The Experts below are selected from a list of 177 Experts worldwide ranked by ideXlab platform
Ronald L Davis - One of the best experts on this subject based on the ideXlab platform.
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gilgamesh is required for rutabaga independent olfactory learning in drosophila
Neuron, 2010Co-Authors: Dinghui Yu, Jennifer Pletting, Ronald L DavisAbstract:Summary Cyclic AMP signaling in Drosophila mushroom body neurons, anchored by the adenylyl cyclase encoded by the rutabaga gene, is indispensable for olfactory memory formation. From a screen for new memory mutants, we identified alleles of the gilgamesh ( gish ) gene, which encodes a casein kinase Iγ homolog that is preferentially expressed in the mushroom body neurons. The gish -encoded kinase participates in the physiology of these neurons underlying memory formation since the mutant memory deficit was rescued with expression of a gish cDNA in these neurons only during adulthood. A cellular memory trace, detected as increased calcium influx into the α′/β′ neuron processes in response to the odor used for conditioning, was disrupted in gish mutants. Epistasis experiments indicated a lack of genetic interactions between gish and rutabaga . Therefore, gish participates in a rutabaga -independent pathway for memory formation and accounts for some of the residual learning that occurs in rutabaga mutants.
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dynamics of learning related camp signaling and stimulus integration in the drosophila olfactory pathway
Neuron, 2009Co-Authors: Seth M Tomchik, Ronald L DavisAbstract:Summary Functional imaging with genetically encoded calcium and cAMP reporters was used to examine the signal integration underlying learning in Drosophila . Dopamine and octopamine modulated intracellular cAMP in spatially distinct patterns in mushroom body neurons. Pairing of neuronal depolarization with subsequent dopamine application revealed a synergistic increase in cAMP in the mushroom body lobes, which was dependent on the rutabaga adenylyl cyclase. This synergy was restricted to the axons of mushroom body neurons, and occurred only following forward pairing with time intervals similar to those required for behavioral conditioning. In contrast, forward pairing of neuronal depolarization and octopamine produced a subadditive effect on cAMP. Finally, elevating intracellular cAMP facilitated calcium transients in mushroom body neurons, suggesting that cAMP elevation is sufficient to induce presynaptic plasticity. These data suggest that rutabaga functions as a coincidence detector in an intact neuronal circuit, with dopamine and octopamine bidirectionally influencing the generation of cAMP.
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pharmacogenetic rescue in time and space of the rutabaga memory impairment by using gene switch
Proceedings of the National Academy of Sciences of the United States of America, 2004Co-Authors: Gregg Roman, Lin Zong, Ronald L DavisAbstract:The GAL4-based Gene-Switch system has been engineered to regulate transgene expression in Drosophila in both time and space. We constructed a Gene-Switch transgene in which Gene-Switch expression is restricted spatially by a defined mushroom body enhancer. This system allows Gene-Switch to be active only in the mushroom bodies and only on administration of the pharmacological Gene-Switch ligand RU486. This line was used to drive the expression of a rutabaga cDNA in otherwise rutabaga mutant flies. Induction of the rutabaga cDNA in the mushroom bodies only during adulthood, or during adulthood along with the larval and pupal developmental stages, corrects the olfactory memory impairment found in rutabaga mutants. Induction of the cDNA only during the larval and pupal stages was inconsequential to performance in olfactory memory tasks. These data indicate that normal rutabaga function must be expressed in adulthood for normal memory and conclusively delimit the time and space expression requirements for correcting the rutabaga memory impairment. Such combined pharmacogenetic regulation of transgene expression now allows this time and space dissection to be made for other behavioral mutants.
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spatiotemporal rescue of memory dysfunction in drosophila
Science, 2003Co-Authors: Sean E Mcguire, Alexander J Osborn, Kunihiro Matsumoto, Ronald L DavisAbstract:We have developed a method for temporal and regional gene expression targeting (TARGET) in Drosophila and show the simultaneous spatial and temporal rescue of a memory defect. The transient expression of the rutabaga-encoded adenylyl cyclase in the mushroom bodies of the adult brain was necessary and sufficient to rescue the rutabaga memory deficit, which rules out a developmental brain defect in the etiology of this deficit and demonstrates an acute role for rutabaga in memory formation in these neurons. The TARGET system offers general utility in simultaneously addressing issues of when and where gene products are required.
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tissue specific expression of a type i adenylyl cyclase rescues the rutabaga mutant memory defect in search of the engram
Learning & Memory, 2000Co-Authors: Troy Zars, Reinhard Wolf, Ronald L Davis, Martin HeisenbergAbstract:Most attempts to localize physical correlates of memory in the central nervous system (CNS) rely on ablation techniques. This approach has the limitation of defining just one of an unknown number of structures necessary for memory formation. We have used the Drosophila rutabaga type I Ca2+/CaM-dependent adenylyl cyclase (AC) gene to determine in which CNS region AC expression is sufficient for memory formation. Using pan-neural and restricted CNS expression with the GAL4 binary transcription activation system, we have rescued the memory defect of the rutabaga mutant in a fast robust spatial learning paradigm. The ventral ganglion, antennal lobes, and median bundle are likely the CNS structures sufficient for rutabaga AC- dependent spatial learning.
Mini V Mathew - One of the best experts on this subject based on the ideXlab platform.
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pkc a differentially affects rutabaga and wild type drosophila neuronal potassium current
International Journal of Neuroscience, 2004Co-Authors: Waleed B Alshuaib, Mini V Mathew, M Y Hasan, Mohammed A FahimAbstract:Learning and memory are defective in the Drosophila mutant rutabaga, which has a low intracellular cyclic adenosine monophosphate (cAMP) concentration. The aim of this study was to compare modulation effects of protein kinase C activator (PKC-A) on the delayed-rectifier potassium current (IKDR) in wild-type and rutabaga neurons. IKDR was measured from cultured (2 days) wild-type and rutabaga neurons. The authors examined the effects of PKC-A on IKDR in wild-type and rutabaga neurons. IKDR was measured from neurons before and after addition of PKC-A to the external solution. IKDR was smaller in rutabaga neurons (380 ± 25 pA) than in wild-type neurons (529 ± 44 pA). IKDR was reduced by PKC-A more in wild-type (↓55 ± 6%) than in rutabaga (↓35 ± 8%) neurons (single-cell studies). In the presence of PKC-A, there was no difference in IKDR between wild-type (229 ± 31 pA) and rutabaga (242 ± 26 pA) neurons (population studies). These results indicate that PKC-A differentially affects the delayed--rectifier channe...
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differential effects of dopamine on a potassium current in cultured rutabaga and wild type drosophila cells
Neuroscience Research Communications, 2003Co-Authors: Waleed B Alshuaib, Mini V Mathew, M Y Hasan, Mohammed A FahimAbstract:The rutabaga mutation which has a low intracellular cyclic adenosine monophosphate (cAMP) concentration is defective in short-term memory. The aim of this study was to compare modulation effects of dopamine on the delayed-rectifier potassium current (IKDR) in rutabaga and wild-type Drosophila neurons. The conventional whole-cell patch-clamp technique was applied to cultured Drosophila neurons derived from embryonic neuroblasts. IKDR was measured from cultured (2 days) wild-type and rutabaga neurons. IKDR was smaller in rutabaga neurons (373 ± 38 pA) than in wild-type neurons (519 ± 40 pA) but there was no difference in IKDR activation in wild-type inactivation between the two genotypes. We examined the effects of dopamine on IKDR in wild-type and rutabaga neurons. IKDR was measured from neurons before and after addition of dopamine to the external solution. Dopamine application reduced IKDR in wild-type neurons but did not significantly affect IKDR in rutabaga neurons (single-cell studies). In the presence of dopamine there was no difference in IKDR between wild-type (344 ± 29 pA) and rutabaga (338 ± 27pA) neurons (population studies). These results indicate that dopamine differentially affects the delayed-rectifier channel in wild-type and rutabaga neurons. This can alter neuronal excitability in rutabaga and may affect the processing of neural signals necessary for learning and memory.
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serotonin reduces potassium current in rutabaga and wild type drosophila neurons
International Journal of Neuroscience, 2003Co-Authors: Waleed B Alshuaib, Mini V Mathew, M Y Hasan, Mohammed A FahimAbstract:The Drosophila learning mutant rutabaga is defective in short-term memory and has a reduced intracellular cyclic adenosine monophosphate (cAMP) concentration. The delayed-rectifier potassium current (IKDR) was measured from cultured (2 days) wild-type and rutabaga neurons. IKDR was smaller in rutabaga neurons (382 - 41 pA) than in wild-type neurons (542 - 33 pA). IKDR was measured from neurons before and after addition of serotonin to the external solution. IKDR was reduced by serotonin in wildtype ( O 37 - 7%) and rutabaga ( O 33 - 6%) neurons (single-cell studies). In the presence of serotonin, IKDR was smaller in rutabaga (218 - 24 pA) than in wild-type (426 - 35 pA) neurons (population studies). These results indicate that serotonin has affected IKDR so that the inherent difference between the two genotypes was preserved.
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reduced delayed rectifier k current in the learning mutant rutabaga
Learning & Memory, 2002Co-Authors: Waleed B Alshuaib, Mini V MathewAbstract:The Drosophila mutations rutabaga and dunce affect learning and memory due to defects in cAMP metabolism. The dunce mutant has a high intracellular cAMP concentration owing to cAMP-specific phosphodiesterase (PDE) disruption (Byers et al. 1981). The rutabaga mutant has a low intracellular cAMP concentration due to elimination of a calcium/cadmodulin-responsive adenylyl cyclase. The ability of the cyclase catalytic subunit to interact with calcium/cadmodulin may be affected in rutabaga (Livingstone et al. 1984; Levin et al. 1992). dunce and rutabaga, originally identified for affecting learning and memory (Dudai et al. 1976) have been shown to alter synaptic plasticity (Zhong and Wu 1991), disrupt habituation (Engel and Wu 1996), and reduce growth cone motility (Kim and Wu 1996). cAMP-dependent modulation of ion channels has been shown to modify impulse activity of neurons (Kaczmarek and Kauer 1983). Modulation of neuronal electrical properties can change the operation of neural networks, it may be an important cellular mechanism for activity-dependent conditioning of behavior. Classical conditioning of the Aplysia siphon and tail-withdrawal reflex is believed to rely on presynaptic facilitation (Kandel et al. 1983). However, this form of simple learning, which depends on the synapse, cannot occur in complete isolation from the cell body, because changes in neuronal function can impact synaptic function. K+ current is one of the fundamental factors that regulate neuronal excitability (Klee et al. 1995) and neuronal function (Le Masson et al. 1993). Investigation of somal K+ current is required to elucidate possible changes in neuronal function of the Drosophila learning mutants. The learning deficit in rutabaga has been demonstrated in the adult fly, nonetheless, the embryonic cell culture system provides an excellent preparation that can be manipulated easily in electrophysiological studies. Furthermore, embryonic neurons can be used to show whether the K+ current is altered in early life of the fly. It has been shown previously that short-term (10 min) treatment with dibutyryl (db) cAMP does not affect neuronal K+ current (Alshuaib and Byerly 1996), whereas long-term (2 d) treatment with db-cAMP enhances neuronal K+ current (Alshuaib and Mathew 1998). Moreover, neuronal K+ current was shown to be greater in dunce than in wild-type neurons (Alshuaib and Mathew 1998). dunce and rutabaga were shown to display altered firing patterns in giant (cleavage-arrested) cultured neurons (Zhao and Wu 1997). However, neuronal K+ current of normal embryonic cultures has not been investigated in the rutabaga mutant. In the present study, we compared the delayed-rectifier K+ current (IKDR) in wild-type and rutabaga neurons from normal embryonic cultures. IKDR was reduced in rutabaga neurons as compared with the wild-type, a defect that can impact neuronal excitability and, ultimately, learning and memory.
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reduced delayed rectifier k current in the learning mutant rutabaga
Learning & Memory, 2002Co-Authors: Waleed B Alshuaib, Mini V MathewAbstract:The Drosophila mutations rutabaga and dunce affect learning and memory due to defects in cAMP metabolism. The dunce mutant has a high intracellular cAMP concentration owing to cAMP-specific phosphodiesterase (PDE) disruption (Byers et al. 1981). The rutabaga mutant has a low intracellular cAMP concentration due to elimination of a calcium/cadmodulin-responsive adenylyl cyclase. The ability of the cyclase catalytic subunit to interact with calcium/cadmodulin may be affected in rutabaga (Livingstone et al. 1984; Levin et al. 1992). dunce and rutabaga, originally identified for affecting learning and memory (Dudai et al. 1976) have been shown to alter synaptic plasticity (Zhong and Wu 1991), disrupt habituation (Engel and Wu 1996), and reduce growth cone motility (Kim and Wu 1996). cAMP-dependent modulation of ion channels has been shown to modify impulse activity of neurons (Kaczmarek and Kauer 1983). Modulation of neuronal electrical properties can change the operation of neural networks, it may be an important cellular mechanism for activity-dependent conditioning of behavior. Classical conditioning of the Aplysia siphon and tail-withdrawal reflex is believed to rely on presynaptic facilitation (Kandel et al. 1983). However, this form of simple learning, which depends on the synapse, cannot occur in complete isolation from the cell body, because changes in neuronal function can impact synaptic function. K+ current is one of the fundamental factors that regulate neuronal excitability (Klee et al. 1995) and neuronal function (Le Masson et al. 1993). Investigation of somal K+ current is required to elucidate possible changes in neuronal function of the Drosophila learning mutants. The learning deficit in rutabaga has been demonstrated in the adult fly, nonetheless, the embryonic cell culture system provides an excellent preparation that can be manipulated easily in electrophysiological studies. Furthermore, embryonic neurons can be used to show whether the K+ current is altered in early life of the fly. It has been shown previously that short-term (10 min) treatment with dibutyryl (db) cAMP does not affect neuronal K+ current (Alshuaib and Byerly 1996), whereas long-term (2 d) treatment with db-cAMP enhances neuronal K+ current (Alshuaib and Mathew 1998). Moreover, neuronal K+ current was shown to be greater in dunce than in wild-type neurons (Alshuaib and Mathew 1998). dunce and rutabaga were shown to display altered firing patterns in giant (cleavage-arrested) cultured neurons (Zhao and Wu 1997). However, neuronal K+ current of normal embryonic cultures has not been investigated in the rutabaga mutant. In the present study, we compared the delayed-rectifier K+ current (IKDR) in wild-type and rutabaga neurons from normal embryonic cultures. IKDR was reduced in rutabaga neurons as compared with the wild-type, a defect that can impact neuronal excitability and, ultimately, learning and memory.
Waleed B Alshuaib - One of the best experts on this subject based on the ideXlab platform.
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pkc a differentially affects rutabaga and wild type drosophila neuronal potassium current
International Journal of Neuroscience, 2004Co-Authors: Waleed B Alshuaib, Mini V Mathew, M Y Hasan, Mohammed A FahimAbstract:Learning and memory are defective in the Drosophila mutant rutabaga, which has a low intracellular cyclic adenosine monophosphate (cAMP) concentration. The aim of this study was to compare modulation effects of protein kinase C activator (PKC-A) on the delayed-rectifier potassium current (IKDR) in wild-type and rutabaga neurons. IKDR was measured from cultured (2 days) wild-type and rutabaga neurons. The authors examined the effects of PKC-A on IKDR in wild-type and rutabaga neurons. IKDR was measured from neurons before and after addition of PKC-A to the external solution. IKDR was smaller in rutabaga neurons (380 ± 25 pA) than in wild-type neurons (529 ± 44 pA). IKDR was reduced by PKC-A more in wild-type (↓55 ± 6%) than in rutabaga (↓35 ± 8%) neurons (single-cell studies). In the presence of PKC-A, there was no difference in IKDR between wild-type (229 ± 31 pA) and rutabaga (242 ± 26 pA) neurons (population studies). These results indicate that PKC-A differentially affects the delayed--rectifier channe...
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differential effects of dopamine on a potassium current in cultured rutabaga and wild type drosophila cells
Neuroscience Research Communications, 2003Co-Authors: Waleed B Alshuaib, Mini V Mathew, M Y Hasan, Mohammed A FahimAbstract:The rutabaga mutation which has a low intracellular cyclic adenosine monophosphate (cAMP) concentration is defective in short-term memory. The aim of this study was to compare modulation effects of dopamine on the delayed-rectifier potassium current (IKDR) in rutabaga and wild-type Drosophila neurons. The conventional whole-cell patch-clamp technique was applied to cultured Drosophila neurons derived from embryonic neuroblasts. IKDR was measured from cultured (2 days) wild-type and rutabaga neurons. IKDR was smaller in rutabaga neurons (373 ± 38 pA) than in wild-type neurons (519 ± 40 pA) but there was no difference in IKDR activation in wild-type inactivation between the two genotypes. We examined the effects of dopamine on IKDR in wild-type and rutabaga neurons. IKDR was measured from neurons before and after addition of dopamine to the external solution. Dopamine application reduced IKDR in wild-type neurons but did not significantly affect IKDR in rutabaga neurons (single-cell studies). In the presence of dopamine there was no difference in IKDR between wild-type (344 ± 29 pA) and rutabaga (338 ± 27pA) neurons (population studies). These results indicate that dopamine differentially affects the delayed-rectifier channel in wild-type and rutabaga neurons. This can alter neuronal excitability in rutabaga and may affect the processing of neural signals necessary for learning and memory.
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serotonin reduces potassium current in rutabaga and wild type drosophila neurons
International Journal of Neuroscience, 2003Co-Authors: Waleed B Alshuaib, Mini V Mathew, M Y Hasan, Mohammed A FahimAbstract:The Drosophila learning mutant rutabaga is defective in short-term memory and has a reduced intracellular cyclic adenosine monophosphate (cAMP) concentration. The delayed-rectifier potassium current (IKDR) was measured from cultured (2 days) wild-type and rutabaga neurons. IKDR was smaller in rutabaga neurons (382 - 41 pA) than in wild-type neurons (542 - 33 pA). IKDR was measured from neurons before and after addition of serotonin to the external solution. IKDR was reduced by serotonin in wildtype ( O 37 - 7%) and rutabaga ( O 33 - 6%) neurons (single-cell studies). In the presence of serotonin, IKDR was smaller in rutabaga (218 - 24 pA) than in wild-type (426 - 35 pA) neurons (population studies). These results indicate that serotonin has affected IKDR so that the inherent difference between the two genotypes was preserved.
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reduced delayed rectifier k current in the learning mutant rutabaga
Learning & Memory, 2002Co-Authors: Waleed B Alshuaib, Mini V MathewAbstract:The Drosophila mutations rutabaga and dunce affect learning and memory due to defects in cAMP metabolism. The dunce mutant has a high intracellular cAMP concentration owing to cAMP-specific phosphodiesterase (PDE) disruption (Byers et al. 1981). The rutabaga mutant has a low intracellular cAMP concentration due to elimination of a calcium/cadmodulin-responsive adenylyl cyclase. The ability of the cyclase catalytic subunit to interact with calcium/cadmodulin may be affected in rutabaga (Livingstone et al. 1984; Levin et al. 1992). dunce and rutabaga, originally identified for affecting learning and memory (Dudai et al. 1976) have been shown to alter synaptic plasticity (Zhong and Wu 1991), disrupt habituation (Engel and Wu 1996), and reduce growth cone motility (Kim and Wu 1996). cAMP-dependent modulation of ion channels has been shown to modify impulse activity of neurons (Kaczmarek and Kauer 1983). Modulation of neuronal electrical properties can change the operation of neural networks, it may be an important cellular mechanism for activity-dependent conditioning of behavior. Classical conditioning of the Aplysia siphon and tail-withdrawal reflex is believed to rely on presynaptic facilitation (Kandel et al. 1983). However, this form of simple learning, which depends on the synapse, cannot occur in complete isolation from the cell body, because changes in neuronal function can impact synaptic function. K+ current is one of the fundamental factors that regulate neuronal excitability (Klee et al. 1995) and neuronal function (Le Masson et al. 1993). Investigation of somal K+ current is required to elucidate possible changes in neuronal function of the Drosophila learning mutants. The learning deficit in rutabaga has been demonstrated in the adult fly, nonetheless, the embryonic cell culture system provides an excellent preparation that can be manipulated easily in electrophysiological studies. Furthermore, embryonic neurons can be used to show whether the K+ current is altered in early life of the fly. It has been shown previously that short-term (10 min) treatment with dibutyryl (db) cAMP does not affect neuronal K+ current (Alshuaib and Byerly 1996), whereas long-term (2 d) treatment with db-cAMP enhances neuronal K+ current (Alshuaib and Mathew 1998). Moreover, neuronal K+ current was shown to be greater in dunce than in wild-type neurons (Alshuaib and Mathew 1998). dunce and rutabaga were shown to display altered firing patterns in giant (cleavage-arrested) cultured neurons (Zhao and Wu 1997). However, neuronal K+ current of normal embryonic cultures has not been investigated in the rutabaga mutant. In the present study, we compared the delayed-rectifier K+ current (IKDR) in wild-type and rutabaga neurons from normal embryonic cultures. IKDR was reduced in rutabaga neurons as compared with the wild-type, a defect that can impact neuronal excitability and, ultimately, learning and memory.
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reduced delayed rectifier k current in the learning mutant rutabaga
Learning & Memory, 2002Co-Authors: Waleed B Alshuaib, Mini V MathewAbstract:The Drosophila mutations rutabaga and dunce affect learning and memory due to defects in cAMP metabolism. The dunce mutant has a high intracellular cAMP concentration owing to cAMP-specific phosphodiesterase (PDE) disruption (Byers et al. 1981). The rutabaga mutant has a low intracellular cAMP concentration due to elimination of a calcium/cadmodulin-responsive adenylyl cyclase. The ability of the cyclase catalytic subunit to interact with calcium/cadmodulin may be affected in rutabaga (Livingstone et al. 1984; Levin et al. 1992). dunce and rutabaga, originally identified for affecting learning and memory (Dudai et al. 1976) have been shown to alter synaptic plasticity (Zhong and Wu 1991), disrupt habituation (Engel and Wu 1996), and reduce growth cone motility (Kim and Wu 1996). cAMP-dependent modulation of ion channels has been shown to modify impulse activity of neurons (Kaczmarek and Kauer 1983). Modulation of neuronal electrical properties can change the operation of neural networks, it may be an important cellular mechanism for activity-dependent conditioning of behavior. Classical conditioning of the Aplysia siphon and tail-withdrawal reflex is believed to rely on presynaptic facilitation (Kandel et al. 1983). However, this form of simple learning, which depends on the synapse, cannot occur in complete isolation from the cell body, because changes in neuronal function can impact synaptic function. K+ current is one of the fundamental factors that regulate neuronal excitability (Klee et al. 1995) and neuronal function (Le Masson et al. 1993). Investigation of somal K+ current is required to elucidate possible changes in neuronal function of the Drosophila learning mutants. The learning deficit in rutabaga has been demonstrated in the adult fly, nonetheless, the embryonic cell culture system provides an excellent preparation that can be manipulated easily in electrophysiological studies. Furthermore, embryonic neurons can be used to show whether the K+ current is altered in early life of the fly. It has been shown previously that short-term (10 min) treatment with dibutyryl (db) cAMP does not affect neuronal K+ current (Alshuaib and Byerly 1996), whereas long-term (2 d) treatment with db-cAMP enhances neuronal K+ current (Alshuaib and Mathew 1998). Moreover, neuronal K+ current was shown to be greater in dunce than in wild-type neurons (Alshuaib and Mathew 1998). dunce and rutabaga were shown to display altered firing patterns in giant (cleavage-arrested) cultured neurons (Zhao and Wu 1997). However, neuronal K+ current of normal embryonic cultures has not been investigated in the rutabaga mutant. In the present study, we compared the delayed-rectifier K+ current (IKDR) in wild-type and rutabaga neurons from normal embryonic cultures. IKDR was reduced in rutabaga neurons as compared with the wild-type, a defect that can impact neuronal excitability and, ultimately, learning and memory.
Randall R Reed - One of the best experts on this subject based on the ideXlab platform.
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preferential expression of the drosophila rutabaga gene in mushroom bodies neural centers for learning in insects
Neuron, 1992Co-Authors: Lonny R Levin, Randall R Reed, Ronald L DavisAbstract:Abstract Seven lines were isolated with P element insertions in the cytogenetic vicinity of the learning and memory gene, rutabaga , from an enhancer detector screen designed to mark genes preferentially expressed in mushroom bodies. Six of these lines performed poorly in learning and memory tests, and several failed to complement an existing rutabaga allele. Molecular cloning revealed that the P elements were inserted in the putative promoter of the rutabaga gene. RNA in situ hybridization and immunohistochemistry demonstrated that the expression of the rutabaga gene, which encodes a Ca 2+ /calmodulin-responsive adenylyl cyclase, is markedly elevated in the mushroom bodies of normal flies and that the insertion elements compromised its expression in the new rutabaga mutants. The reisolation of a known learning and memory gene, but with a heretofore unknown expression pattern, strongly supports the postulate that mushroom bodies are principal sites mediating olfactory learning and memory.
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the drosophila learning and memory gene rutabaga encodes a ca2 calmodulin responsive adenylyl cyclase
Cell, 1992Co-Authors: Lonny R Levin, Paul Feinstein, Ronald L Davis, Paul M Hwang, Randall R ReedAbstract:Abstract Four putative adenylyl cyclase genes from Drosophila melanogaster were identified by virtue of their extensive sequence homology with mammalian cyclases. One corresponds to the learning and memory gene rutabaga and is most similar to the mammalian brain Ca2+calmodulin (CaM)-responsive cyclase. In a mammalian expression system, rutabaga cyclase activity was stimulated approximately 5-fold by the presence of Ca2+CaM. A point mutation, identified at this locus in rut1 mutant flies, resulted in loss of detectable adenylyl cyclase activity. New P element insertion-induced rutabaga mutations mapped to within 200 nucleotides of the 5′ end of the rutabaga cDNA. These data confirm the identity of the rutabaga locus as the structural gene for the Ca2+CaM-responsive adenylyl cyclase and show that the inactivation of this cyclase leads to a learning and memory defect.
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The Drosophila learning and memory gene rutabaga encodes a Ca2+/Calmodulin-responsive adenylyl cyclase.
Cell, 1992Co-Authors: Lonny R Levin, Paul Feinstein, Ronald L Davis, Paul M Hwang, Randall R ReedAbstract:Abstract Four putative adenylyl cyclase genes from Drosophila melanogaster were identified by virtue of their extensive sequence homology with mammalian cyclases. One corresponds to the learning and memory gene rutabaga and is most similar to the mammalian brain Ca2+calmodulin (CaM)-responsive cyclase. In a mammalian expression system, rutabaga cyclase activity was stimulated approximately 5-fold by the presence of Ca2+CaM. A point mutation, identified at this locus in rut1 mutant flies, resulted in loss of detectable adenylyl cyclase activity. New P element insertion-induced rutabaga mutations mapped to within 200 nucleotides of the 5′ end of the rutabaga cDNA. These data confirm the identity of the rutabaga locus as the structural gene for the Ca2+CaM-responsive adenylyl cyclase and show that the inactivation of this cyclase leads to a learning and memory defect.
Lonny R Levin - One of the best experts on this subject based on the ideXlab platform.
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preferential expression of the drosophila rutabaga gene in mushroom bodies neural centers for learning in insects
Neuron, 1992Co-Authors: Lonny R Levin, Randall R Reed, Ronald L DavisAbstract:Abstract Seven lines were isolated with P element insertions in the cytogenetic vicinity of the learning and memory gene, rutabaga , from an enhancer detector screen designed to mark genes preferentially expressed in mushroom bodies. Six of these lines performed poorly in learning and memory tests, and several failed to complement an existing rutabaga allele. Molecular cloning revealed that the P elements were inserted in the putative promoter of the rutabaga gene. RNA in situ hybridization and immunohistochemistry demonstrated that the expression of the rutabaga gene, which encodes a Ca 2+ /calmodulin-responsive adenylyl cyclase, is markedly elevated in the mushroom bodies of normal flies and that the insertion elements compromised its expression in the new rutabaga mutants. The reisolation of a known learning and memory gene, but with a heretofore unknown expression pattern, strongly supports the postulate that mushroom bodies are principal sites mediating olfactory learning and memory.
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the drosophila learning and memory gene rutabaga encodes a ca2 calmodulin responsive adenylyl cyclase
Cell, 1992Co-Authors: Lonny R Levin, Paul Feinstein, Ronald L Davis, Paul M Hwang, Randall R ReedAbstract:Abstract Four putative adenylyl cyclase genes from Drosophila melanogaster were identified by virtue of their extensive sequence homology with mammalian cyclases. One corresponds to the learning and memory gene rutabaga and is most similar to the mammalian brain Ca2+calmodulin (CaM)-responsive cyclase. In a mammalian expression system, rutabaga cyclase activity was stimulated approximately 5-fold by the presence of Ca2+CaM. A point mutation, identified at this locus in rut1 mutant flies, resulted in loss of detectable adenylyl cyclase activity. New P element insertion-induced rutabaga mutations mapped to within 200 nucleotides of the 5′ end of the rutabaga cDNA. These data confirm the identity of the rutabaga locus as the structural gene for the Ca2+CaM-responsive adenylyl cyclase and show that the inactivation of this cyclase leads to a learning and memory defect.
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The Drosophila learning and memory gene rutabaga encodes a Ca2+/Calmodulin-responsive adenylyl cyclase.
Cell, 1992Co-Authors: Lonny R Levin, Paul Feinstein, Ronald L Davis, Paul M Hwang, Randall R ReedAbstract:Abstract Four putative adenylyl cyclase genes from Drosophila melanogaster were identified by virtue of their extensive sequence homology with mammalian cyclases. One corresponds to the learning and memory gene rutabaga and is most similar to the mammalian brain Ca2+calmodulin (CaM)-responsive cyclase. In a mammalian expression system, rutabaga cyclase activity was stimulated approximately 5-fold by the presence of Ca2+CaM. A point mutation, identified at this locus in rut1 mutant flies, resulted in loss of detectable adenylyl cyclase activity. New P element insertion-induced rutabaga mutations mapped to within 200 nucleotides of the 5′ end of the rutabaga cDNA. These data confirm the identity of the rutabaga locus as the structural gene for the Ca2+CaM-responsive adenylyl cyclase and show that the inactivation of this cyclase leads to a learning and memory defect.