Pleural Ganglia Research Articles

Identification and characterization of pleural neurons that inhibit tail sensory neurons and motor neurons in Aplysia: correlation with FMRFamide immunoreactivity

Neurons on the rostral edge of the ventral surface of the right pleural ganglion were identified as elements of the circuit mediating the defensive tail withdrawal reflex of Aplysia. These neurons produced IPSPs in tail sensory neurons and were classified into two groups, RPI4 and RPI5, according to their affinity for an antibody directed against FMRFamide. RPI4 was not FMRFamide immunoreactive, and RPI5 was. RPI4 and RPI5 were found to have different electrophysiological profiles. The summated IPSPs in sensory neurons produced by RPI4 developed more rapidly and had a shorter duration than those produced by RPI5. In addition, RPI4 produced IPSPs in the tail motor neurons, whereas RPI5 did not. Both RPI4 and RPI5 received excitatory synaptic inputs from stimulation of the pleural-abdominal connective as well as peripheral nerves P8 and P9, which innervate the tail and posterior part of the animal's body. These inputs were sufficient to elicit spikes. In RPI4, the excitatory synaptic inputs were followed by short and transient hyperpolarization, whereas in RPI5, the excitatory synaptic inputs were followed by slow and long-lasting hyperpolarization. Excitatory inputs elicited in RPI4 by stimulation of peripheral nerves appeared to be mediated, at least in part, by activation of tail sensory neurons. Intracellular stimulation of sensory neurons produced EPSPs in RPI4 that appeared to be monosynaptic. These results suggest that inhibitory interneurons underlying the circuit of the tail withdrawal reflex may play roles in mediating or modulating neuronal responses to tail stimulation. By inhibiting tail sensory and motor neurons, these interneurons may reduce the effectiveness of an animal's response to stimulation of the tail.

Distributed input to the tail-siphon withdrawal circuit in Aplysia from neurons in the J cluster of the cerebral ganglion

Plasticity in the circuits for the withdrawal reflexes has been correlated with several simple forms of nonassociative and associative learning in Aplysia, and biochemical, biophysical, and molecular mechanisms of plasticity in these circuits have been described. In order to examine network features of this plasticity, we identified and characterized a component of the modulatory circuitry for the tail-siphon withdrawal circuit. Activation of mechanoafferent neurons in the J cluster of the cerebral ganglion produced strong and distributed input to the tail-siphon withdrawal circuit. Stimulation of the J cells led to excitatory and inhibitory effects in the sensory neurons in the pleural ganglion, the tail motor neurons in the pedal ganglion, and several classes of interneurons in the pleural ganglion, including the multifunctional neuron LPI17. Activation of the J cells produced both fast and slow post-synaptic potentials in neurons of the tail-siphon withdrawal circuit. Of particular interest was the ability of the J cells to produce slow EPSPs in the pleural sensory neurons. These slow EPSPs were associated with an increase in the excitability of the sensory neurons, but no effect of the J cells on spike duration in the sensory neurons was observed. The J cells appear to mediate both sensory and modulatory inputs to the circuit for tail withdrawal.

Changes Occur in the Central Nervous System of the Nudibranch Berghia verrucicornis (Mollusca, Opisthobranchia) During Metamorphosis.

The structure of the larval and juvenile central nervous system (CNS) in Berghia verrucicornis, an aeolid nudibranch, was examined using 1-{mu}m serial sections. The CNS consists of paired optic, cerebral, pleural (also known as sub- and supra-intestinal ganglia), pedal, and buccal ganglia, and a single visceral ganglion. A pleurovisceral loop is present. The organization of the CNS changes as the nudibranch undergoes metamorphosis. In general, there is a condensation of the CNS. The cerebral and pleural ganglia fuse to form the prominent cerebropleural ganglia. The single visceral ganglion fuses with the pleural portion of the left cerebropleural ganglion. The buccal ganglia enlarge and fully organize into a cortex of nerve cell bodies and medulla of nerve fibers. Rhinophoral ganglia develop anterior to each cerebropleural ganglion and a pair of nervous processes extend from each: one to the developing rhinophore and the other anteroventral toward the mouth and associated structures. These metamorphic changes are similar to those seen in other commonly studied opisthobranch species, suggesting that Berghia verrucicornis is an appropriate model for the developmental examination of structure and function in molluscan nervous systems.

Defense reaction in the pond snail Planorbis corneus. II. Central pattern generator.

1. In the isolated CNS of the pond snail Planorbis corneus, spontaneous bursts of activity in the motor neurons (MNs) supplying the columellar muscle were occasionally observed. The biphasic pattern of this activity, with a shorter (3-5 s) initial burst and longer (20-40 s) subsequent burst, was similar to that of the motor output during the general ("whole-body") defense reaction. In preparations consisting of the CNS isolated with the columellar muscle or with the lung, spontaneous biphasic contractions of the muscle as well as openings of the pneumostome with a temporal pattern characteristic of the defense reaction were observed. These findings demonstrated that the efferent pattern of the defense reaction in the snail is, to a large extent, produced by a special neuronal mechanism (the central pattern generator, CPG) triggered by the sensory input, rather than generated by ongoing processing of sensory input. The CPG consists of two components responsible for generation of two phases of the defense reaction. A characteristic feature of the CPG is that the magnitude of its response depends in a graded fashion on the strength of the initial stimulus. 2. In the pleural ganglia there are at least two electrically connected interneurons (DRN1s) that play an important role in generation of the first phase of the defense reaction. Processes of the DRN1s form a ring passing through all (except pedal and buccal) ganglia. The DRN1s received an excitatory input when a peripheral nerve was stimulated. They generated action potentials of long (0.2-2 s) duration. The DRN1 from the right ganglion was studied in more detail.(ABSTRACT TRUNCATED AT 250 WORDS)

Mapping of neurons participating in the innervation of the body wall of the snail.

The results of experiments on the retrograde staining of the left-sided cutaneous nerves of the pedal ganglia of the snail Helix lucorum L. are presented in this paper. The bodies of nerve cells contributing processes to these nerves were identified by means of the precipitation of nickel and cobalt ions by rubeanic acid. A large number of neurons were found, including the parietal command neurons, in all the ganglia, with the exception of the buccal. An especially large number of neurons were stained in the ipsilateral pedal, pleural, and parietal ganglia.

Identification and characterization of a multifunction neuron contributing to defensive arousal in Aplysia.

1. The tail withdrawal reflex is mediated by a monosynaptic circuit composed of tail sensory and motor neurons, but there appear to be additional neuronal elements that also contribute to the reflex. A newly identified interneuron, called LP117, was located in the pleural ganglion. This neuron formed a parallel excitatory pathway between sensory and motor neurons. The distinguishing feature of LP117 was its ability to elicit a long-lasting (5-100 s) excitatory postsynaptic potential (EPSP) in the motor neuron. 2. Intracellular labeling of LP117 revealed axons projecting to the cerebral and abdominal as well as the pedal ganglia. Simultaneous intracellular recordings confirmed the widely divergent output of LP117 to tentacle motor neurons in the cerebral ganglion, as well as to gill, siphon, and ink motor neurons in the abdominal ganglion. 3. Also receiving input were abdominal neurons L29, which excites LFs motor neurons and facilitates LE sensory neurons, and L25, which is part of the pattern-generating network underlying respiratory pumping. Thus LP117 appears to be a neural element important for the conduction of information about tail stimulation to ganglia that are not innervated by tail sensory neurons themselves. Moreover, the divergent outputs suggest that LP117 is an element of a neural circuit underlying defensive arousal. 4. LP117 produced slow EPSPs in several motor neurons. The long time course of the EPSP could prolong the burst in the motor neuron produced by LP117 itself as well as increase the effectiveness of coincident synaptic input. This suggests that an important function of this interneuron is to extend the duration of the response to tail stimulation in the motor neuron. This could account for the relatively long time course of the motor neuron response to tail stimulation compared with that of the sensory neuron. 5. Sensitization is a form of nonassociative learning that produces changes in the amplitude and duration of reflex responses. It seems unlikely that all of these changes can be attributed to enhanced amplitude of the sensory-motor synapse, however. Therefore LP117 may itself be a site of plasticity for reflexes elicited by tail stimulation.

Activity-dependent depression of mechanosensory discharge in Aplysia.

1. Inhibition of action potential discharge in Aplysia mechanosensory neurons after noxious stimulation has not been described previously. The present studies investigated depressive effects of prolonged noxious stimulation and repetitive intracellular activation on the number and latency of action potentials evoked by test stimuli applied to the tail or the nerve innervating the tail. Action potential discharge was monitored in the somata of mechanonociceptors in the pleural ganglia. 2. Repeated brief pinches delivered at 5-s intervals to a sensory neuron's receptive field on the tail initially caused intense activation (10-25 spikes recorded in the soma) followed by a progressive decrease or "wind-down" of spike number during subsequent pinches. 3. Repeated application to the tail of noxious shock that caused intense activation of sensory neurons (10-22 spikes during the initial shock) produced progressive wind-down of discharge similar to that produced by repeated tail pinch. However, sensory neurons that showed lower activation (1-9 spikes) to the same shock displayed wind-up of discharge during the 10 shocks. These results suggested that prolonged, intense activation depresses subsequent action potential discharge. 4. Changes in the time required for spikes evoked in the tail to reach the central soma were used as an indicator of changes in the excitability and/or conduction velocity of peripheral branches. Repeated pinch within a sensory neuron's receptive field caused an increase in the latency of discharge elicited by test shocks within the receptive field that lasted > or = 10 min. Repetitive intracellular stimulation of the sensory neuron soma caused a similar increase in latency. 5. Repetitive soma activation decreased the number of spikes evoked 10 s later by a test shock in the sensory neuron's receptive field, indicating that spike activity depresses the initiation and/or conduction of spikes in peripheral branches. Surprisingly, repeated pinch to the receptive field caused no significant change in the number of spikes evoked by the same test shock. This difference suggests that tail pinch produces concomitant facilitatory effects that oppose the depressive effects of intense spike activity. 6. Depressive effects of repeated pinch and repetitive soma activation were expressed in the axon between the receptive field and the CNS. Spikes evoked by brief test shocks delivered to the nerve containing the axon of the recorded sensory neuron showed a transient increase in latency (perhaps due to a decrease in conduction velocity) after either procedure. Repeated pinch, but not repetitive soma activation, also caused an increase in spike threshold in the nerve.(ABSTRACT TRUNCATED AT 400 WORDS)

Rapid amplification and facilitation of mechanosensory discharge in Aplysia by noxious stimulation

1. Little is known about modulation of action potential discharge in Aplysia mechanosensory neurons during defensive responses. The present studies examined rapid effects of noxious stimulation (occurring within 0.5-10 s) on the number of action potentials evoked by test stimuli delivered to the tail. Responses were monitored in the somata of mechanonociceptors in the pleural ganglion. A major hypothesis to be tested was that an important function of previously described alterations of membrane conductances in the sensory neuron soma is to generate an after-discharge that amplifies sensory signals during severe noxious stimulation of the cell's receptive field. 2. Discharge of spikes evoked by a moderate tap to one part of a sensory neuron's receptive field on the tail was enhanced by strong shock delivered 10 s earlier to another part of the field. Part of this enhancement appears to be due to a decrease in conduction block in central regions of the sensory neuron. 3. Repeated delivery of innocuous, moderately intense tail shock at 5-s intervals caused a progressive increase ("wind-up") of discharge, whereas repeated delivery of weak tail shock had no significant effect on discharge. In some cases the increase in action potential number involved a buildup of afterdischarge. 4. A single strong tail pinch sometimes induced an afterdischarge lasting < or = 2 s. Afterdischarge could also be induced in the isolated nervous system by intense electrical stimulation of the nerve containing the sensory neuron's main axon. 5. Several observations suggest that afterdischarge requires cooperative effects of a relatively large number of coactivated fibers in the test pathway. In contrast to pinching stimuli (which stimulated a larger part of the tail), intense, punctate stimulation with von Frey hairs failed to produce afterdischarge. Weaker tail or nerve stimulation failed to produce afterdischarge, even when short-latency, high-frequency discharge was evoked in the sensory neuron. 6. Cooperative effects on afterdischarge may differ from those involved in activity-dependent enhancement of presynaptic facilitation because simultaneous pairing of high-frequency activation of a single test sensory neuron with strong stimulation of a peripheral nerve lacking an axon of the tested sensory neuron was not sufficient to produce afterdischarge. The cooperative effects on afterdischarge may function to encode information about both the severity and spatial extensiveness of an injury. 7. Artificial hyperpolarization of the soma often reversibly reduced or abolished afterdischarge evoked by stimulating the nerve or tail. Thus the afterdischarge is often generated in or near the sensory neuron soma.(ABSTRACT TRUNCATED AT 400 WORDS)

Neural structures in the receptive field of pleural ganglion mechanosensory neurons of Aplysia californica

The peripheral processes of the mechanoafferents that, when stimulated, initiate the much-studied tail withdrawal reflex of Aplysia californica have not been characterized. We show that immunofluorescence staining for class III β-tubulin highlights neurons and reveals nerve tracts and fine neuronal processes in Aplysia tissue. Coupled with transmission and scanning electron microscopy, class III β-tubulin immunofluorescence is consistent with the possibility that mechanoafferents in the receptive field of pleural ganglion mechanosensory neurons penetrate the tail epidermis and terminate as ciliated endings. This view is reinforced by comparisons among neuronal processes in several mechanosensory epidermal regions and in a chemosensory epidermis.

The sodium influx stimulating peptide of the pulmonate freshwater snail Lymnaea stagnalis

In Lymnaea stagnalis integumental Na + uptake is stimulated by the sodium influx stimulating (SIS)-peptide. Its primary structure was determined as: SRTQSRFASYELMGTEGTECVTTKTISQICYQCATRHEDSFVQVYQECCKKEMGLREYCEEIYTELPIRSGLWQPN. Antisera raised against parts of SIS-peptide stained neurons in the visceral, parietal, and pleural ganglia, and in the proximal parts of the intestinal, anal, and right internal pallial nerves. Locations and axon projection patterns of these neurons suggest that they represent the previously described neurosecretory yellow cells.

New Interpretation of a Nudibranch Central Nervous System Based on Ultrastructural Analysis of Neurodevelopment in Melibe leonina. I. Cerebral and Visceral Loop Ganglia.

Development of the `cerebropleural' ganglia in the dendronotid nudibranch Melibe leonina (Gould, 1852) was examined by electron microscopy of semi-serial sections through larval stages. Although comparative neuroanatomical studies suggest that the paired cerebropleurals of nudibranchs are formed by fusion of cerebral and pleural ganglia, plus all other ancestral ganglia of the visceral loop, my study indicates that the pleural ganglia are not part of these compound ganglionic masses. In Melibe larvae, the cerebral, optic, and rhinophoral ganglia, arise from pre-trochal cephalopedal ectoderm. At hatching stage, the visceral loop extends from the two cerebral ganglia, is non-ganglionated, and forms a complete circuit beneath the esophagus. Ganglia that subsequently develop along the visceral loop, which were identified as subintestinal, visceral, supraintestinal, and possibly right parietal ganglia, arise from placodes of visceropallial ectoderm that show torsional displacements. In addition, a cluster of neurons, presumed to be osphradial, lies close to the rim of the right mantle fold. Detorsion of the visceral loop is accomplished by migration of subintestinal neurons along the visceral loop fiber tract, not by visceral loop shortening. Localized elongation of a different segment of this fiber tract during metamorphosis displaces the visceral ganglion to the left, where it fuses with subintestinal and left cerebral ganglia.

New Interpretation of a Nudibranch Central Nervous System Based on Ultrastructural Analysis of Neurodevelopment in Melibe leonina. II. Pedal, Pleural, and Labial Ganglia.

Electron microscopical analysis of semi-serial sections through larval stages of the dendronotid nudi-branch Melibe leonina (Gould, 1852) revealed paired placodes of neurogenic ectoderm at the base of the foot. The location of these laterocephalic placodes corresponds to descriptions of the ectodermal site generating pleural neurons in prosobranchs. In Melibe, there are two sites of neuronal ingression within each laterocephalic placode. Neurons ingressing from one of these sites join the cerebral ganglia, and their initial axons extend into the cerebrobuccal connectives or run distally along the esophagus. I identify these neurons as homologues of labial ganglia neurons in archeogastropods. However, neurons derived from the second ingression site within each laterocephalic placode join the pedal ganglia. Pedal ganglia are present in hatching veligers and are linked to the cerebral ganglia by cerebropedal connectives associated with the statocyst nerves. A second connective between each cerebral and pedal ganglia appears at the onset of neuronal ingression from the laterocephalic placodes. Peripheral axons branching from this second pair of connectives are associated with laterocephalic neurons that ingress to the pedal ganglia. I argue that these are pleural neurons, meaning that the pleural ganglia in Melibe are uncoupled from the visceral loop.

Identified FMRFamide-immunoreactive neuron LPL16 in the left pleural ganglion of Aplysia produces presynaptic inhibition of siphon sensory neurons

The gill- and siphon-withdrawal reflex of Aplysia undergoes transient inhibition following noxious stimuli such as tail shock. This behavioral inhibition appears to be due in part to transient presynaptic inhibition of the siphon sensory cells, which can be mimicked by application of the peptide FMRFamide. Although FMRFamide is widespread in the Aplysia nervous system, an FMRFamide-containing inhibitory neuron has not previously been identified. We have searched for such a neuron by combining FMRFamide immunofluorescence with fluorescent dye backfilling from the abdominal ganglion, the location of the siphon sensory cells. These methods localized a neuron in the left pleural ganglion, which we have named LPL16. LPL16 is FMRFamide immunoreactive; it is excited by tail shock; and stimulation of LPL16 produces inhibition of siphon sensory cell-to-motor cell postsynaptic potentials and narrowing of action potentials in the sensory cells in tetraethylammonium solution. These results indicate that LPL16 participates in the inhibitory effects of tail shock, and support the idea that FMRFamide plays a physiological role in the inhibition.

Identification of putative egg-laying hormone containing neuronal systems in gastropod molluscs

Of gastropod molluscs, only in the Aplysiidae and the Lymnaeidae have the genes encoding the respective egg-laying hormones been cloned and the neurons controlling egg laying and egg-laying behavior been identified. Immunocytochemistry, using antibodies raised against α-CDCP (one of the neuropeptides encoded on the egg-laying hormone gene of Lymnaea stagnalis), identified neurons in various species of gastropods. In the basommatophoran snail, Biomphalaria glabrata, large and small neurons were observed in areas of the central nervous system similar to where immunoreactive cells exist in L. stagnalis, i.e., in the cerebral and pleural ganglia. In the stylommatophoran snail ( Helix aspersa) and the slug ( Limax maximus), large immunopositive neurons occur in the visceral and right parietal ganglia. In L. maximus, small immunoreactive neurons were found in the cerebral ganglia while in H. aspersa similar cells were observed intermingled with the large cells in the visceral and right parietal ganglia. Similar to the situation in L. stagnalis, in the female part of the reproductive tract of B. glabrata, L. maximus, and A. californica, but not in H. aspersa, neurons and/or fiber tracts are present. The results indicate that egg-laying hormone precursor molecules of gastropod molluscs are phylogenetically closely related. The α-CDCP antiserum may allow the identification of hitherto unknown egg-laying regulating systems of gastropod molluscs.

Inhibitory neuron produces heterosynaptic inhibition of the sensory-to-motor neuron synapse in Aplysia

We have identified an inhibitory neuron (RPL4) in the right pleural ganglion of Aplysia, which produced hyperpolarization of the sensory and motor neurons involved in the tail withdrawal reflex. Activation of RPL4 significantly reduced the amplitude of excitatory postsynaptic potentials produced in tail motor neurons by action potentials triggered in sensory neurons. This example of heterosynaptic inhibition was due, at least in part, to an increase in membrane input conductance in the motor neuron. Since the synaptic strength of the sensory-to-motor neuron connection has been associated with the strength of the tail withdrawal reflex, RPL4 may contribute to modulation of that reflex.

Characterization of neuronal protein phosphatases in Aplysia californica.

Biochemical properties of neuronal protein phosphatases from Aplysia californica were characterized. Dephosphorylation of phosphorylase alpha by extracts of abdominal ganglia and clusters of sensory neurons from pleural ganglia was demonstrated. Type-1 protein phosphatase (PrP-1) was identified in these extracts by the dephosphorylation of the beta-subunit of phosphorylase kinase and its inhibition by the protein, inhibitor-2. Type-2A protein phosphatase (PrP-2A) was demonstrated by the dephosphorylation of the alpha-subunit of phosphorylase kinase, which was insensitive to inhibitor-2. As in vertebrate tissues, only four enzymes, PrP-1 (47%), PrP-2A (42%), PrP-2B (11%), and PrP-2C (less than 1%), accounted for all the cellular protein phosphatase activity dephosphorylating phosphorylase kinase. Aplysia PrP-1 and PrP-2A were potently inhibited by okadaic acid, with PrP-1 being approximately 20-fold more sensitive than PrP-2A. By comparison, purified PrP-2A from rabbit skeletal muscle was 15- to 20-fold more sensitive to okadaic acid than PrP-1 from the same source. Only PrP-1 was associated with the particulate fractions from Aplysia neurons, whereas PrP-1 and PrP-2A, -2B, and -2C were all present in the cytosol. Extraction of the particulate PrP-1 decreased its sensitivity to okadaic acid by sixfold, suggesting that cellular factor(s) affect its sensitivity to this inhibitor. In most respects, protein phosphatases from Aplysia neurons resemble their mammalian counterparts, and their biochemical characterization sets the stage for examining the role of these enzymes in neuronal plasticity, and in learning and memory.

Serotoninergic varicosities make synaptic contacts with pleural sensory neurons of Aplysia

Serotonin is a modulatory neurotransmitter that produces many of the cellular changes associated with sensitization of reflexes in Aplysia. These changes have been carefully documented in sensory neurons located in the abdominal ganglion that mediate the gill-siphon withdrawal reflex and in sensory neurons located in the pleural ganglion that mediate the tail-siphon withdrawal reflex. Although serotonin appears to be necessary for sensitization, there is no direct evidence that serotoninergic neurons make synaptic contacts with sensory neurons. In this study, the immunoperoxidase technique was used to label serotonin-immunoreactive neurites surrounding the cell bodies of sensory neurons in the pleural ganglion. Serotonin-immunoreactive neurites had varicosities whose mean short axis diameter was 1.1 +/- 0.6 microns (mean +/- S.D.). The shape of the size distribution was skewed toward larger sizes, however, suggesting that there were multiple subpopulations of varicosities. One subpopulation was that of varicosities located at branch points whose average short axis diameter was larger than normal (1.7 +/- 0.5 microns). Serotonin-immunoreactive varicosities were directly apposed to the sensory neurons without intervening glial cells. In most contacts, serotonin-immunoreactive neurites invaginated into the plasma membranes of the sensory neurons. There were also a few contacts onto spinelike processes, but these were flat rather than invaginated. Serotoninergic neurons whose activity produces changes in the electrophysiological properties of sensory neurons have been identified, but this study provides the first direct evidence for synaptic connections between serotoninergic neurons and sensory neurons in Aplysia.

Urotensin I-like immunoreactivity in the central nervous system of Aplysia californica

In the present study the occurrence and localization of urotensin I (UI, a corticotropin releasing factor-like peptide) in the CNS of Aplysia californica were investigated by immunocytochemistry and radioimmunoassay. The RIA cross-reactivity pattern indicated that the UI antiserum used recognized an epitope in the C-terminal region of the UI, but it did not cross-react with mammalian corticotropin-releasing factor (CRF) and partially recognized sauvagine (SVG, a frog CRF-like peptide). The use of CRF-specific and sauvagine-specific antisera failed to give positive immunostaining. The application of UI antiserum (which does not cross-react with CRF in RIA) gave a positive staining, which was blocked by synthetic sucker ( Catostomus commersoni) UI, but not by rat/human CRF (10 μM). On the basis of immunostaining and RIA parallel to fish UI displacement curves of cerebral ganglia extracts, the unknown UI/CRF-like substance in the Aplysia ganglia is likely to have greater homology with sucker UI than with the known CRF peptides. Urotensin I-immunoreactive (UI-ir) neurons were seen mainly in the F neuron clusters, located in the midline and rostrodorsal portion of the cerebral ganglia. Few UI-ir neurons were also found in the C and D neuron clusters of the cerebral ganglia, as well as in the left pleural and abdominal ganglia. In addition, numerous fine and coarse, and beaded UI-ir fibers were found in the cerebral commissure. UI-ir fibers were also seen in the neuropile of the buccal, pedal and pleural ganglia, and abdominal ganglion. A cuff-like arrangement of UI-ir fibers was seen in the supralabial nerves. Fewer fibers were seen in the anterior tentacular nerves. No UI-ir fibers were seen in other nerves. Coarse and fine UI-ir fibers in the connectives from the circumesophageal ganglia suggest that a putative UI-like peptide may affect the function of these ganglia.

Functional and morphological evidence for the existence of neurites from abdominal ganglion bag cell neurons in the head-ring ganglia of Aplysia

Three lines of evidence are presented indicating that axons of the Aplysia neuroendocrine bag cells extend into the head-ring ganglia of the CNS. When the abdominal ganglion was bisected longitudinally, separating the two bag cell clusters, an afterdischarge induced in one cluster generated an afterdischarge in the other via activity through the head-ring ganglia to which each half abdominal ganglion was attached by connective nerves. This suggests that some axons of bag cells in each cluster communicate through the head-ring ganglia. Retrograde labelling of bag cells occurred when rhodamine-conjugated latex microspheres were injected into the cerebral or either pleural ganglion, a direct demonstration that bag cell axons extend into these ganglia. Finally, cell LP1 in the left pleural ganglion was inhibited during a bag cell afterdischarge, an action mimicked by application of alpha-bag cell peptide (alpha BCP). Since alpha BCP can act only close to its site of release due to susceptibility to peptidase activity, it is likely that LP1 inhibition is dependent on the local release of alpha BCP from bag cell neurites in the pleural ganglion. These results open new possibilities for how bag cell afterdischarges may be initiated and broaden the distribution of their effects.

Axons of orcadian pacemaker neurons in the eye of Bulla project to the central nervous system and the contralateral eye

1. 1. Orcadian pacemaker neurons located in the eye of Bulla have optic nerve axons. Their projections in the CNS were labeled with either tritiated leucine or HRP and confirmed by electrical recordings. 2. 2. Axons labeled with tritium or HRP project to the cerebral and pleural ganglia and into the abdominal connective. Many fibers cross to the contralateral ganglia. Labeling with HRP revealed fine fiber terminations within the cerebral neuropil. 3. 3. Electrical recording of autogenous compound action potentials (CAPS) that originated in an eye appeared as small CAPs in the cerebral commissure, the contralateral optic nerve and the ipsi- and contralateral pleural-abdominal connectives.