On the Role of the Protocerebral Bridge in the Central Complex of Drosophila melanogaster Brain in Control of Courtship Behavior and Sound Production

2003 ◽  
Vol 39 (6) ◽  
pp. 655-666 ◽  
Author(s):  
A. V. Popov ◽  
A. I. Peresleni ◽  
P. V. Ozerskii ◽  
E. E. Shchekanov ◽  
E. V. Savvateeva-Popova
Keyword(s):  
Drosophila Melanogaster ◽  
Sound Production ◽  
Courtship Behavior ◽  
Central Complex ◽  
Protocerebral Bridge

scholarly journals Protocerebral bridge neurons that regulate sleep in Drosophila melanogaster

2020 ◽  
Author(s):  
Jun Tomita ◽  
Gosuke Ban ◽  
Yoshiaki S. Kato ◽  
Kazuhiko Kume
Keyword(s):  
Drosophila Melanogaster ◽  
Brain Regions ◽  
Central Complex ◽  
Neuronal Circuit ◽  
Sleep Regulation ◽  
Synaptic Contacts ◽  
Protocerebral Bridge ◽  
Dopamine Signaling

AbstractThe central complex is one of the major brain regions that control sleep in Drosophila, but the circuitry details of sleep regulation have yet to be elucidated. Here, we show a novel sleep-regulating neuronal circuit in the protocerebral bridge (PB) of the central complex. Activation of the PB interneurons labeled by the R59E08-Gal4 and the PB columnar neurons in the R52B10-Gal4 promoted sleep and wakefulness, respectively. A targeted GFP reconstitution across synaptic partners (t-GRASP) analysis demonstrated synaptic contacts between these two groups of sleep-regulating PB neurons. Furthermore, we found that activation of a pair of dopaminergic (DA) neurons projecting to the PB (T1 DA neurons) decreased sleep. The wake-promoting T1 DA neurons and the sleep-promoting PB interneurons formed close associations. Dopamine 2-like receptor (Dop2R) knockdown in the sleep-promoting PB interneurons increased sleep. These results indicated that the neuronal circuit in the PB regulated by dopamine signaling mediates sleep-wakefulness.

scholarly journals Protocerebral Bridge Neurons That Regulate Sleep in Drosophila melanogaster

2021 ◽  
Vol 15 ◽  
Author(s):  
Jun Tomita ◽  
Gosuke Ban ◽  
Yoshiaki S. Kato ◽  
Kazuhiko Kume
Keyword(s):  
Drosophila Melanogaster ◽  
Synaptic Contact ◽  
Brain Regions ◽  
Central Complex ◽  
Neuronal Circuit ◽  
Sleep Regulation ◽  
Protocerebral Bridge ◽  
Dopamine Signaling

The central complex is one of the major brain regions that control sleep in Drosophila. However, the circuitry details of sleep regulation have not been elucidated yet. Here, we show a novel sleep-regulating neuronal circuit in the protocerebral bridge (PB) of the central complex. Activation of the PB interneurons labeled by the R59E08-Gal4 and the PB columnar neurons with R52B10-Gal4 promoted sleep and wakefulness, respectively. A targeted GFP reconstitution across synaptic partners (t-GRASP) analysis demonstrated synaptic contact between these two groups of sleep-regulating PB neurons. Furthermore, we found that activation of a pair of dopaminergic (DA) neurons projecting to the PB (T1 DA neurons) decreased sleep. The wake-promoting T1 DA neurons and the sleep-promoting PB interneurons formed close associations. Dopamine 2-like receptor (Dop2R) knockdown in the sleep-promoting PB interneurons increased sleep. These results indicated that the neuronal circuit in the PB, regulated by dopamine signaling, mediates sleep-wakefulness.

mAChRs in the Grasshopper Brain Mediate Excitation by Activation of the AC/PKA and the PLC Second-Messenger Pathways

2002 ◽  
Vol 87 (2) ◽  
pp. 876-888 ◽  
Author(s):  
B. Wenzel ◽  
N. Elsner ◽  
R. Heinrich
Keyword(s):  
Signaling Pathways ◽  
Intracellular Signaling ◽  
Sound Production ◽  
Courtship Behavior ◽  
Second Messenger ◽  
Muscarinic Acetylcholine Receptors ◽  
Muscarinic Agonists ◽  
Second Messenger Pathways

The species-specific sound production of acoustically communicating grasshoppers can be stimulated by pressure injection of both nicotinic and muscarinic agonists into the central body complex and a small neuropil situated posterior and dorsal to it. To determine the role of muscarinic acetylcholine receptors (mAChRs) in the control of acoustic communication behavior and to identify the second-messenger pathways affected by mAChR-activation, muscarinic agonists and membrane-permeable drugs known to interfere with specific mechanisms of intracellular signaling pathways were pressure injected to identical sites in male grasshopper brains. Repeated injections of small volumes of muscarine elicited stridulation of increasing duration associated with decreased latencies. This suggested an accumulation of excitation over time that is consistent with the suggested role of mAChRs in controling courtship behavior: to provide increasing arousal leading to higher intensity of stridulation and finally initiating a mating attempt. At sites in the brain where muscarine stimulation was effective, stridulation could be evoked by forskolin, an activator of adenylate cyclase (AC); 8-Br-cAMP-activating protein kinase A (PKA); and 3-isobuty-1-methylxanthine, leading to the accumulation of endogenously generated cAMP through inhibition of phosphodiesterases. This suggested that mAChRs mediate excitation by stimulating the AC/cAMP/PKA pathway. In addition, muscarine-stimulated stridulation was inhibited by 2′-5′-dideoxyadenonsine and SQ 22536, two inhibitors of AC; H-89 and Rp-cAMPS, two inhibitors of PKA; and by U-73122 and neomycin, two agents that inhibit phospholipase C (PLC) by independent mechanisms. Because the inhibition of AC, PKA, or PLC by various individually applied substances entirely suppressed muscarine-evoked stridulation in a number of experiments, activation of both pathways, AC/cAMP/PKA and PLC/IP3/diacylglycerine, appeared to be necessary to mediate the excitatory effects of mAChRs. With these studies on an intact “behaving” grasshopper preparation, we present physiological relevance for mAChR-evoked excitation mediated by sequential activation of the AC- and PLC-initiated signaling pathways that has been reported in earlier in vitro studies.

scholarly journals MULTIPLE ALLELE APPROACH TO THE STUDY OF GENES IN DROSOPHILA MELANOGASTER THAT ARE INVOLVED IN IMAGINAL DISC DEVELOPMENT

Genetics ◽  
1978 ◽  
Vol 89 (2) ◽  
pp. 355-370 ◽  
Author(s):  
Allen Shearn ◽  
Grafton Hersperger ◽  
Evelyn Hersperger ◽  
Ellen Steward Pentz ◽  
Paul Denker
Keyword(s):  
Drosophila Melanogaster ◽  
Phenotypic Variation ◽  
Mutant Allele ◽  
Imaginal Disc ◽  
Reference Allele ◽  
Multiple Allele ◽  
Significant Difference ◽  
Chromosome Mutations ◽  
Cold Sensitive

ABSTRACT The phenotypes of five different lethal mutants of Drosophila melanogaster that have small imaginal discs were analyzed in detail. From these results, we inferred whether or not the observed imaginal disc phenotype resulted exclusively from a primary imaginal disc defect in each mutant. To examine the validity of these inferences, we employed a multiple-allele method. Lethal alleles of the five third-chromosome mutations were identified by screening EMS-treated chromosomes for those which fail to complement with a chromosome containing all five reference mutations. Twenty-four mutants were isolated from 13,197 treated chromosomes. Each of the 24 was then tested for complementation with each of the five reference mutants. There was no significant difference in the mutation frequencies at these five loci. The stage of lethality and the imaginal disc morphology of each mutant allele were compared to those of its reference allele in order to examine the range of defects to be found among lethal alleles of each locus. In addition, hybrids of the alleles were examined for intracistronic complementation. For two of the five loci, we detected no significant phenotypic variation among lethal alleles. We infer that each of the mutant alleles at these two loci cause expression of the null activity phenotype. However, for the three other loci, we did detect significant phenotypic variation among lethal alleles. In fact, one of the mutant alleles at each of these three loci causes no detectable imaginal disc defect. This demonstrates that attempting to assess the developmental role of a gene by studying a single mutant allele may lead to erroneous conclusions. As a byproduct of the mutagenesis procedure, we have isolated two dominant, cold-sensitive mutants.

Sign in / Sign up

Export Citation Format

Share Document