Serotonin mediates a learned increase in attraction to high concentrations of benzaldehyde in aged <i>C. elegans</i>

Tsui, David Chun Cheong; Kooy, Derek van der

doi:10.1101/lm.1188208

Cited by 21 publications

(21 citation statements)

References 41 publications

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“…Diacetyl is normally one such chemoattractant, but Morrison et al (1999) showed that worms could learn to avoid it if it was previously presented with an aversive acetic acid solution. Conversely, Torayama et al (2007) found that C. elegans became more attracted to butanone after pre-exposure to it in the presence of food, and Tsui and van der Kooy (2008) proposed that older worms displayed enhanced chemotaxis to benzaldehyde because of increased exposure to the pairing of volatile metabolites with the presence of an appetitive bacterial food source. Interestingly, increased attraction to benzaldehyde in aged worms was mediated by serotonin (Tsui and van der Kooy 2008) while butanone enhancement was not (Torayama et al 2007), suggesting that there are multiple mechanisms for sensory integration.…”

Section: Smell As the Conditioned Stimulusmentioning

confidence: 99%

“…Conversely, Torayama et al (2007) found that C. elegans became more attracted to butanone after pre-exposure to it in the presence of food, and Tsui and van der Kooy (2008) proposed that older worms displayed enhanced chemotaxis to benzaldehyde because of increased exposure to the pairing of volatile metabolites with the presence of an appetitive bacterial food source. Interestingly, increased attraction to benzaldehyde in aged worms was mediated by serotonin (Tsui and van der Kooy 2008) while butanone enhancement was not (Torayama et al 2007), suggesting that there are multiple mechanisms for sensory integration. Zhang et al (2005) demonstrated that worms could learn to avoid odors associated with pathogenic bacteria, preferring those associated with familiar nonpathogenic strains.…”

Section: Smell As the Conditioned Stimulusmentioning

confidence: 99%

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An elegant mind: Learning and memory in Caenorhabditis elegans

Ardiel¹,

Rankin²

2010

Learn. Mem.

276

191

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This article reviews the literature on learning and memory in the soil-dwelling nematode Caenorhabditis elegans. Paradigms include nonassociative learning, associative learning, and imprinting, as worms have been shown to habituate to mechanical and chemical stimuli, as well as learn the smells, tastes, temperatures, and oxygen levels that predict aversive chemicals or the presence or absence of food. In each case, the neural circuit underlying the behavior has been at least partially described, and forward and reverse genetics are being used to elucidate the underlying cellular and molecular mechanisms. Several genes have been identified with no known role other than mediating behavior plasticity.Historically, it was believed that even if they were capable of learning, the nervous systems of invertebrates were too different to be instructive on human cognition. In the 1960s, Kandel and colleagues began studying learning in the marine mollusc Aplysia (Kandel and Tauc 1965). Using this system, they were able to relate behavioral plasticity to changes at specific synapses of identified neurons, and began a biochemical analysis of these neuronal changes, uncovering a role for cAMP, PKA, and CREB. In the 1970s, Benzer and colleagues began a genetic dissection of learning in the fruit fly Drosophila melanogaster (Quinn et al. 1974;Dudai et al. 1976). They established an associative learning assay (Quinn et al. 1974) and conducted a forward genetic screen, identifying the first learning mutant, dunce (Dudai et al. 1976). Since then, many genes have been cloned, and the biological basis of learning has proven to be highly conserved (Barco et al. 2006;Skoulakis and Grammenoudi 2006). Today there is no question as to the relevance of invertebrate research in the field of learning and memory.At about the same time that Kandel was beginning his work with Aplysia, Sydney Brenner chose Caenorhabditis elegans as the organism in which to study development and the nervous system (Brenner 1974). Today this transparent nematode is the world's best understood animal. It's small size ( 1 mm), short life cycle (,3 d), and ease of cultivation make it perfect for the laboratory, and its mode of reproduction is ideal for genetic analysis-selffertilizing hermaphrodites can be easily inbred or crossed with males. The genome has been mapped and sequenced, and there are thousands of mutants and RNAi constructs readily available for researchers. Furthermore, C. elegans has an invariant cell lineage and relatively simple morphology-959 cells make up the entire adult hermaphrodite (Sulston and Horvitz 1977;Sulston et al. 1983). Using serial section electron micrographs, White et al. (1986) were able to construct a neural wiring diagram of the hermaphrodite's 302 neurons. They found about 5000 chemical synapses, 600 gap junctions, and 2000 neuromuscular junctions, the location of which were fairly consistent between animals. With its invariant cell lineage and reproducible connectome, C. elegans was initially viewed as a genetically hardwired ...

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Section: Smell As the Conditioned Stimulusmentioning

confidence: 99%

Section: Smell As the Conditioned Stimulusmentioning

confidence: 99%

An elegant mind: Learning and memory in Caenorhabditis elegans

Ardiel¹,

Rankin²

2010

Learn. Mem.

276

191

View full text Add to dashboard Cite

show abstract

“…4a), indicating that other Gα probably works in sensing undiluted isoamyl alcohol and driving attractive behaviour. ODR-3 is also known to mediate attraction to various odorants such as benzaldehyde and diacetyl at lower concentrations 20 , and initial attraction to but not subsequent avoidance of undiluted benzaldehyde 21 . In contrast to isoamyl alcohol, ODR-3 is not involved in avoidance of higher concentrations of benzaldehyde or diacetyl, as previously reported 14 (Fig.…”

Section: A Gα Odr-3 Mediates Bidirectional Behavioural Responsesmentioning

confidence: 99%

“…These results indicate that AWC and AWA are not involved in the response to higher concentrations of isoamyl alcohol. To determine which sensory neurons mediate avoidance of isoamyl alcohol, we examined the involvement of AWB and ADL neurons which were previously reported to be required for avoidance of repellents and higher concentrations of benzaldehyde 9,10,12,21,22 . AWB-ablated animals showed defects in avoidance of isoamyl alcohol at a higher concentration (Fig.…”

Section: A Gα Odr-3 Mediates Bidirectional Behavioural Responsesmentioning

confidence: 99%

Odour concentration-dependent olfactory preference change in C. elegans

et al. 2012

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“…elegans is controlled by serotonin signaling, making it a suitable indicator of proper serotonin signaling [501]. MICA has no affinity for serotonin receptors [502] and has no effect on serotonin sensitivity in no-Aβ controls.…”

Section: Discussionmentioning

confidence: 99%

Metabolic study of Alzheimer’s disease using mutant C. elegans

Ahmad¹

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Alzheimer's disease (AD) is associated with chronic neurodegeneration and is the cause of the most common form of dementia. The main hallmarks of AD are aggregates of amyloid beta (Aβ) and formation of hyperphosphorylated tau neurofibrillary tangles (NFTs). Unfortunately, after more than 100 years of research the exact cause(s) and mechanisms involved in AD progression remain unclarified. Evidence indicates that impaired mitochondrial bioenergetics may precede by decades, the neurodegeneration and cognitive decline associated with AD. Moreover, a genetic association of the core metabolic enzyme dihydrolipoamide dehydrogenase (DLD) with late-onset AD and reduced activity of DLD-containing enzymes suggests glucose hypo-metabolism as a possible cause of AD. Contrary to this, improvements of AD symptoms under caloric restriction or other means of reducing-glucose dependent energy metabolism supports an alternative hypothesis that a decrease in glucose metabolism may be protective. In the present study, we used mutant Caenorhabditis elegans (C. elegans) to investigate the effect of glucose metabolism on AD progression. We initially looked at the role of suppressed DLD-1, and then we focused on the effect of high glucose in AD pathogenesis.Transgenic expression of Aβ in C. elegans causes both phenotypic and behavioral defects and results in accumulation of toxic Aβ oligomers, culminating in protein aggregation as is normally associated with AD pathophysiology. Aβ expression in worm muscle causes agedependent progressive paralysis and impaired acetylcholine neurotransmission while neuronal Aβ expression results in defective chemotaxis and impaired serotonin sensitivity as well as reduced fecundity and egg hatching. Suppression of the dld-1 gene alleviated paralysis, improved acetylcholine neurotransmission, enhanced chemotaxis and restored normal sensitivity to serotonin.dld-1 gene suppression also protects vitality as indicated by improved fecundity and egg hatching.Interestingly, protective effects of dld-1 suppression could be reversed using the calcium ionophore (CaI), indicating that the protective mechanism involves calcium signaling. Each of these beneficial effects of dld-1 gene suppression could be mimicked using a specific, small molecule inhibitor of the DLD-1 enzyme, 5-methoxyindole-2-carboxylic acid (MICA).High glucose levels are associated with the metabolic disorder, diabetes, which is a major risk factor for AD. In fact, it has been suggested that AD is a neural form of diabetes, type 3 diabetes. If true, drugs used to treat diabetes could act as possible treatments for AD. In this study, I investigated the effect of elevated glucose, the glucose metabolism inhibitor, 2-deoxy-d-glucose ii (2DOG) as well as the anti-diabetes drugs, metformin and 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR), on AD progression. Elevated glucose in the growth medium induced hyperactivity, which interfered with the paralysis assays, but it was seen to impair cholinergic neurotransmission, egg laying and hatc...

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Serotonin mediates a learned increase in attraction to high concentrations of benzaldehyde in aged C. elegans

Cited by 21 publications

References 41 publications

An elegant mind: Learning and memory in Caenorhabditis elegans

An elegant mind: Learning and memory in Caenorhabditis elegans

Odour concentration-dependent olfactory preference change in C. elegans

Metabolic study of Alzheimer’s disease using mutant C. elegans

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