Worm Breeder's Gazette 9(2): 53
These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.
Previous studies reported from this laboratory, using a wholemount immunocytochemical technique, indicate that a physiologically identified set of inhibitory motorneurons in Ascaris (the ventral and dorsal inhibitors) stain intensely with an antiserum prepared against the neurotransmitter gamma-aminobutyric acid (GABA) (WBG, vol. 8(2), p. 33). We have also observed staining of four neurons located at the anterior margin of the nerve ring which are probably analogous to the RME neurons (V,D,L,R) in C. elegans as well as staining in a variable number of other neurons in the head. We are now extending these immunocytochemical studies to sectioned material which, together with an analysis of H-GABA uptake, gives us a more complete view of GABA-related mechanisms in Ascaris.Staining of nerve cord sections with the GABA antiserum reveals a cluster of immunoreactive neuronal profiles in both the ventral and dorsal cords. The position of these neurites within the cords strongly suggests that they represent the processes of the inhibitory motorneurons. Staining of profiles on the side of the cord containing the excitatory motorneurons is not seen. In addition, none of the ventral cord interneurons stain with this antiserum, indicating that, if there are inhibitory interneurons in the ventral cord, they are probably not GABAnergic. A single stained profile, located just below the excitatory cluster, is seen in the ventral cord, and a single stained profile, located at the base of the dorsal cord, are also observed. Based on comparisons between sectioned material and wholemounts, we believe that these profiles represent the ventral and dorsal processes of RMEV and RMED, respectively. As autoradiographic analysis of specimens incubated with 0.5uM H- GABA shows that several neurons in the head are labeled, among them the RME cells, suggesting that these neurons possess an active uptake mechanism for this neurotransmitter. In the ventral and dorsal nerve cords, single processes, whose position and morphology suggest that they are the nerve cord processes of RMEV and RMED, are also labeled. However, the inhibitory motorneurons, which stain so intensely with the GABA antiserum, are not labeled with H-GABA. Heavy labeling of muscle (both cephalic and somatic) is also seen, but the functional significance of this is unknown. Thus, there appear to be at least two classes of nematode neurons with GABA-related markers: one class, which possesses a GABA-like immunoreactive substance as well as an uptake system for GABA (e.g., the RME cells); and a second class which possesses a GABA-like immunoreactive substance, but which lacks an uptake system for GABA (e. g., the inhibitory motorneurons). It is interesting to note that GABA uptake, a marker traditionally used by mammalian neuroanatomists to visualize neurons thought to use GABA as a neurotransmitter, does not result in the labeling of a class of physiologically identified inhibitory neurons in the nematode.