment in terms of stimulation of the sense of smell, and different studies have suggested effectiveness of smell training, i.e., daily exposition to certain odors. To obtain reliable and precise estimates of overall treatment benefit on the olfactory function, we meta-analyzed the effects of smell training reported in 13 previous studies. We analyzed the smell training effectiveness across three different olfactory abilities, smell identification, discrimination and threshold for odor detection. We found a significant, positive effect of olfactory training for all olfactory abilities, with large effects of training on identification, discrimination and TDI-score and small-to-moderate effect in the case of threshold for odor detection. Interestingly, the pattern of results differed across Sniffin Sticks subtests depending on the origin of participants smell disorder, and the smell training duration influenced its effectiveness in the case of identification and the TDI score. Although the exact mechanism of olfactory recovery following the smell training still requires further investigation, our meta-analysis showed that such training should be considered an addition or alternative to existing smell treatment methods.
215 citations
TL;DR: This work links olfactory ecology to structural and regulatory genetic changes influencing nervous system anatomy and function to show that D. sechellia exhibits derived odor-evoked attraction and physiological sensitivity to the abundant Morinda volatile hexanoic acid.
209 citations
TL;DR: It is suggested that olfaction and depression interact in two ways: first, olfactory function in depression is impaired as a consequence of reducedOlfactory attention and diminished olfatory receptor turnover rates; and second, the OB may constitute a marker for enhanced vulnerability to depression.
Abstract: Olfactory and emotional higher processing pathways share common anatomical substrates. Hence, depression is often accompanied by alterations in olfactory function. These alterations are negative in nature and may involve decreased activation in olfactory eloquent structures or decreased volume in the olfactory bulb (OB). We suggest that olfaction and depression interact in two ways. First, olfactory function in depression is impaired as a consequence of reduced olfactory attention and diminished olfactory receptor turnover rates. Second, the OB may constitute a marker for enhanced vulnerability to depression. Closer analysis of these interactions may help to explain observed experimental data, as well as to elucidate new therapeutic strategies involving olfaction. Because of the difficulties to disentangle cause from consequence in the relationship between olfaction and depression, longitudinal and intervention studies are necessary to elucidate this further.
201 citations
TL;DR: A primacy coding model is tested using an optogenetic masking paradigm in mice to show that a set of earliest activated receptors are sufficient to make decisions about odor identity across concentrations, and a computational model is proposed demonstrating how such a code can be read by neural circuits of the olfactory system.
Abstract: Humans can identify visual objects independently of view angle and lighting, words independently of volume and pitch, and smells independently of concentration. The computational principles underlying invariant object recognition remain mostly unknown. Here we propose that, in olfaction, a small and relatively stable set comprised of the earliest activated receptors forms a code for concentration-invariant odor identity. One prediction of this "primacy coding" scheme is that decisions based on odor identity can be made solely using early odor-evoked neural activity. Using an optogenetic masking paradigm, we define the sensory integration time necessary for odor identification and demonstrate that animals can use information occurring <100 ms after inhalation onset to identify odors. Using multi-electrode array recordings of odor responses in the olfactory bulb, we find that concentration-invariant units respond earliest and at latencies that are within this behaviorally-defined time window. We propose a computational model demonstrating how such a code can be read by neural circuits of the olfactory system.
186 citations
TL;DR: It is demonstrated that mice upon conditional ablation of mature olfactory sensory neurons (OSNs) are resistant to diet-induced obesity accompanied by increased thermogenesis in brown and inguinal fat depots, unraveling a new bidirectional function for the o aroma system in controlling energy homeostasis in response to sensory and hormonal signals.
174 citations
TL;DR: Calcium imaging is used to determine how odor identity is encoded in olfactory cortex and it is proposed that distinct perceptual features of odors are encoded in independent subnetworks of neurons in the o aroma cortex.
Abstract: Olfactory perception and behaviors critically depend on the ability to identify an odor across a wide range of concentrations. Here, we use calcium imaging to determine how odor identity is encoded in olfactory cortex. We find that, despite considerable trial-to-trial variability, odor identity can accurately be decoded from ensembles of co-active neurons that are distributed across piriform cortex without any apparent spatial organization. However, piriform response patterns change substantially over a 100-fold change in odor concentration, apparently degrading the population representation of odor identity. We show that this problem can be resolved by decoding odor identity from a subpopulation of concentration-invariant piriform neurons. These concentration-invariant neurons are overrepresented in piriform cortex but not in olfactory bulb mitral and tufted cells. We therefore propose that distinct perceptual features of odors are encoded in independent subnetworks of neurons in the olfactory cortex.
142 citations
TL;DR: This work aimed to determine whether the pattern of olfactory impairment seen in psychophysical testing reflects underlying disease etiology.
Abstract: Objective
We aimed to determine whether the pattern of olfactory impairment seen in psychophysical testing reflects underlying disease etiology.
Study Design
Retrospective cohort.
Methods
We performed a retrospective analysis of 1,226 patients from our tertiary referral center. Only hyposmic patients with the following conditions were included: postinfectious hyposmia, posttraumatic hyposmia, hyposmia secondary to sinonasal disease, and hyposmia secondary to Parkinson disease. Patients with anosmia were excluded.
Results
Using a repeated measures analysis of variance (within subject factor “test”: threshold [T], discrimination [D], identification [I]; between subject factor: “etiology”) with posthoc Bonferroni corrected t tests, we found significant interaction between the factors “test” and “etiology” (F6,2444 = 8.46, P < 0.001), indicating that different causes of hyposmia produce different patterns of olfactory loss with respect to the individual subtests T, D, and I . Specifically, patients with Parkinson disease performed relatively well in odor threshold testing, but poorly in odor identification and discrimination compared with the other etiology groups. Conversely, patients with sinonasal disease performed well in odor identification and discrimination but poorly in odor threshold. Patients with postinfectious and posttraumatic hyposmia performed relatively well in both thresholds and discrimination but poorly in identification. However, patients with posttraumatic hyposmia had globally reduced scores compared with the other groups.
Conclusion
This is the first study to comprehensively show that patterns of olfactory impairment reflect underlying disease etiology. We suggest that multicomponent olfactory testing should be performed, especially if there is diagnostic uncertainty. However, to clearly separate different patterns of olfactory loss to the various causes at an individual level, more work is needed.
Level of Evidence
4. Laryngoscope, 2016
TL;DR: A novel model in which multiple interneuron types with distinct abundances, connectivity patterns, and physiologies complement one another to regulate M/TC activity and sensory processing is yields a novel model.
Abstract: Synaptic inhibition critically influences sensory processing throughout the mammalian brain, including the main olfactory bulb (MOB), the first station of sensory processing in the olfactory system...
TL;DR: This review of sensory coding from the vinegar fly Drosophila melanogaster will outline the relevant steps of the olfactory code and describe its progress along the Olfactory pathway, i.e., from the peripheral ofactory organs to the first olf factory center in the brain and then to the higher processing areas where the odor perception takes place, enabling an organism to make odor-guided decisions.
Abstract: Sensory coding represents a basic principle of all phyla in nature: species attempt to perceive their natural surroundings and to make sense of them. Ultimately, sensory coding is the only way to allow a species to make the kinds of crucial decisions that lead to a behavioral response. In this manner, animals are able to detect numerous parameters, ranging from temperature and humidity to light and sound to volatile or non-volatile chemicals. Most of these environmental cues represent a clearly defined stimulus array that can be described along a single physical parameter, such as wavelength or frequency; odorants, in contrast, cannot. The odor space encompasses an enormous and nearly infinite number of diverse stimuli that cannot be classified according to their positions along a single dimension. Hence, the olfactory system has to encode and translate the vast odor array into an accurate neural map in the brain. In this review, we will outline the relevant steps of the olfactory code and describe its progress along the olfactory pathway, i.e., from the peripheral olfactory organs to the first olfactory center in the brain and then to the higher processing areas where the odor perception takes place, enabling an organism to make odor-guided decisions. We will focus mainly on studies from the vinegar fly Drosophila melanogaster, but we will also indicate similarities to and differences from the olfactory system of other invertebrate species as well as of the vertebrate world.
TL;DR: This non-systematic review provides an overview of olfactory habituation and adaptation in humans, and techniques that have been used to measure them.
2 May 2017
TL;DR: Essence, the first olfactory computational necklace that can be remotely controlled through a smartphone and can vary the intensity and frequency of the released scent based on biometric or contextual data is presented.
Abstract: The sense of smell is perhaps the most pervasive of all senses, but it is also one of the least understood and least exploited in HCI. We present Essence, the first olfactory computational necklace that can be remotely controlled through a smartphone and can vary the intensity and frequency of the released scent based on biometric or contextual data. This paper discusses the role of smell in designing pervasive systems that affect one's mood and cognitive performance while being asleep or awake. We present a set of applications for this type of technology as well as the implementation of the olfactory display and the supporting software. We also discuss the results of an initial test of the prototype that show the robustness and usability of Essence while wearing it for long periods of time in multiple environments.
TL;DR: A novel olfactory mechanism for ATP sensing in zebrafish is discovered, providing conclusive evidence for a sophisticated enzyme-linked receptor mechanism underlying detection of ATP as a food-derived attractive odorant linking to foraging behavior that is crucial and common to aquatic lower vertebrates.
TL;DR: The aims of this study were to use combined data to report the prevalence of olfactory dysfunction and to calculate weighted averages of Olfactory test scores in CRS patients.
Abstract: Objectives
Many studies have reported that olfactory dysfunction frequently occurs in chronic rhinosinusitis (CRS) populations; however, the prevalence and degree of olfactory loss has not been systematically studied. The aims of this study were to use combined data to report the prevalence of olfactory dysfunction and to calculate weighted averages of olfactory test scores in CRS patients.
Data Sources
A search was conducted in PubMed and Scopus, following the methods of Preferred Reporting Items for Systematic Review and Meta-Analysis guidelines.
Review Methods
Studies reporting the prevalence of olfactory dysfunction using objective measures or olfactory test scores using validated scales were included.
Results
A total of 47 articles were included in a systematic review and 35 in the pooled data analysis. The prevalence of olfactory dysfunction in chronic rhinosinusitis was found to be 30.0% using the Brief Smell Identification Test, 67.0% using the 40-item Smell Identification Test, and 78.2% using the total Sniffin' Sticks score. Weighted averages ± standard deviation of olfactory test scores were 25.96 ± 7.11 using the 40-item Smell Identification Test, 8.60 ± 2.81 using the Brief Smell Identification Test, 21.96 ± 8.88 using total Sniffin' Sticks score, 5.65 ± 1.51 using Sniffin' Sticks–Threshold, 9.21 ± 4.63 using Sniffin' Sticks–Discrimination, 9.47 ± 3.92 using Sniffin' Sticks–Identification, and 8.90 ± 5.14 using the Questionnaire for Olfactory Disorders–Negative Statements.
Conclusions
In CRS populations, a significant percentage of patients experience olfactory dysfunction, and mean olfactory scores are within the dysosmic range.
Laryngoscope, 2016 127:309–320, 2017
TL;DR: The results reveal that the unpleasant odour had a statistically significant effect on the sense of Presence (as measured by repeated brief measures of Presence and the Independent Television Commission Sense of Presence Inventory), but the pleasant one did not.
Abstract: While olfactory cues affect the everyday human experience in the physical world, few studies have empirically examined the effect they could have on the human experience in virtual reality (VR). This project's goal was to determine whether the exposure to olfactory stimuli would affect the senses of Presence (primary measure), Reality and Realism (exploratory measures) in VR. In a virtual kitchen devoid of obvious visual cues linking the visual scene to an odour, three groups of 20 randomly assigned participants (12 females and 8 males per group), unaware of the potential exposure to olfactory stimuli, were exposed to either ambient air, a pleasant odour, or an unpleasant odour. The results reveal that the unpleasant odour had a statistically significant effect on the sense of Presence (as measured by repeated brief measures of Presence and the Independent Television Commission Sense of Presence Inventory), but the pleasant one did not. The lower perceived intensity of the pleasant odour may have contributed to its lower detection rate which, in turn, may have contributed to the pleasant odour's lack of effect on the sense of Presence. Neither of the olfactory stimuli had an effect on either the sense of Reality or the sense of Realism.
TL;DR: It is shown that brain regions mediating odor-driven innate behaviors can, like brain areas involved in odor learning, represent odor objects using distributive population codes; these findings suggest both alternative mechanisms for the generation of innate odor- driven behaviors and additional roles for the plCoA in odor perception.
TL;DR: An olfactory channel is discovered in D. melanogaster with a dual affinity to sex and food odorants and the underlying gene yields a collaboration between natural and sexual selection, which has the potential to drive speciation.
Abstract: Mate finding and recognition in animals evolves during niche adaptation and involves social signals and habitat cues. Drosophila melanogaster and related species are known to be attracted to fermenting fruit for feeding and egg-laying, which poses the question of whether species-specific fly odours contribute to long-range premating communication. We have discovered an olfactory channel in D. melanogaster with a dual affinity to sex and food odorants. Female flies release a pheromone, (Z)-4-undecenal (Z4-11Al), that elicits flight attraction in both sexes. Its biosynthetic precursor is the cuticular hydrocarbon (Z,Z)-7,11-heptacosadiene (7,11-HD), which is known to afford reproductive isolation between the sibling species D. melanogaster and D. simulans during courtship. Twin olfactory receptors, Or69aB and Or69aA, are tuned to Z4-11Al and food odorants, respectively. They are co-expressed in the same olfactory sensory neurons, and feed into a neural circuit mediating species-specific, long-range communication; however, the close relative D. simulans, which shares food resources with D. melanogaster, does not respond to Z4-11Al. The Or69aA and Or69aB isoforms have adopted dual olfactory traits. The underlying gene yields a collaboration between natural and sexual selection, which has the potential to drive speciation.
TL;DR: Intranasal vitamin A at a dose of 10,000 IU per day for 2 months may be useful in the treatment of post-infectious olfactory loss and further work with prospective, placebo-controlled studies is required to confirm these findings.
Abstract: Vitamin A plays a decisive role in the regeneration of olfactory receptor neurons. In this retrospective study we investigated the effectiveness of topical vitamin A in patients with post-infectious and posttraumatic smell disorders. Retrospective cohort. A total of 170 patients (age range 18–70 years, mean age 52 years) participated. Forty-six patients were treated with smell training only. The remaining 124 patients received smell training and topical vitamin A. Olfactory function was assessed using the Sniffin’ Sticks test kit, a validated technique to measure odor thresholds, discrimination and identification. The duration of olfactory training was 12 weeks. In patients receiving vitamin A, this was applied topically (head back position) at a dose of 10,000 IU/day for 8 weeks. Follow-up testing was performed approximately 10 months after the first assessment. Thirty-seven per cent of all post-infectious patients treated with vitamin A exhibited clinical improvement, whereas only 23% improved in controls. Using a Chi-square test, this was a significant result (χ
2 = 7.06, df = 2, p = 0.03). In addition, when comparing change in score after treatment, olfactory training + vitamin A produced significantly greater improvement compared with training alone, in discrimination score for all patients (1.4 points, p = 0.008), and in threshold and discrimination in the post-infectious group (1.6 points, p = 0.01 and 1.4 points, p = 0.04, respectively). Intranasal vitamin A at a dose of 10,000 IU per day for 2 months may be useful in the treatment of post-infectious olfactory loss. Further work with prospective, placebo-controlled studies is required to confirm these findings.
TL;DR: The deletion of BmOrco gene in the Lepidopteran model insect, Bombyx mori, using a binary transgene-based clustered regulatory interspaced short palindromic repeats (CRISPR)/Cas9 system provides insights into the insect olfactory system and provides a paradigm for agroforestry pest control.
TL;DR: Data show for the first time in humans that olfactory training may involve top-down process, which ultimately lead to a bilateral increase in Olfactory bulb volume.
Abstract: Repeated exposure to odors modifies olfactory function. Consequently, "olfactory training" plays a significant role in hyposmia treatment. In addition, numerous studies show that the olfactory bulb (OB) volume changes in disorders associated with olfactory dysfunction. Aim of this study was to investigate whether and how olfactory bulb volume changes in relation to lateralized olfactory training in healthy people. Over a period of 4 months, 97 healthy participants (63 females and 34 males, mean age: 23.74 ± 4.16 years, age range: 19-43 years) performed olfactory training by exposing the same nostril twice a day to 4 odors (lemon, rose, eucalyptus and cloves) while closing the other nostril. Before and after olfactory training, magnetic resonance imaging (MRI) scans were performed to measure OB volume. Furthermore, participants underwent lateralized odor threshold and odor identification testing using the "Sniffin' Sticks" test battery.OB volume increased significantly after olfactory training (11.3 % and 13.1 % respectively) for both trained and untrained nostril. No significant effects of sex, duration and frequency of training or age of the subjects were seen. Interestingly, PEA odor thresholds worsened after training, while olfactory identification remained unchanged.These data show for the first time in humans that olfactory training may involve top-down process, which ultimately lead to a bilateral increase in olfactory bulb volume.
TL;DR: It is found that the VTA (DAergic)-mOT pathway could be activated by different types of naturalistic rewards as well as odors in DAT-cre mice and mediates a variety of preferences including odor-preference in mice.
Abstract: Odor-preferences are usually influenced by life experiences. However, the neural circuit mechanisms remain unclear. The medial olfactory tubercle (mOT) is involved in both reward and olfaction, whereas the ventral tegmental area (VTA) dopaminergic (DAergic) neurons are considered to be engaged in reward and motivation. Here, we found that the VTA (DAergic)-mOT pathway could be activated by different types of naturalistic rewards as well as odors in DAT-cre mice. Optogenetic activation of the VTA-mOT DAergic fibers was able to elicit preferences for space, location and neutral odor, while pharmacological blockade of the dopamine receptors in the mOT fully prevented the odor-preference formation. Furthermore, inactivation of the mOT-projecting VTA DAergic neurons eliminated the previously formed odor-preference and strongly affected the Go-no go learning efficiency. In summary, our results revealed that the VTA (DAergic)-mOT pathway mediates a variety of naturalistic reward processes and different types of preferences including odor-preference in mice.
TL;DR: This review summarizes the locations and release of vesicular zinc in the central nervous system (CNS), including in the OB, and summarizes the effects of zinc on various amino acid receptors and ion channels involved in regulating synaptic transmission and neuronal excitability.
Abstract: The olfactory bulb (OB) is central to the sense of smell, as it is the site of the first synaptic relay involved in the processing of odor information. Odor sensations are first transduced by olfactory sensory neurons before being transmitted, by way of the OB, to higher olfactory centers that mediate olfactory discrimination and perception. Zinc is a common trace element, and it is highly concentrated in the synaptic vesicles of subsets of glutamatergic neurons in some brain regions including the hippocampus and OB. In addition, zinc is contained in the synaptic vesicles of some glycinergic and GABAergic neurons. Thus, zinc released from synaptic vesicles is available to modulate synaptic transmission mediated by excitatory (e.g., NMDA, AMPA) and inhibitory (e.g., GABA, glycine) amino acid receptors. Furthermore, extracellular zinc can alter the excitability of neurons through effects on a variety of voltage-gated ion channels. Consistent with the notion that zinc acts as a regulator of neuronal activity, we and others have shown zinc modulation (inhibition and/or potentiation) of amino acid receptors and voltage-gated ion channels expressed by OB neurons. This review summarizes the locations and release of vesicular zinc in the central nervous system, including in the OB. It also summarizes the effects of zinc on various amino acid receptors and ion channels involved in regulating synaptic transmission and neuronal excitability, with a special emphasis on the actions of zinc as a neuromodulator in the OB. An understanding of how neuroactive substances such as zinc modulate receptors and ion channels expressed by OB neurons will increase our understanding of the roles that synaptic circuits in the OB play in odor information processing and transmission.
TL;DR: A possible solution that could eliminate the lack of clarity and reduce variation would be to adhere to a single, thorough methodology that examines and separates central and peripheral olfactory processing.
Abstract: Background. Research has demonstrated a reduction in olfactory functioning in patients with schizophrenia. This research has led to examination of olfactory functioning in other mental disorders, such as depression. There is a great deal of variation in the results generated from such research and it remains unclear as to how olfactory functioning is associated with or impacted by depression. Method. The current review examined the literature in accordance with PRISMA guidelines in order to generate a better understanding of this relationship and to identify if and what aspects of olfactory processing are altered. Through examination of the available literature from the databases PubMed, Ovid Medline, CINAL, and PsychINFO, fifteen manuscripts were selected to determine if there was a difference in olfactory processing - specifically central and peripheral processing – between depressed individuals and non-depressed controls. Results. The comparison of the fifteen studies showed that the majority of studies (9/15, 60%) found a difference in overall olfactory functioning between depressed individuals and non-depressed controls (p <0.05). Limitations. There is still a lack of definitive conclusions due to variation of which olfactory process was altered. Conclusions. Given the differences in the methodology and design of these studies, a possible solution that could eliminate the lack of clarity and reduce variation would be to adhere to a single, thorough methodology that examines and separates central and peripheral olfactory processing. Future research employing a uniform and validated methodology could provide more definitive conclusions as to how and if olfactory functioning is related depression.
TL;DR: The no-odor condition, allowing investigation of activation patterns when the peripheral olfactory system was not directly involved, elicited the same functional response as the odor condition for each of the three groups, indicating that the olfFactory activation deficits present in AD and MCI patients are most likely caused by degeneration of the central Olfactory nervous system.
Abstract: BACKGROUND Olfactory deficits are present in early Alzheimer's disease (AD) and mild cognitively impaired (MCI) patients. However, whether these deficits are due to dysfunction of the central or peripheral olfactory nervous system remains uncertain. This question is fundamentally important for developing imaging biomarkers for AD using olfactory testing. OBJECTIVE This study sought to use olfactory functional magnetic resonance imaging (fMRI) to further demonstrate the involvement of the central olfactory system in olfactory deficits in MCI and AD. METHODS We investigated the central olfactory system in 27 cognitively normal controls (CN), 21 MCI, and 15 AD subjects using olfactory fMRI with an odor-visual association paradigm during which a visual cue was paired with lavender odorant (odor condition) or odorless air (no-odor condition). RESULTS The CN subjects had significantly greater activated volume in the primary olfactory cortex during both the odor and no-odor conditions compared to either the MCI or AD groups (p < 0.05). No significant differences were observed between the odor and no-odor conditions within each group. No-odor condition activation in AD and MCI correlated with the cognitive and olfactory assessments. CONCLUSION The no-odor condition, allowing investigation of activation patterns when the peripheral olfactory system was not directly involved, elicited the same functional response as the odor condition for each of the three groups. Thus, the olfactory activation deficits present in AD and MCI patients are most likely caused by degeneration of the central olfactory nervous system.
TL;DR: Rather than highlighting the weaknesses of olfaction, this review presents a positive perspective by focusing on factors that make someone a better smeller by considering three driving forces in improving olfactory ability: one's biological makeup, one’s experience, and the environment.
Abstract: Olfaction is often viewed as difficult, yet the empirical evidence suggests a different picture. A closer look shows people around the world differ in their ability to detect, discriminate, and name odors. This gives rise to the question of what influences our ability to smell. Instead of focusing on olfactory deficiencies, this review presents a positive perspective by focusing on factors that make someone a better smeller. We consider three driving forces in improving olfactory ability: one's biological makeup, one's experience, and the environment. For each factor, we consider aspects proposed to improve odor perception and critically examine the evidence; as well as introducing lesser discussed areas. In terms of biology, there are cases of neurodiversity, such as olfactory synesthesia, that serve to enhance olfactory ability. Our lifetime experience, be it typical development or unique training experience, can also modify the trajectory of olfaction. Finally, our odor environment, in terms of ambient odor or culinary traditions, can influence odor perception too. Rather than highlighting the weaknesses of olfaction, we emphasize routes to harnessing our olfactory potential.
TL;DR: This study relied on multielectrode recordings to investigate how single GC neurons respond to intraorally delivered tastants and tasteless odorants dissolved in water and whether/how these two modalities converge in the same neurons and found that neurons in gustatory cortex can respond either exclusively to taste, exclusively to odorants, or to both (bimodal).
Abstract: The integration of gustatory and olfactory information is essential to the perception of flavor. Human neuroimaging experiments have pointed to the gustatory cortex (GC) as one of the areas involved in mediating flavor perception. Although GC9s involvement in encoding the chemical identity and hedonic value of taste stimuli is well studied, it is unknown how single GC neurons process olfactory stimuli emanating from the mouth. In this study, we relied on multielectrode recordings to investigate how single GC neurons respond to intraorally delivered tastants and tasteless odorants dissolved in water and whether/how these two modalities converge in the same neurons. We found that GC neurons could either be unimodal, responding exclusively to taste (taste-only) or odor (odor-only), or bimodal, responding to both gustatory and olfactory stimuli. Odor responses were confirmed to result from retronasal olfaction: monitoring respiration revealed that exhalation preceded odor-evoked activity and reversible inactivation of olfactory receptors in the nasal epithelium significantly reduced responses to intraoral odorants but not to tastants. Analysis of bimodal neurons revealed that they encode palatability significantly better than the unimodal taste-only group. Bimodal neurons exhibited similar responses to palatable tastants and odorants dissolved in water. This result suggested that odorized water could be palatable. This interpretation was further supported with a brief access task, where rats avoided consuming aversive taste stimuli and consumed the palatable tastants and dissolved odorants. These results demonstrate the convergence of the chemosensory components of flavor onto single GC neurons and provide evidence for the integration of flavor with palatability coding. SIGNIFICANCE STATEMENT Food perception and choice depend upon the concurrent processing of olfactory and gustatory signals from the mouth. The primary gustatory cortex has been proposed to integrate chemosensory stimuli; however, no study has examined the single-unit responses to intraoral odorant presentation. Here we found that neurons in gustatory cortex can respond either exclusively to tastants, exclusively to odorants, or to both (bimodal). Several differences exist between these groups9 responses; notably, bimodal neurons code palatability significantly better than unimodal neurons. This group of neurons might represent a substrate for how odorants gain the quality of tastants.
TL;DR: An analysis of data obtained by a systematic literature review regarding the possible association between olfaction and ASDs suggested a possible involvement of olfactory impairment in ASDs, underlining the importance of Olfactory evaluation in the clinical assessment of ASDs.
Abstract: Olfactory function is a well-known early biomarker for neurodegeneration and neural functioning in the adult population, being supported by a number of brain structures that could be dysfunctioning in neurodegenerative processes. Evidence has suggested that atypical sensory and, particularly, olfactory processing is present in several neurodevelopmental conditions, including autism spectrum disorders (ASDs). In this paper, we present data obtained by a systematic literature review, conducted according to PRISMA guidelines, regarding the possible association between olfaction and ASDs, and analyze them critically in order to evaluate the occurrence of olfactory impairment in ASDs, as well as the possible usefulness of olfactory evaluation in such conditions. The results obtained in this analysis suggested a possible involvement of olfactory impairment in ASDs, underlining the importance of olfactory evaluation in the clinical assessment of ASDs. This assessment could be potentially included as a complementary evaluation in the diagnostic protocol of the condition. Methods for study selection and inclusion criteria were specified in advance and documented in PROSPERO protocol #CRD42014013939.