The research report should be a detailed narrative explaining the function, biological processes, and localization of the gene product. Citations should be given for all claims.
You should prioritize authoritative reviews and primary scientific literature when conducting research. You can supplement
this with annotations you find in gene/protein databases, but these can be outdated or inaccurate.
We are specifically interested in the primary function of the gene - for enzymes, what reaction is catalyzed, and what is the substrate specificity? For transporters, what is the substrate? For structural proteins or adapters, what is the broader structural role? For signaling molecules, what is the role in the pathway.
We are interested in where in or outside the cell the gene product carries out its function.
We are also interested in the signaling or biochemical pathways in which the gene functions. We are less interested in broad pleiotropic effects, except where these elucidate the precise role.
Include evidence where possible. We are interested in both experimental evidence as well as inference from structure, evolution, or bioinformatic analysis. Precise studies should be prioritized over high-throughput, where available.
The requested identity is verified. The target is the Drosophila melanogaster dunce gene, symbol dnc, also designated Pde4/CG32498, rather than an unrelated gene with a similar abbreviation. Its product is an intracellular, high-affinity, cAMP-specific 3′,5′-cyclic-nucleotide phosphodiesterase of the PDE4 family. Its primary molecular function is:
3′,5′-cAMP + H₂O → 5′-AMP
Dnc therefore terminates and spatially restricts cAMP signals. In neurons—most prominently in mushroom-body neuropil—it controls the amplitude, duration, and subcellular spread of cAMP and thereby regulates PKA and other cAMP effectors involved in synaptic plasticity and memory. The most informative recent work suggests that Dnc is not simply a bulk cAMP “off switch”: it helps confine learning-related cAMP to the correct axonal compartments.
| Annotation dimension | Best-supported conclusion | Evidence type / key quantitative result | Confidence / limitation |
|---|---|---|---|
| Identity | dnc (dunce; Pde4/CG32498) in Drosophila melanogaster encodes the cAMP-specific phosphodiesterase corresponding to UniProt Q9W4S9, not an unrelated similarly named gene. | X-chromosomal dosage and deletion mapping linked region 3D3–3D4 to the relevant PDE activity; molecular cloning identified dnc as its structural gene. Comparative evidence identifies Dunce as the fly PDE4 ortholog. (wilson1995characterisationandanalysis pages 45-48, davis2004thecyclicamp pages 7-8, richter2013pde4asa pages 12-12) | High. Genetic, biochemical, and molecular evidence converge. Literature concerning C. elegans PDE-4 or “DNC” as dorsal nerve cord is not evidence about this protein. |
| Catalytic reaction and specificity | Dunce catalyzes 3′,5′-cAMP + H₂O → 5′-AMP, thereby terminating intracellular cAMP signals. It is a high-affinity, Mg²⁺-dependent, Ca²⁺-insensitive PDE with strong specificity for cAMP over cGMP. | The dnc-associated “Form II” activity was selectively lost after deletion of 3D3–3D4; expression studies produced high-affinity cAMP PDE activity. Dunce reportedly did not hydrolyze cGMP even at 1 mM. Loss of activity can elevate fly cAMP by as much as eightfold. (wilson1995characterisationandanalysis pages 45-48, davis2004thecyclicamp pages 2-3, wilson1995characterisationandanalysis pages 52-56) | High for cAMP hydrolysis and preference; moderate for exact biochemical limits because kinetic constants and original assay details were unavailable in the retrieved excerpts. |
| PDE4 domains and isoforms | The protein belongs to the cyclic-nucleotide PDE/PDE4 family and contains a conserved C-terminal catalytic region plus PDE4 upstream-conserved regulatory architecture. The locus produces multiple transcripts, including the UniProt N/G isoforms. | Early molecular analysis reported approximately six RNAs and a conserved 200–270-aa C-terminal region; truncations lacking that region had no PDE activity. A mammalian PDE4-related protein showed about 80% identity to Dunce within the conserved region. (wilson1995characterisationandanalysis pages 45-48, wilson1995characterisationandanalysis pages 52-56) | High for the catalytic-domain assignment and multiple transcripts; moderate for complete isoform annotation. Retrieved studies do not resolve the individual localization or biochemical behavior of UniProt isoforms N and G. |
| Cellular and anatomical localization | Dunce is an intracellular enzyme concentrated in adult-brain mushroom-body neuropil, particularly neuronal axonal and dendritic compartments; recent tagged-protein observations suggest bouton-associated organization. | Histological analysis localized the PDE to mushroom-body neuropil. Reviews describe axonal and dendritic enrichment; endogenous tagged Dnc appeared circularly distributed within boutons in recent imaging. (davis2004thecyclicamp pages 7-8, davis2004thecyclicamp pages 1-2, deimel2024learningdependentplasticityof pages 467-471) | High for mushroom-body neuropil enrichment; moderate for precise sub-bouton topology because the newest observation comes from a 2024 thesis rather than a peer-reviewed primary paper. |
| cAMP–PKA pathway role | Dunce negatively regulates PDE4-sensitive cAMP pools: it opposes adenylyl-cyclase activity, limits cAMP amplitude, duration, and spatial spread, and consequently constrains PKA and other cAMP effectors during neuronal plasticity. | dnc mutants have reduced PDE activity, elevated cAMP, defective learning, and rapid memory loss. Pathway analyses place Dunce with Rutabaga adenylyl cyclase and PKA in canonical learning signaling. Individual-synapse studies reported approximately 50% lower spontaneous vesicle-release frequency in dnc larvae, although whole-cell studies did not reproduce this difference. (davis2004thecyclicamp pages 2-3, davis2004thecyclicamp pages 1-2, charlie2006theduncecamp pages 1-2, davis2004thecyclicamp pages 5-6) | High for negative regulation of cAMP and learning; moderate for specific synaptic-release effects because electrophysiological results differ by preparation. |
| 2024 mushroom-body compartmentalization | Dnc appears to confine shock- and conditioning-evoked cAMP to appropriate Kenyon-cell γ-lobe compartments. Reducing Dnc allowed cAMP to spread into γ4–γ5 and may mislocalize learning-induced presynaptic depression. | Optophysiological thesis experiments found significant cAMP elevation in γ5 after shock and in γ4–γ5 during conditioning. Dnc downregulation also produced an additional CS⁺-associated calcium depression in γ5 while preserving γ1 plasticity. Exact effect sizes, sample sizes, and p values were not supplied in the retrieved text. (deimel2024learningdependentplasticityof pages 51-56, deimel2024learningdependentplasticityof pages 467-471, deimel2024learningdependentplasticityof pages 35-39) | Preliminary/moderate. Mechanistically compelling but reported in a 2024 doctoral thesis, with signals near sensor baseline and some work described as in preparation; independent peer-reviewed replication is needed. |
| 2024 socialization behavior | dnc is required for normal persistence of some experience-dependent behavioral changes after socialization, particularly reduced feeding; sleep effects are more complex and assay-dependent. | In dnc¹¹ mutants, socialized versus isolated flies showed no feeding difference at 0–24 h or 24–48 h (Dunn p=1.00 for each). A sleep difference occurred at 24–28 h (Kruskal–Wallis χ²=36.476, df=3, p=5.94×10⁻⁸; Dunn p=3.48×10⁻³). (gilmarti2024socializationcauseslonglasting pages 1-2, gilmarti2024socializationcauseslonglasting pages 7-8, gilmarti2024socializationcauseslonglasting pages 2-3) | Moderate–high for a requirement in persistent feeding plasticity; moderate for sleep interpretation because results depended on motion-analysis method and mutant basal behavior complicates causal interpretation. |
| Fragile-X research application | Genetic reduction of Dunce or pharmacological PDE4 inhibition has been used to restore deficient cAMP signaling and memory in a Drosophila dfmr1 fragile-X model, motivating cross-species therapeutic testing. | Rolipram (50 or 500 μM) and Ro-20-1724 (20 μM) rescued fly immediate and 60-min memory; acute 50 μM rolipram rescued olfactory learning (N=6 performance indices per group, p<0.001). A dnc loss-of-function allele also rescued dfmr1 short-term memory. In mice, rolipram normalized exaggerated LTD at 60–80 min; at 80 min, knockout vehicle was 72.0%±1.2% versus 81.9%±1.8% with rolipram (p<0.0001). (choi2015pde4inhibitionrescues pages 5-6, choi2015pde4inhibitionrescues pages 8-10, choi2015pde4inhibitionrescues pages 2-3, choi2015pde4inhibitionrescues pages 3-5) | High as a preclinical research application; not a direct therapeutic implementation of fly dnc. Drosophila Dunce reportedly differs pharmacologically from mammalian PDE4s, so inhibitor effects and translation require caution. (wilson1995characterisationandanalysis pages 52-56) |
Table: Evidence-graded functional annotation of Drosophila melanogaster dnc/Pde4 (UniProt Q9W4S9), spanning identity, enzymology, localization, signaling, recent findings, and preclinical application. Thesis-based and pharmacological limitations are explicitly identified.
The literature agrees with the supplied UniProt record: dnc/dunce is a D. melanogaster gene encoding a cAMP phosphodiesterase. Classical dosage and deletion experiments mapped the relevant enzyme activity to X-chromosome region 3D3–3D4. Deleting this region removed the heat-labile, cAMP-specific “Form II” PDE activity, and subsequent cloning identified dnc as its structural gene. This establishes correspondence between the genetic learning locus and the enzyme, rather than merely an indirect regulatory association. (wilson1995characterisationandanalysis pages 45-48, davis2004thecyclicamp pages 7-8)
The target is therefore consistent across all required identifiers:
Search results using “DNC” also retrieved unrelated meanings—notably “dorsal nerve cord” in Caenorhabditis elegans—and C. elegans PDE-4 papers. Those were not treated as evidence about Q9W4S9.
Molecular analysis identified a conserved approximately 200–270-residue C-terminal region shared with cyclic-nucleotide PDEs; truncations lacking this region lacked PDE activity, supporting its assignment as the catalytic domain. Comparative sequence work found approximately 80% identity between Dunce and a mammalian PDE4-related protein within the conserved region. These observations agree with the supplied InterPro assignments for PDEase/PDEase catalytic domains and the PDE4 upstream-conserved regulatory region. (wilson1995characterisationandanalysis pages 45-48, wilson1995characterisationandanalysis pages 52-56)
Early molecular studies detected approximately six dnc RNAs, consistent with a complex locus and multiple products. UniProt designates N/G isoforms, but the retrieved experimental literature does not adequately resolve the individual biochemical properties or subcellular distributions of those two isoforms. Consequently, isoform-specific claims should not be inferred from observations made with pan-Dnc reagents. (wilson1995characterisationandanalysis pages 45-48)
Dnc hydrolyzes the 3′,5′-phosphodiester bond of cyclic AMP, consuming water and yielding noncyclic 5′-AMP. Functionally, it lowers intracellular cAMP and terminates signaling initiated by adenylyl cyclases. It is therefore a signal-terminating enzyme, not a receptor, transporter, or structural protein.
Classical fractionation distinguished the Dnc-associated activity from a separate calcium/calmodulin-regulated PDE. Dnc/Form II was heat-labile, relatively low molecular weight, Mg²⁺-dependent, calcium-insensitive, and cAMP-specific. The other activity hydrolyzed both cAMP and cGMP and was calcium activated. Loss of the Form II activity in dnc deletions is strong genetic-biochemical evidence for the annotation. (wilson1995characterisationandanalysis pages 45-48)
The best-supported substrate is cAMP. Expression and kinetic studies identified Dunce as a high-affinity cAMP PDE, and the enzyme reportedly failed to hydrolyze cGMP even when cGMP was supplied at concentrations as high as 1 mM. Loss of dnc activity can elevate fly cAMP by as much as eightfold, providing an in-vivo biochemical consequence consistent with its catalytic assignment. (davis2004thecyclicamp pages 2-3, davis2004thecyclicamp pages 1-2, wilson1995characterisationandanalysis pages 52-56)
Thus, “cAMP-specific” is more precise than the broader phrase “cyclic-nucleotide phosphodiesterase.” Exact modern values for Km, kcat, metal dependence, and isoform N/G kinetics were not available in the retrieved primary excerpts.
Although Dunce is evolutionarily related to mammalian PDE4 enzymes, comparative work reported that the fly enzyme was insensitive to the prototypic mammalian PDE4 inhibitors rolipram and Ro-20-1724 in some biochemical assays. Therefore, results from administering these drugs to flies should not automatically be interpreted as direct inhibition of Q9W4S9; effects on other fly PDE activities or differences between assay contexts remain possible. (wilson1995characterisationandanalysis pages 52-56)
Dnc is an intracellular enzyme and is especially concentrated in the mushroom-body neuropil, the principal associative-learning center of the fly brain. Histological work localized Dnc to neuronal processes rather than describing it as a secreted or integral-membrane protein. Reviews further describe enrichment in mushroom-body axonal and dendritic compartments. (davis2004thecyclicamp pages 7-8, davis2004thecyclicamp pages 1-2)
This localization is functionally important. Mushroom-body Kenyon cells receive sensory and reinforcement information, and their compartmentalized axons contain synapses at which associative plasticity is expressed. Placing a cAMP-hydrolyzing enzyme in these processes allows signaling to be controlled near its sites of production and action rather than only through whole-cell cAMP clearance.
Recent endogenous-tag observations described Dnc in a circular pattern within boutons. That supports local organization of the enzyme around signaling microdomains, but this observation comes from a 2024 doctoral thesis and requires peer-reviewed confirmation and higher-resolution structural analysis. (deimel2024learningdependentplasticityof pages 467-471)
Dnc operates in the pathway:
receptor/G-protein and Ca²⁺ inputs → adenylyl cyclase, including Rutabaga → cAMP → PKA and other cAMP effectors → synaptic/neuronal responses, with Dnc hydrolyzing cAMP to terminate and delimit the signal.
Dnc, Rutabaga adenylyl cyclase, and PKA were historically identified as major components of the cAMP pathway required for associative learning. dnc mutants have reduced PDE activity, elevated cAMP, impaired acquisition, and rapid memory loss, while altered PKA activity is considered a major downstream consequence of disturbing either cAMP synthesis or degradation. (davis2004thecyclicamp pages 1-2, davis2004thecyclicamp pages 5-6)
The key mechanistic interpretation is homeostatic and spatial: both insufficient and excessive/mislocalized cAMP can impair memory. Consequently, the phenotype is not evidence that cAMP simply promotes learning monotonically. Dnc shapes an appropriate cAMP pulse and prevents activation of downstream targets at the wrong time or place.
A 2024 optophysiological study provides the most direct recent model of this spatial function. Reducing Dnc allowed shock-evoked cAMP, normally concentrated largely in γ1–γ3 mushroom-body compartments, to spread into γ4–γ5 boutons, with a significant increase in γ5. During odor–shock conditioning, redistribution was stronger and produced significant increases in γ4 and γ5. (deimel2024learningdependentplasticityof pages 467-471, deimel2024learningdependentplasticityof pages 35-39)
Presynaptic calcium imaging showed the expected aversive-conditioning-associated depression in γ1. Dnc reduction did not abolish that plasticity but was associated with an additional CS+-related depression in γ5, a compartment linked to appetitive learning. The authors therefore propose that loss of Dnc misallocates plasticity to an inappropriate compartment, rather than eliminating plasticity globally. (deimel2024learningdependentplasticityof pages 51-56, deimel2024learningdependentplasticityof pages 467-471)
This is an attractive mechanistic refinement: Dnc may establish biochemical boundaries that permit distinct mushroom-body compartments to encode different reinforcements. However, the calcium signals were close to sensor baseline, bleaching was problematic, exact effect sizes and sample sizes were unavailable in the retrieved text, and some underlying work was described as in preparation. The finding should therefore be considered preliminary rather than settled.
Learning and memory are the best-established organismal functions of dnc. Mutants perform poorly and forget rapidly in associative and non-associative paradigms. Dnc enrichment in mushroom-body neuropil, elevated cAMP after enzyme loss, and disruption of downstream cAMP/PKA signaling connect the behavioral phenotype to a defined molecular pathway. (davis2004thecyclicamp pages 2-3, davis2004thecyclicamp pages 1-2, wilson1995characterisationandanalysis pages 52-56)
The approximately 5,000 mushroom-body neurons described in the reviewed literature provide an anatomical substrate for this enrichment, although this cell count is not a measurement of Dnc-expressing cells specifically. (davis2004thecyclicamp pages 1-2)
The synaptic evidence is informative but not fully uniform. Individual-synapse recordings reportedly found an approximately 50% reduction in spontaneous vesicle-release frequency in dnc larvae. Other whole-cell embryonic recordings found no spontaneous-release difference, and nerve-evoked release at individual synapses was not significantly altered in some experiments. Effects were also reported on facilitation, vesicle-pool mobilization, and the ratio of docked to undocked vesicles. (charlie2006theduncecamp pages 1-2)
These results suggest that Dnc-dependent cAMP regulation affects presynaptic organization and plasticity, but preparation, developmental stage, and recording scale materially influence the measured phenotype. It is safer to annotate a role in synaptic modulation than to claim a universal increase or decrease in transmitter release.
A peer-reviewed September 2024 study used the dnc¹¹ allele to test persistent behavioral effects of social experience. Wild-type flies reduced feeding after five days of socialization, and the effect persisted after social interaction ended. In dnc mutants, socialized and isolated groups did not differ in feeding during either 0–24 h or 24–48 h; the reported Dunn post-hoc value was p=1.00 in both intervals. This supports a requirement for intact Dnc-dependent memory signaling in persistent feeding plasticity. (gilmarti2024socializationcauseslonglasting pages 1-2, gilmarti2024socializationcauseslonglasting pages 7-8)
Sleep results were more complex. Socialized and isolated dnc mutants differed during the 24–28-h interval, with Kruskal–Wallis χ²=36.476, df=3, p=5.94×10⁻⁸, and a relevant Dunn comparison of p=3.48×10⁻³. Reduced walking and micromovements produced increased inferred sleep, but conclusions depended on whether sensitive ethoscope or conventional activity analysis was used. Altered basal behavior in dnc mutants also complicates simple “memory required” interpretations. (gilmarti2024socializationcauseslonglasting pages 7-8, gilmarti2024socializationcauseslonglasting pages 2-3)
The authors place these effects within cAMP/CREB-dependent, mushroom-body plasticity mechanisms. The direct dnc experiment establishes a genetic requirement for aspects of persistent behavioral change; it does not by itself prove that Dnc directly regulates CREB phosphorylation in the tested cells. (gilmarti2024socializationcauseslonglasting pages 1-2)
dnc is a foundational genetic tool for determining how cyclic-nucleotide turnover affects learning, synaptic physiology, and spatially restricted second-messenger signals. Loss-of-function alleles, RNA interference, tagged endogenous protein, cAMP sensors, and pharmacological manipulations can be combined to distinguish signal production from degradation and to map where memory-associated cAMP is allowed to act.
A major preclinical application was reported in January 2015 using Drosophila dfmr1 fragile-X mutants, which have reduced head cAMP and memory defects. Chronic rolipram or Ro-20-1724 treatment improved immediate-recall and 60-min memory in courtship and olfactory assays. Acute 50 μM rolipram for 12 h rescued olfactory immediate-recall learning without changing wild-type performance, odor avoidance, or shock avoidance; the reported olfactory experiment used N=6 performance indices per group and found p<0.001. A dnc loss-of-function allele also rescued dfmr1 short-term memory, providing genetic support for the idea that reducing cAMP degradation can compensate for deficient cAMP signaling. (choi2015pde4inhibitionrescues pages 5-6, choi2015pde4inhibitionrescues pages 2-3, choi2015pde4inhibitionrescues pages 3-5)
The study used 50 or 500 μM rolipram and 20 μM Ro-20-1724 in fly experiments. Fifty micromolar rolipram rescued memory but not mushroom-body α/β-lobe midline crossing, whereas 500 μM reduced that structural defect. Thus, behavioral rescue did not require correction of the developmental brain phenotype. (choi2015pde4inhibitionrescues pages 5-6, choi2015pde4inhibitionrescues pages 2-3)
The fly findings motivated cross-species testing. In Fmr1-knockout mouse hippocampal slices, vehicle-treated LTD remained enhanced at 72.0%±1.2% of baseline at 80 min, whereas acute rolipram produced 81.9%±1.8% (p<0.0001). At 60 min, the corresponding statistical comparison was p=0.0002. Chronic mouse treatment used 0.03 mg/kg rolipram daily for eight weeks, followed by a 3–5-week washout, and also eliminated exaggerated LTD. (choi2015pde4inhibitionrescues pages 8-10, choi2015pde4inhibitionrescues pages 2-3)
These experiments show the practical value of dnc as a pathway-validation model. They do not constitute a therapeutic implementation of the fly protein itself, and the reported pharmacological divergence between Dunce and mammalian PDE4s cautions against assuming identical inhibitor–target relationships across species. (wilson1995characterisationandanalysis pages 52-56)
Authoritative reviews describe PDE4 enzymes as organizers of signaling cross-talk, desensitization, and cAMP compartmentalization, and identify Dunce as the canonical fly PDE4 ortholog whose discovery linked PDE activity to memory. This framework is strongly supported for Dnc by genetic loss, biochemical activity, molecular cloning, anatomical enrichment, and behavioral rescue experiments. (davis2004thecyclicamp pages 7-8, richter2013pde4asa pages 12-12)
The evidence hierarchy is:
Overall, the most defensible functional annotation is: Dnc is a mushroom-body-enriched, intracellular PDE4-family enzyme that selectively degrades cAMP and establishes the temporal and spatial boundaries of neuronal cAMP signaling required for correctly localized synaptic plasticity and memory.
References
(wilson1995characterisationandanalysis pages 45-48): Moira Ann Wilson. Characterisation and analysis of pde4a phosphodiesterase isoforms. Text, Jan 1995. URL: https://doi.org/10.5525/gla.thesis.71682, doi:10.5525/gla.thesis.71682. This article has 0 citations and is from a peer-reviewed journal.
(davis2004thecyclicamp pages 7-8): Ronald L. Davis, Jim Cherry, Brigitte Dauwalder, Pyung-Lim Han, and Efthimios Skoulakis. The cyclic amp system anddrosophila learning. Molecular and Cellular Biochemistry, 149-150:271-278, Aug 2004. URL: https://doi.org/10.1007/bf01076588, doi:10.1007/bf01076588. This article has 190 citations and is from a peer-reviewed journal.
(richter2013pde4asa pages 12-12): Wito Richter, Frank S. Menniti, Han-Ting Zhang, and Marco Conti. Pde4 as a target for cognition enhancement. Expert Opinion on Therapeutic Targets, 17:1011-1027, Aug 2013. URL: https://doi.org/10.1517/14728222.2013.818656, doi:10.1517/14728222.2013.818656. This article has 183 citations and is from a peer-reviewed journal.
(davis2004thecyclicamp pages 2-3): Ronald L. Davis, Jim Cherry, Brigitte Dauwalder, Pyung-Lim Han, and Efthimios Skoulakis. The cyclic amp system anddrosophila learning. Molecular and Cellular Biochemistry, 149-150:271-278, Aug 2004. URL: https://doi.org/10.1007/bf01076588, doi:10.1007/bf01076588. This article has 190 citations and is from a peer-reviewed journal.
(wilson1995characterisationandanalysis pages 52-56): Moira Ann Wilson. Characterisation and analysis of pde4a phosphodiesterase isoforms. Text, Jan 1995. URL: https://doi.org/10.5525/gla.thesis.71682, doi:10.5525/gla.thesis.71682. This article has 0 citations and is from a peer-reviewed journal.
(davis2004thecyclicamp pages 1-2): Ronald L. Davis, Jim Cherry, Brigitte Dauwalder, Pyung-Lim Han, and Efthimios Skoulakis. The cyclic amp system anddrosophila learning. Molecular and Cellular Biochemistry, 149-150:271-278, Aug 2004. URL: https://doi.org/10.1007/bf01076588, doi:10.1007/bf01076588. This article has 190 citations and is from a peer-reviewed journal.
(deimel2024learningdependentplasticityof pages 467-471): Stephan Hubertus Deimel. Learning-dependent plasticity of the drosophila mushroom body: an optophysiological approach. ArXiv, 2024. URL: https://doi.org/10.53846/goediss-10629, doi:10.53846/goediss-10629. This article has 0 citations.
(charlie2006theduncecamp pages 1-2): Nicole K. Charlie, Angela M. Thomure, Michael A. Schade, and K. Miller. The dunce camp phosphodiesterase pde-4 negatively regulates gαs-dependent and gαs-independent camp pools in the caenorhabditis elegans synaptic signaling network. Genetics, 173:111-130, May 2006. URL: https://doi.org/10.1534/genetics.105.054007, doi:10.1534/genetics.105.054007. This article has 65 citations and is from a domain leading peer-reviewed journal.
(davis2004thecyclicamp pages 5-6): Ronald L. Davis, Jim Cherry, Brigitte Dauwalder, Pyung-Lim Han, and Efthimios Skoulakis. The cyclic amp system anddrosophila learning. Molecular and Cellular Biochemistry, 149-150:271-278, Aug 2004. URL: https://doi.org/10.1007/bf01076588, doi:10.1007/bf01076588. This article has 190 citations and is from a peer-reviewed journal.
(deimel2024learningdependentplasticityof pages 51-56): Stephan Hubertus Deimel. Learning-dependent plasticity of the drosophila mushroom body: an optophysiological approach. ArXiv, 2024. URL: https://doi.org/10.53846/goediss-10629, doi:10.53846/goediss-10629. This article has 0 citations.
(deimel2024learningdependentplasticityof pages 35-39): Stephan Hubertus Deimel. Learning-dependent plasticity of the drosophila mushroom body: an optophysiological approach. ArXiv, 2024. URL: https://doi.org/10.53846/goediss-10629, doi:10.53846/goediss-10629. This article has 0 citations.
(gilmarti2024socializationcauseslonglasting pages 1-2): Beatriz Gil-Martí, Julia Isidro-Mézcua, Adriana Poza-Rodriguez, Gerson S. Asti Tello, Gaia Treves, Enrique Turiégano, Esteban J. Beckwith, and Francisco A. Martin. Socialization causes long-lasting behavioral changes. Sep 2024. URL: https://doi.org/10.1038/s41598-024-73218-w, doi:10.1038/s41598-024-73218-w. This article has 10 citations and is from a peer-reviewed journal.
(gilmarti2024socializationcauseslonglasting pages 7-8): Beatriz Gil-Martí, Julia Isidro-Mézcua, Adriana Poza-Rodriguez, Gerson S. Asti Tello, Gaia Treves, Enrique Turiégano, Esteban J. Beckwith, and Francisco A. Martin. Socialization causes long-lasting behavioral changes. Sep 2024. URL: https://doi.org/10.1038/s41598-024-73218-w, doi:10.1038/s41598-024-73218-w. This article has 10 citations and is from a peer-reviewed journal.
(gilmarti2024socializationcauseslonglasting pages 2-3): Beatriz Gil-Martí, Julia Isidro-Mézcua, Adriana Poza-Rodriguez, Gerson S. Asti Tello, Gaia Treves, Enrique Turiégano, Esteban J. Beckwith, and Francisco A. Martin. Socialization causes long-lasting behavioral changes. Sep 2024. URL: https://doi.org/10.1038/s41598-024-73218-w, doi:10.1038/s41598-024-73218-w. This article has 10 citations and is from a peer-reviewed journal.
(choi2015pde4inhibitionrescues pages 5-6): Catherine H. Choi, Brian P. Schoenfeld, Eliana D. Weisz, Aaron J. Bell, Daniel B. Chambers, Joseph Hinchey, Richard J. Choi, Paul Hinchey, Maria Kollaros, Michael J. Gertner, Neal J. Ferrick, Allison M. Terlizzi, Nicole Yohn, Eric Koenigsberg, David A. Liebelt, R. Suzanne Zukin, Newton H. Woo, Michael R. Tranfaglia, Natalia Louneva, Steven E. Arnold, Steven J. Siegel, Francois V. Bolduc, Thomas V. McDonald, Thomas A. Jongens, and Sean M. J. McBride. Pde-4 inhibition rescues aberrant synaptic plasticity in drosophila and mouse models of fragile x syndrome. The Journal of Neuroscience, 35:396-408, Jan 2015. URL: https://doi.org/10.1523/jneurosci.1356-12.2015, doi:10.1523/jneurosci.1356-12.2015. This article has 70 citations.
(choi2015pde4inhibitionrescues pages 8-10): Catherine H. Choi, Brian P. Schoenfeld, Eliana D. Weisz, Aaron J. Bell, Daniel B. Chambers, Joseph Hinchey, Richard J. Choi, Paul Hinchey, Maria Kollaros, Michael J. Gertner, Neal J. Ferrick, Allison M. Terlizzi, Nicole Yohn, Eric Koenigsberg, David A. Liebelt, R. Suzanne Zukin, Newton H. Woo, Michael R. Tranfaglia, Natalia Louneva, Steven E. Arnold, Steven J. Siegel, Francois V. Bolduc, Thomas V. McDonald, Thomas A. Jongens, and Sean M. J. McBride. Pde-4 inhibition rescues aberrant synaptic plasticity in drosophila and mouse models of fragile x syndrome. The Journal of Neuroscience, 35:396-408, Jan 2015. URL: https://doi.org/10.1523/jneurosci.1356-12.2015, doi:10.1523/jneurosci.1356-12.2015. This article has 70 citations.
(choi2015pde4inhibitionrescues pages 2-3): Catherine H. Choi, Brian P. Schoenfeld, Eliana D. Weisz, Aaron J. Bell, Daniel B. Chambers, Joseph Hinchey, Richard J. Choi, Paul Hinchey, Maria Kollaros, Michael J. Gertner, Neal J. Ferrick, Allison M. Terlizzi, Nicole Yohn, Eric Koenigsberg, David A. Liebelt, R. Suzanne Zukin, Newton H. Woo, Michael R. Tranfaglia, Natalia Louneva, Steven E. Arnold, Steven J. Siegel, Francois V. Bolduc, Thomas V. McDonald, Thomas A. Jongens, and Sean M. J. McBride. Pde-4 inhibition rescues aberrant synaptic plasticity in drosophila and mouse models of fragile x syndrome. The Journal of Neuroscience, 35:396-408, Jan 2015. URL: https://doi.org/10.1523/jneurosci.1356-12.2015, doi:10.1523/jneurosci.1356-12.2015. This article has 70 citations.
(choi2015pde4inhibitionrescues pages 3-5): Catherine H. Choi, Brian P. Schoenfeld, Eliana D. Weisz, Aaron J. Bell, Daniel B. Chambers, Joseph Hinchey, Richard J. Choi, Paul Hinchey, Maria Kollaros, Michael J. Gertner, Neal J. Ferrick, Allison M. Terlizzi, Nicole Yohn, Eric Koenigsberg, David A. Liebelt, R. Suzanne Zukin, Newton H. Woo, Michael R. Tranfaglia, Natalia Louneva, Steven E. Arnold, Steven J. Siegel, Francois V. Bolduc, Thomas V. McDonald, Thomas A. Jongens, and Sean M. J. McBride. Pde-4 inhibition rescues aberrant synaptic plasticity in drosophila and mouse models of fragile x syndrome. The Journal of Neuroscience, 35:396-408, Jan 2015. URL: https://doi.org/10.1523/jneurosci.1356-12.2015, doi:10.1523/jneurosci.1356-12.2015. This article has 70 citations.