Flies lacking all synapsins are unexpectedly healthy but are impaired in complex behaviour.
Vertebrate synapsins are abundant synaptic vesicle phosphoproteins that have been proposed to fine-regulate neurotransmitter release by phosphorylation-dependent control of synaptic vesicle motility. However, the consequences of a total lack of all synapsin isoforms due to a knock-out of all three mouse synapsin genes have not yet been investigated. In Drosophila a single synapsin gene encodes several isoforms and is expressed in most synaptic terminals. Thus the targeted deletion of the synapsin gene of Drosophila eliminates the possibility of functional knock-out complementation by other isoforms. Unexpectedly, synapsin null mutant flies show no obvious defects in brain morphology, and no striking qualitative changes in behaviour are observed. Ultrastructural analysis of an identified 'model' synapse of the larval nerve muscle preparation revealed no difference between wild-type and mutant, and spontaneous or evoked excitatory junction potentials at this synapse were normal up to a stimulus frequency of 5 Hz. However, when several behavioural responses were analysed quantitatively, specific differences between mutant and wild-type flies are noted. Adult locomotor activity, optomotor responses at high pattern velocities, wing beat frequency, and visual pattern preference are modified. Synapsin mutant flies show faster habituation of an olfactory jump response, enhanced ethanol tolerance, and significant defects in learning and memory as measured using three different paradigms. Larval behavioural defects are described in a separate paper. We conclude that Drosophila synapsins play a significant role in nervous system function, which is subtle at the cellular level but manifests itself in complex behaviour.
Godenschwege
Tanja A
TA
Theodor Boveri-Institut für Biowissenschaften, Lehrstuhl für Genetik und Neurobiologie, Am Hubland D-97074 Wuerzburg, Germany.
Reisch
Dietmar
D
Diegelmann
Sören
S
Eberle
Kai
K
Funk
Natalja
N
Heisenberg
Martin
M
Hoppe
Viviane
V
Hoppe
Jürgen
J
Klagges
Bert R E
BR
Martin
Jean-René
JR
Nikitina
Ekaterina A
EA
Putz
Gabi
G
Reifegerste
Rita
R
Reisch
Natascha
N
Rister
Jens
J
Schaupp
Michael
M
Scholz
Henrike
H
Schwärzel
Martin
M
Werner
Ursula
U
Zars
Troy D
TD
Buchner
Sigrid
S
Buchner
Erich
E
D000200:Action Potentials / Q000187:drug effects / Q000235:genetics / Q000502:physiology; D000818:Animals; D030801:Animals, Genetically Modified; D001522:Behavior, Animal / Q000187:drug effects / Q000502:physiology*; D015153:Blotting, Western / Q000379:methods; D002492:Central Nervous System Depressants / Q000494:pharmacology; D003001:Cloning, Molecular / Q000379:methods; D003216:Conditioning, Operant / Q000502:physiology; D004252:DNA Mutational Analysis; D004330:Drosophila / Q000235:genetics / Q000502:physiology*; D004558:Electric Stimulation / Q000379:methods; D000431:Ethanol / Q000494:pharmacology; D019706:Excitatory Postsynaptic Potentials / Q000235:genetics; D007150:Immunohistochemistry / Q000379:methods; D007163:Immunosorbent Techniques; D008564:Membrane Potentials / Q000235:genetics / Q000502:physiology; D008854:Microscopy, Electron; D009043:Motor Activity / Q000187:drug effects / Q000502:physiology; D016296:Mutagenesis / Q000502:physiology; D009469:Neuromuscular Junction / Q000235:genetics / Q000378:metabolism / Q000502:physiology; D011597:Psychomotor Performance / Q000502:physiology; D012725:Sexual Behavior / Q000187:drug effects / Q000502:physiology; D013569:Synapses / Q000378:metabolism / Q000648:ultrastructure; D016704:Synapsins / Q000172:deficiency* / Q000235:genetics / Q000502:physiology; D013572:Synaptic Vesicles / Q000235:genetics / Q000378:metabolism / Q000648:ultrastructure; D013997:Time Factors; D014018:Tissue Distribution; D014796:Visual Perception / Q000235:genetics / Q000502:physiology; D016138:Walking / Q000502:physiology; D014921:Wings, Animal / Q000502:physiology
D002492:Central Nervous System Depressants; D016704:Synapsins; D000431:Ethanol