On mechanical agitation, bas1 flies show a stereotypical behavioral sequence of initial spasm, paralysis, delayed spasm and recovery of normal posture. The two spasms are manifested by collapse of the body, high-frequency wing flapping, leg extension, and fully curved abdomen. Seizing females often lay eggs. Electroconvulsive stimulation delivered to the brain of bas1 flies reproducibly induces the bang-sensitive repertoire of seizure behaviour; such electroconvulsive seizures can actually be induced in wild-type flies but this requires more extreme stimulus intensities than for bas1 flies. The failure and recovery of the giant fibre (GF) pathway during seizure can be detected by recording the dorsal longitudinal muscle (DLM) physiological response. Following 1 Hz brain stimulation, bas1 mutants have a significantly longer period of DLM response failure compared to wild type. Additionally, the maximal initial discharge induction is shifted toward lower stimulus intensities in the mutant flies. Delivery of a second stimulus after the onset of the delayed discharge (DD) phase of the DLM response causes a brief suppression of DD and a slight delay in response recovery, an effect that is more pronounced in bas1 mutants than wild type. Delivery of a second stimulus after seizure recovery induces a refractory period during which DLM response failure is shortened and the DD stage is earlier and for a shorter duration; this refractory period is shorter in bas1 flies than in wild type.
Bang-sensitive mutant. Flies usually show abnormal spontaneous activity ("seizures") in the dorsal longitudinal muscle (DLM) lasting approximately 0.5-3 seconds after the delivery of an electrical buzz (50-400 msec) to the brain. Stimulation of the giant fibre (GF) usually fails to evoke DLM potentials following the buzz. This failure lasts for 46 +/- 20 seconds. There is a close correlation between the seizure and failure phenotypes; if a seizure occurs, a failure also occurs in greater than 95% of cases, while failures without seizures occurred in approximately 10% of cases. GF evoked responses by the DLM are abnormal during recovery from the buzz. After recovery, there is a refactory period during which a buzz is less effective at inducing seizures and failures.
Physiological defect: a striking reduction of spike frequency in the anterior postalar (APA) and anterior notopleural (ANP) after mechanical stimulus.
Slow recovery from the prolonged depolarization after potential (PDA). Affect retinula cell physiology.
Bang sensitive paralytic mutant. At 38oC bas mutants become paralysed, without banging, within 12-20 seconds.
Striking culture vial sharply on hard surface immobilizes bas flies for 30-40 seconds. Rapid recovery followed by refractory period of an hour. Suppressed by mlenap-ts1 at permissive temperatures; at temperatures above 37.5oC bas flies quickly paralyzed; no detectable physiological abnormalities at neuromuscular junction in bas larvae (Ganetzky and Wu). In experiments on photoreceptor function, recovery of prolonged depolarization afterpotentials (induced by strong blue light) abnormally slow following exposure to orange light (Homyk and Pye, 1989).
bas1 has abnormal neurophysiology phenotype, enhanceable by parabss1
bas1 has bang sensitive phenotype, enhanceable by parabss1
bas1 has abnormal behavior phenotype, non-enhanceable by Df(2L)TW1/+
bas1 has abnormal behavior phenotype, non-suppressible by Df(2L)TW1/+
bas1 is an enhancer of abnormal neurophysiology phenotype of parabss1
bas1 is an enhancer of bang sensitive phenotype of parabss1
bas1 has muscle cell of abdominal 1 dorsal longitudinal muscle phenotype, enhanceable by parabss1
bas1 is an enhancer of muscle cell of abdominal 1 dorsal longitudinal muscle phenotype of parabss1
bas1, parabss1 has mesothoracic tergotrochanter muscle cell phenotype
Following mechanical agitation, bss1 bas1 double mutant flies have a prolonged paralysis and take longer to recover following spasm than single mutants. These double mutants also have an enhanced susceptibility to electroconvulsion compared to single mutants with a prolonged DLM response failure. The sensitivity for response failure induction and maximal initial discharge induction is similar in the double mutants to bss1 single mutants. Delivery of a second stimulus after the onset of DD causes a greater suppression of DD and a more delayed response recovery in double mutants than either single mutant. Additionally, delivery of a second stimulus after seizure recovery induces a shorter refractory period in bss1 bas1 double mutants. The jump muscle TTMs have an earlier response recovery following electroconvulsive stimuli, compared to DLMs; this effect is much more pronounced in bss1 bas1 mutants than in wild-type flies. Gynandromorph analysis shows that the recovery time of DLM responses to test stimuli applied to the brain is progressively lengthened as the number of bss1 bas1 mutant neurons in the GF pathway increases.
No apparent defect in the larval neuromuscular junction preparation. Behavioral phenotype suppressed by mlenap-ts1, even at permissive temperatures.