Identification of the neuropeptide transmitter proctolin in Drosophila larvae: characterization of muscle fiber-specific neuromuscular endings.

The cellular localization of the peptide neurotransmitter proctolin was determined for larvae of the fruitfly Drosophila melanogaster. Proctolin was recovered from the CNS, hindgut, and segmental bodywall using reverse-phase HPLC, and characterized by bioassay, immunoassay, and enzymatic analysis. A small, stereotyped population of proctolin-immunoreactive neurons was found in the larval CNS. Several of the identified neurons may be efferents. In the periphery, proctolin-immunoreactive neuromuscular endings were identified on both visceral and skeletal muscle fibers. On the hindgut, the neuropeptide is associated with endings on intrinsic circular muscle fibers. We propose that the hindgut muscle fibers are innervated by central neurons homologous to previously described proctolinergic efferents of grasshoppers. The segmental bodywall innervation consists of a pattern of segment-specific junctions on several singly identifiable muscle fibers. While it is generally accepted that Drosophila muscle fibers are innervated by glutamatergic motoneurons, our data indicate that a specialized subset of muscle fibers are also innervated by peptidergic efferents.

Chemical characterization of persistent immunoreactive glucagon in eviscerated rats.

Extraction of rat submaxillary salivary glands and ileal mucosa yielded a single immunoreactive glucagon component of 25,000 daltons and a major peak of approximately 9,000 daltons respectively. Eviscerated rats with and without functional livers were found to have decreased, but persistent levels of immunoreactive glucagon and total immunoreactive glucagon, as measured with a pancreatic specific and cross reacting antiserum respectively. Gel filtration of serum samples on Sephadex G-50 fine and G-200 superfine demonstrated that there was no measurable 3485, 9000 or 25,000 dalton glucagon immunoreactivity. The persistent immunoreactive glucagon in the serum of eviscerated rats is a heterogeneous mixture of nonspecific materials and does not contain submaxillary or intestinal glucagon-related materials. These findings suggest caution in the interpretation of glucagon immunoreactivity in serum and demonstrate the necessity for chromatographic analysis of circulating IRG.

Neutrophils dysfunction during the course of intra-abdominal infection.

Twenty-four patients with intra-peritoneal infections were studied sequentially to evaluate neutrophil chemotaxis, spontaneous migration, and chemiluminescence. In six patients, infection was due to spontaneous disease processes and 18 others, infection was a sequel of intra-abdominal operation. In the patients studied prior to drainage, operation chemotaxis, spontaneous migration and chemiluminescence were all significantly depressed. Operation resulted in a further depression of these functions, and recovery of neutrophil migratory responses was delayed for two weeks. During the period of functional depression, 16 patients developed recurrent infections (nine episodes of intra-abdominal abscess, and 12 episodes of extra-abdominal infection). These infection were associated with a fall-off in neutrophil migratory and chemiluminescence responses prior to clinical evidence of infection. This study suggests that the delayed recovery of neutrophil function may be related to the recurrent infection seen in this patient population. Further, monitoring of neutrophil function in patients recovering from intra-abdominal infection may provide early evidence of recurrent infection.

The autoimmune response to male reproductive tissues of rabbits. IV. Induction of autosensitization to central accessory tissue by the intraabdominal release of endogenous secretions.

A study is described in which tissue- and secretion-specific autosensitization was induced in adult male rabbits through intraabdominal cannulation of one or more of their central accessory glands. Both primary and secondary humoral antibodies were elicited by this procedure, as determined by tanned cell hemagglutination and passive hemolysis, i.e., complement fixation. The secondary antibody responses were elicited by (i) cannulation of animals which had been previously stimulated by cryosurgery or combined cryosurgery and injection of pooled accessory tissue extract, and (ii) isoinjection of previously cannulated animals with accessory tissue extract. Primary antibody responses were less in animals castrated at the time of cannulation compared to those in noncastrated animals; but, paradoxically, subsequent challenges with tissue extract induced higher secondary antibody titers in castrated animals. These observations may be explained in castrates by (i) reduced uptake of antibodies--a result of the sparing effect on circulating antibodies in castrated animals because of accessory tissue atrophy, or (ii) increased production of antibodies through postcastration immune enhancement. In noncastrates secondary antibody depression may be related to (i) increased absorption of antibodies by an accessory gland complex which is much larger than that found in castrates, or (ii) tolerance, due to exposure of the antibody-producing system to excess accessory tissue antigen.

PIP: Tissue- and secretion-specific autosensitization was produced in adult male rabbits by intraabdominal cannulation of 1 or more of the accessory sex glands. Tanned cell hemagglutination and passive hemolysis confirmed the presence of both primary and secondary humoral antibodies. The secondary antibody responses resulted from cannulation of animals which had been stimulated by cryosurgery alone or in combination with injection of pooled accessory extract tissue, and isoinjection of cannulated rabbits with accessory tissue extract. The primary antibody response elicited in rabbits castrated at the time of cannulation was less than that in noncastrated animals. However, the introduction of tissue extract produced higher titers of secondary antibodies in castrates than in noncastrated animals. In castrated animals, this may be due to either a reduced uptake of antibodies caused by atrophy of the accessory glands, or an increased production of antibodies which enhances the immune effect. In the case of noncastrated rabbits, this result may be explained by an increased absorption of antibodies by the accessory sex glands, or tolerance resulting from exposure of the antibody-producing system to excess antigens in accessory gland tissue.