title: Gustatory habituation in Drosophila relies on rutabaga (adenylate cyclase)-dependent plasticity of GABAergic inhibitory neurons.
abstract: In some situations, animals seem to ignore stimuli which in other contexts elicit a robust response. This attenuation in behavior, which enables animals to ignore a familiar, unreinforced stimulus, is called habituation. Despite the ubiquity of this phenomenon, it is generally poorly understood in terms of the underlying neural circuitry. Hungry fruit flies show a proboscis extension reflex (PER) when sensory receptors are stimulated by sugars. The PER is usually followed by feeding. However, if feeding is disallowed following sugar stimulation, PER is no longer robust, and the animal is considered to be habituated to this stimulus. Our results suggest that PER habituation requires an adenylate cyclase-dependent enhancement of inhibitory output of GABAergic neurons in the subesophageal ganglion (SOG), which mediates PER. GABA synthesis in and release from glutamic acid decarboxylase (GAD1) expressing neurons is necessary, and GABA(A) receptors on cholinergic neurons are required for PER habituation. The proposed inhibitory potentiation requires glutamate/NMDA-receptor signaling, possibly playing a role in stimulus selectivity. We explain why these data provide significant and independent support for a general model in which inhibitory potentiation underlies habituation in multiple neural systems and species.
authors.affiliation: National Centre for Biological Sciences, Tata Institute of Fundamental Research, Bangalore 560065, India. pushkarp@ncbs.res.in
authors.forename: Pushkar
authors.initials: P
authors.lastname: Paranjpe
authors.forename: Veronica
authors.initials: V
authors.lastname: Rodrigues
authors.forename: K
authors.initials: K
authors.lastname: VijayRaghavan
authors.forename: Mani
authors.initials: M
authors.lastname: Ramaswami
mesh_terms: D000262:Adenylyl Cyclases / Q000235:genetics / Q000378:metabolism*; D000344:Afferent Pathways / Q000502:physiology; D000818:Animals; D030801:Animals, Genetically Modified; D001921:Brain / Q000378:metabolism; D002241:Carbohydrates / Q000494:pharmacology; D004330:Drosophila; D029721:Drosophila Proteins / Q000235:genetics / Q000378:metabolism*; D059330:GABAergic Neurons / Q000187:drug effects / Q000502:physiology*; D017952:Ganglia, Invertebrate / Q000166:cytology; D041981:Gastrointestinal Tract / Q000294:innervation; D005968:Glutamate Decarboxylase / Q000378:metabolism; D049452:Green Fluorescent Proteins / Q000235:genetics / Q000378:metabolism; D006185:Habituation, Psychophysiologic / Q000235:genetics*; D009433:Neural Inhibition / Q000187:drug effects / Q000235:genetics*; D009473:Neuronal Plasticity / Q000187:drug effects / Q000235:genetics*; D010812:Physical Stimulation; D034622:RNA Interference / Q000502:physiology; D012018:Reflex / Q000235:genetics; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism
chemical_list: D002241:Carbohydrates; D029721:Drosophila Proteins; C557617:GAL4 protein, Drosophila; D014157:Transcription Factors; D049452:Green Fluorescent Proteins; D005968:Glutamate Decarboxylase; C402565:glutamate decarboxylase 1; D000262:Adenylyl Cyclases; C479926:Rut protein, Drosophila