Immunocytochemical and Learning Studies of a Drosophila Melanogaster Neurological Mutant, No-Bridge^KS49 as an Approach to the Possible Role of the Central Complex

Abstract

no-bridge^KS49 (nob) has been shown to have a disturbed protocerebral bridge (pb). Using monoclonal antibodies that stain selectively some central complex regions we found that the protocerebral pridge defect is accompanied by a loss of certain inputs and outputs of the central complex. Mutant nob flies have a reduced climbing activity due to a reduced average walking speed and to a spastic state. Their mean longevity is drastically reduced, suggesting that nob is a pleiotropic gene. The nob mutant is impaired in habituation and in Pavlovian conditioning of the proboscis extension reflex (PER), although its initial reactivity to the sucrose stimulus is normal. Tested in habituation of the PER by ipsi- and contralateral stimulations, the nob mutant shows some difficulties in the “data exchange” between the two brain hemispheres, suggesting that the central complex may coordinate information processing in the two hemispheres.

Key Words:

• Drosophila melanogaster
• no-bridge mutant
• immunocytochemistry
• climbing activity
• longevity
• proboscis extension reflex
• habituation
• Pavlovian conditioning