A tyramine receptor gene mutation causes a defective olfactory behavior in Drosophila melanogaster

Kutsukake, Mayako; Komatsu, Akira; Yamamoto, Daisuke; Ishiwa-Chigusa, Sadao

doi:10.1016/s0378-1119(99)00569-7

Cited by 134 publications

(138 citation statements)

References 31 publications

Supporting

Mentioning

129

Contrasting

Order By: Relevance

“…In mammals, the physiological roles for trace amines such as TA and OA are mostly unknown, but they have been implicated in a variety of neurological disorders (Branchek and Blackburn, 2003), and receptors specific for TA have been identified (Borowsky et al, 2001). In invertebrates, a role of endogenous TA as an important transmitter/modulator has been shown for Drosophila locomotor (Saraswati et al, 2004; this study) and olfactory avoidance (Kutsukake et al, 2000) behavior, as well as for C. elegans motor behavior (Alkema et al, 2005).…”

Section: Ta As Neurotransmitter/modulatormentioning

confidence: 79%

“…Furthermore, OA and TA receptor distributions in the insect CNS differ considerably from each other [J. Erber (Technical University Berlin, Berlin, Germany), personal communication]. Functionally, exogenous TA increases chloride conductances in Drosophila malphigian tubules (Blumenthal, 2003), alters body wall muscle excitatory junction potentials (Kutsukake et al, 2000), and can rescue cocaine sensitization in Drosophila (McClung and Hirsh, 1999). In mammals, the physiological roles for trace amines such as TA and OA are mostly unknown, but they have been implicated in a variety of neurological disorders (Branchek and Blackburn, 2003), and receptors specific for TA have been identified (Borowsky et al, 2001).…”

Section: Ta As Neurotransmitter/modulatormentioning

confidence: 99%

See 1 more Smart Citation

Flight Initiation and Maintenance Deficits in Flies with Genetically Altered Biogenic Amine Levels

Brembs

Christiansen²,

Pflüger³

et al. 2007

J. Neurosci.

145

147

View full text Add to dashboard Cite

Insect flight is one of the fastest, most intense and most energy-demanding motor behaviors. It is modulated on multiple levels by the biogenic amine octopamine. Within the CNS, octopamine acts directly on the flight central pattern generator, and it affects motivational states. In the periphery, octopamine sensitizes sensory receptors, alters muscle contraction kinetics, and enhances flight muscle glycolysis. This study addresses the roles for octopamine and its precursor tyramine in flight behavior by genetic and pharmacological manipulation in Drosophila. Octopamine is not the natural signal for flight initiation because flies lacking octopamine [tyramine-␤-hydroxylase (T␤H) null mutants] can fly. However, they show profound differences with respect to flight initiation and flight maintenance compared with wild-type controls. The morphology, kinematics, and development of the flight machinery are not impaired in T␤H mutants because wing-beat frequencies and amplitudes, flight muscle structure, and overall dendritic structure of flight motoneurons are unaffected in T␤H mutants. Accordingly, the flight behavior phenotypes can be rescued acutely in adult flies. Flight deficits are rescued by substituting octopamine but also by blocking the receptors for tyramine, which is enriched in T␤H mutants. Conversely, ablating all neurons containing octopamine or tyramine phenocopies T␤H mutants. Therefore, both octopamine and tyramine systems are simultaneously involved in regulating flight initiation and maintenance. Different sets of rescue experiments indicate different sites of action for both amines. These findings are consistent with a complex system of multiple amines orchestrating the control of motor behaviors on multiple levels rather than single amines eliciting single behaviors.

show abstract

Section: Ta As Neurotransmitter/modulatormentioning

confidence: 79%

Section: Ta As Neurotransmitter/modulatormentioning

confidence: 99%

Flight Initiation and Maintenance Deficits in Flies with Genetically Altered Biogenic Amine Levels

Brembs

Christiansen²,

Pflüger³

et al. 2007

J. Neurosci.

145

147

View full text Add to dashboard Cite

show abstract

“…The few available studies suggest that tyramine is involved in honey bee motor behavior (Fussnecker et al, 2006). In addition, the tyramine receptor mutant honoka displayed reduced olfactory sensitivity (Kutsukake et al, 2000). In honey bee foragers, tyramine increases sensitivity for sucrose (Scheiner et al, 2002) and increases the rate of habituation (Braun and Bicker, 1992).…”

Section: Introductionmentioning

confidence: 99%

Octopamine improves learning in newly emerged bees but not in old foragers

Behrends

Scheiner

2012

Journal of Experimental Biology

View full text Add to dashboard Cite

SUMMARYHoney bees (Apis mellifera) are well known for their excellent learning abilities. Although most age groups learn quickly to associate an odor with a sucrose reward, newly emerged bees and old foragers often perform poorly. For a long time, the reason for the poor learning performance of these age groups was unclear. We show that reduced sensitivity for sucrose is the cause for poor associative learning in newly emerged bees but not in old foragers. By increasing the sensitivity for sucrose through octopamine, we selectively improved the learning performance of insensitive newly emerged bees. Interestingly, the learning performance of foragers experiencing the same treatment remained low, despite the observed increase in sensitivity for the reward. We thus demonstrate that increasing sensitivity for the reward can improve the associative learning performance of bees when they are young but not when they had foraged for a long time. Importantly, octopamine can have very different effects on bees, depending on their initial sensory sensitivity. These differential effects of octopamine have important consequences for interpreting the action of biogenic amines on insect behavior.

show abstract

“…Several studies have previously shown that OA and TA act antagonistically on muscle contraction, resulting in reduced locomotion in larvae lacking OA, whereas hypomorphic TA receptor mutants show longer track distances (Kutsukake et al 2000;Nagaya et al 2002;Saraswati et al 2004;. A small set of 40 OA/TA neurons within the ventral nerve cord is necessary to control normal locomotor activity in the larva .…”

mentioning

confidence: 99%

Potency of Transgenic Effectors for Neurogenetic Manipulation inDrosophilaLarvae

et al. 2014

View full text Add to dashboard Cite

Genetic manipulations of neuronal activity are a cornerstone of studies aimed to identify the functional impact of defined neurons for animal behavior. With its small nervous system, rapid life cycle, and genetic amenability, the fruit fly Drosophila melanogaster provides an attractive model system to study neuronal circuit function. In the past two decades, a large repertoire of elegant genetic tools has been developed to manipulate and study neural circuits in the fruit fly. Current techniques allow genetic ablation, constitutive silencing, or hyperactivation of neuronal activity and also include conditional thermogenetic or optogenetic activation or inhibition. As for all genetic techniques, the choice of the proper transgenic tool is essential for behavioral studies. Potency and impact of effectors may vary in distinct neuron types or distinct types of behavior. We here systematically test genetic effectors for their potency to alter the behavior of Drosophila larvae, using two distinct behavioral paradigms: general locomotor activity and directed, visually guided navigation. Our results show largely similar but not equal effects with different effector lines in both assays. Interestingly, differences in the magnitude of induced behavioral alterations between different effector lines remain largely consistent between the two behavioral assays. The observed potencies of the effector lines in aminergic and cholinergic neurons assessed here may help researchers to choose the best-suited genetic tools to dissect neuronal networks underlying the behavior of larval fruit flies.

show abstract

A tyramine receptor gene mutation causes a defective olfactory behavior in Drosophila melanogaster

Cited by 134 publications

References 31 publications

Flight Initiation and Maintenance Deficits in Flies with Genetically Altered Biogenic Amine Levels

Flight Initiation and Maintenance Deficits in Flies with Genetically Altered Biogenic Amine Levels

Octopamine improves learning in newly emerged bees but not in old foragers

Potency of Transgenic Effectors for Neurogenetic Manipulation inDrosophilaLarvae

Contact Info

Product

Resources

About