Escape Swim Network Interneurons Have Diverse Roles in Behavioral Switching and Putative Arousal in Pleurobranchaea

2000 ◽  
Vol 83 (3) ◽  
pp. 1346-1355 ◽  
Author(s):  
Jian Jing ◽  
Rhanor Gillette
Keyword(s):  
Escape Response ◽  
Motor Output ◽  
Pedal Ganglion ◽  
Command Neurons ◽  
Food Avoidance ◽  
Sea Slug ◽  
Behavioral Switching ◽  
Arousal System ◽  
Direct Suppression ◽  
Stimulation Of

Escape swimming in the predatory sea slug Pleurobranchaea is a dominant behavior that overrides feeding, a behavioral switch caused by swim-induced inhibition of feeding command neurons. We have now found distinct roles for the different swim interneurons in acute suppression of feeding during the swim and in a longer-term stimulation of excitability in the feeding network. The identified pattern-generating swim neurons A1, A3, A10, and their follower interneuron A-ci1, suppress feeding motor output partly by excitation of the I1 feeding interneurons, which monosynaptically inhibit both the feeding command neurons, PCP, PSE, and other major interneurons, the I2s. This mechanism exerts broad inhibition of the feeding network suitable to an escape response; broader than feeding suppression in learned and satiation-induced food avoidance and acting through a different presynaptic pathway. Four intrinsic neuromodulatory neurons of the swim network, the serotonergic As1–4, add little to direct suppression of feeding. Rather, they monosynaptically excite the serotonergic metacerebral giant (MCG) neurons of the feeding network, themselves intrinsic neuromodulators of feeding, as well as a cluster of adjacent serotonergic feeding neurons, with both fast and slow EPSPs. They also provide mild neuromodulatory excitation of the PCP/PSE feeding command neurons, and I1 and I2 feeding interneurons, which is masked by inhibition during the swim. As1–4 also excite the serotonergic pedal ganglion G neurons for creeping locomotion. These observations further delineate the nature of the putative serotonergic arousal system of gastropods and suggest a central coordinating role to As1–4.

Organization of synaptic inputs to paracerebral feeding command interneurons of Pleurobranchaea californica. III. Modifications induced by experience

1983 ◽  
Vol 49 (6) ◽  
pp. 1557-1572 ◽  
Author(s):  
W. J. Davis ◽  
R. Gillette ◽  
M. P. Kovac ◽  
R. P. Croll ◽  
E. M. Matera
Keyword(s):  
Tactile Stimulation ◽  
Neural Circuitry ◽  
Cellular Model ◽  
Command Neurons ◽  
Food Avoidance ◽  
Pleurobranchaea Californica ◽  
Inhibitory Postsynaptic Potentials ◽  
Food Satiation ◽  
Behavioral Motivation ◽  
Stimulation Of

Phasic paracerebral feeding command interneurons (PCP's) were studied in whole-animal preparations of Pleurobranchaea drawn from four populations with different behavioral histories: food avoidance conditioned, yoked controls, food satiated, and naive. PCP responses to chemosensory food stimuli (liquefied squid) and mechanosensory touch stimuli (tactile stimulation of anterior and posterior structures) were recorded intracellularly, scored blind, and compared quantitatively across the four populations. PCP's from avoidance-conditioned specimens (10, 18, 19) showed decreased excitatory and increased inhibitory responses to food and touch in comparison with naive (untrained) specimens. Control animals did not show these effects. PCP's from satiated specimens showed decreased excitatory and increased inhibitory responses to food and touch in comparison with PCP's from control, naive, and conditioned specimens. Inhibitory postsynaptic potentials (IPSPs) induced in PCP's of conditioned and satiated specimens by food and touch are indistinguishable in amplitude and waveform from IPSPs produced in the same PCP's by the previously described cyclic inhibitory network (CIN; Ref. 13). In addition, tonic paracerebral neurons (PCT's) that lack input from the CIN, are not inhibited but rather are excited in trained and satiated animals. Therefore the inhibitory responses to food and touch by PCP's of conditioned and satiated specimens appear to be mediated by the CIN. This study demonstrates that associative and nonassociative processes (learning and food satiation, respectively) manifest similarly at the level of command interneurons. The findings furnish a neurophysiological explanation for behavioral motivation in Pleurobranchaea, namely, modulation of the balance of excitation/inhibition in command neurons controlling the corresponding behavior. A cellular model of food avoidance learning and food satiation is formulated to account for these data, based on the identified neural circuitry of the paracerebral command system (15, 17).

Higher order neurons in buccal ganglia of Pleurobranchaea elicit vomiting motor activity

1983 ◽  
Vol 50 (3) ◽  
pp. 658-670 ◽  
Author(s):  
A. D. McClellan
Keyword(s):  
High Frequency ◽  
Motor Pattern ◽  
Higher Order ◽  
Root Activity ◽  
Command Neurons ◽  
Sensory Inputs ◽  
Buccal Ganglia ◽  
Output Pattern ◽  
Stimulation Of

The buccal mass of the gastropod Pleurobranchaea is used during a regurgitation response that consists of a writhing phase interrupted by brief periodic bouts of a vomiting phase (17, 20). During transitions from writhing to vomiting, specific changes occur in the motor pattern (19, 20). Evidence is presented suggesting that at least some of the initiation or "command" neurons for vomiting reside in the buccal ganglia. The present paper examines the role of two candidate vomiting-initiation cells, the ventral white cells (VWC) and midganglionic cells (MC), in the buccal ganglia of isolated nervous systems. Stimulation of single VWCs activates a vomiting motor pattern, consisting in part of alternating buccal root activity. Furthermore, the VWCs fire in high-frequency bursts during episodes (i.e., bouts) of this same vomiting pattern. Mutual reexcitation between the VWCs and motor pattern generator (MPG) appears to produce the accelerated buildup and maintenance of vomiting rhythms. Brief stimulation of single MCs "triggers" bouts of a vomiting motor pattern, but the membrane potential of this cell is only modulated during this same pattern, at least in the isolated nervous system. It is proposed that in intact animals the MCs are activated by sensory inputs and briefly excite the VWC-MPG network, thereby turning on the mutual reexcitatory mechanism mentioned above and switching the output pattern. A general implication for gastropod research is that higher order neurons that activate buccal root activity cannot automatically be given the function of "feeding command neuron," as some cells clearly control other responses, such as vomiting.

scholarly journals Giant fiber activation of an intrinsic muscle in the mesothoracic leg of Drosophila melanogaster

1993 ◽  
Vol 177 (1) ◽  
pp. 149-167 ◽  
Author(s):  
J. R. Trimarchi ◽  
A. M. Schneiderman
Keyword(s):  
Drosophila Melanogaster ◽  
Electrical Stimulation ◽  
Motor Neuron ◽  
Cell Body ◽  
Escape Response ◽  
Large Cell ◽  
Giant Fiber ◽  
Leg Muscle ◽  
Muscle Responses ◽  
Stimulation Of

Cinematographic analysis reveals that an important component of the light-elicited escape response of Drosophila melanogaster is the extension of the femur-tibia joint of the mesothoracic leg. During the jumping phase of the response, this extension works synergistically with extension of the femur. Femur extension is generated by contraction of the tergotrochanteral muscle (TTM), one of four previously described escape response muscles. Femur-tibia joint extension in the mesothoracic leg has been thought to be controlled by contraction of the tibial levator (TLM), an intrinsic leg muscle. We investigated the activation of the TLM during the escape response. Electrical stimulation of the giant fiber interneuron that mediates the escape response results in activation of the TLM with a latency of 1.46 +/− 0.02 ms. The TLM is innervated by a motor neuron (TLMn) with a large cell body in the mesothoracic ganglion. The TLMn has extensive arborizations in the lateral mesothoracic leg neuromere and has a prominent medially directed neurite. To investigate possible presynaptic inputs activating the TLMn during the escape response, we analyzed the muscle responses of two mutants, giant fiber A1 and bendless. Our analysis suggests that the TLMn is activated by a novel pathway.

A Preparation of Aplysia Fasciata For Intrasomatic Recording and Stimulation of Single Neurones During Locomotor Movements

1971 ◽  
Vol 54 (3) ◽  
pp. 659-676
Author(s):  
R. G. DE WEEVERS
Keyword(s):  
Ganglion Cells ◽  
Pedal Ganglion ◽  
Preliminary Results ◽  
Single Neurones ◽  
Sensory Responses ◽  
Motor Cells ◽  
Aplysia Fasciata ◽  
Pleural Ganglion ◽  
Somatic Musculature ◽  
Stimulation Of

1. Methods are described for suspending and clamping Aplysia fasciata so as to permit intrasomatic recording from neurones of the head ganglia during locomotor and other behavioural activities. 2. Sensory responses of neurones in the pedal ganglion are classified into four main types, all being distinct from those of pleural ganglion cells. 3. The pedal ganglion may well contain ‘motor cells’ for the greater part of the somatic musculature. 4. Preliminary results suggest that the pleural LGC may be involved in promoting a change from swimming to creeping behaviour.

scholarly journals Reciprocal Stimulation of Decay Between Serotonergic Facilitation and Depression of Synaptic Transmission

2008 ◽  
Vol 100 (2) ◽  
pp. 1113-1126 ◽  
Author(s):  
Sun Hee Cho Lee ◽  
Karen Taylor ◽  
Franklin B. Krasne
Keyword(s):  
Protein Kinase ◽  
Synaptic Transmission ◽  
Protein Kinase A ◽  
The Other ◽  
Command Neurons ◽  
Wide Range ◽  
History Of ◽  
Depressive States ◽  
Kinase A ◽  
Stimulation Of

Serotonin can produce multiple, contradictory modulatory effects on strength of synaptic transmission in both vertebrate and invertebrate nerve circuits. In crayfish, serotonin (5-HT) can both facilitate and depress transmission to lateral giant escape command neurons; however, which effect is manifest during application, as well as the sign and duration of effects that may continue long after 5-HT washout, may depend on history of application as well as on concentration. We report that protein kinase A (PKA) signaling is essential to the production of facilitation but depression is mediated by non-cAMP/PKA signaling pathways. However, we unexpectedly found that PKA activity is essential for the decay of depression when serotonin is washed out. This, and evidence from the effects of a variety of serotonin application regimens, suggest that facilitatory and depressive states coexist and compete and that the decay of each is dependent on stimulation by the other. A computational model that incorporates these assumptions can account for and rationalize the varied effects of a wide range of serotonin application regimens.

Electrophysiological identification of vagally innervated enteric neurons in guinea pig stomach

1992 ◽  
Vol 263 (5) ◽  
pp. G709-G718 ◽  
Author(s):  
M. Schemann ◽  
D. Grundy
Keyword(s):  
Nicotinic Receptors ◽  
Vagal Stimulation ◽  
Enteric Neurons ◽  
Command Neurons ◽  
Myenteric Neurons ◽  
Release Of Acetylcholine ◽  
Vagal Innervation ◽  
Guinea Pig Stomach ◽  
Stimulation Of

Myenteric "command neurons" are thought to be the interface between extrinsic and intrinsic controls of gut functions and are thought to be responsible for transmission of vagal impulses to enteric microcircuits. To identify, electrophysiologically, myenteric neurons responding to electrical stimulation of the vagus, we developed an in vitro preparation of the gastric myenteric plexus in which the vagal innervation was preserved. The majority of myenteric neurons [102 of 155 (66%)] received fast excitatory postsynaptic potentials (fEPSPs) after stimulation of the vagus. The proportion of neurons receiving vagal input was highest at the lesser curve (98%) and decreased gradually when recordings were made from neurons located toward the greater curve. Only a small proportion of neurons (4 of 85 cells) showed a slow EPSP after a burst of vagal stimulation. No postsynaptic inhibitory potentials were observed. There was no preferential vagal input to either gastric I, gastric II, or gastric III neurons. The fEPSPs were due to the release of acetylcholine acting postsynaptically on nicotinic receptors. The behavior of the fEPSPs suggests multiple vagal inputs to a majority of myenteric neurons. Our observations call into question the concept of enteric command neurons in favor of a divergent vagal input with widespread modulatory influences over gastric enteric neurotransmission.

Load Signals Assist the Generation of Movement-Dependent Reflex Reversal in the Femur–Tibia Joint of Stick Insects

2006 ◽  
Vol 96 (6) ◽  
pp. 3532-3537 ◽  
Author(s):  
Turgay Akay ◽  
Ansgar Büschges
Keyword(s):  
Time Course ◽  
Stick Insect ◽  
Motor Output ◽  
Chordotonal Organ ◽  
Frequency Of Occurrence ◽  
Stick Insects ◽  
Extensor Motoneuron ◽  
Motoneuron Activity ◽  
First Time ◽  
Stimulation Of

Reinforcement of movement is an important mechanism by which sensory feedback contributes to motor control for walking. We investigate how sensory signals from movement and load sensors interact in controlling the motor output of the stick insect femur–tibia (FT) joint. In stick insects, flexion signals from the femoral chordotonal organ (fCO) at the FT joint and load signals from the femoral campaniform sensilla (fCS) are known to individually reinforce stance-phase motor output of the FT joint by promoting flexor and inhibiting extensor motoneuron activity. We quantitatively compared the time course of inactivation in extensor tibiae motoneurons in response to selective stimulation of fCS and fCO. Stimulation of either sensor generates extensor activity in a qualitatively similar manner but with a significantly different time course and frequency of occurrence. Inactivation of extensor motoneurons arising from fCS stimulation was more reliable but more than threefold slower compared with the extensor inactivation in response to flexion signals from the fCO. In contrast, simultaneous stimulation of both sense organs produced inactivation in motoneurons with a time course typical for fCO stimulation alone, but with a frequency of occurrence characteristic for fCS stimulation. This increase in probability of occurrence was also accompanied by a delayed reactivation of the extensor motoneurons. Our results indicate for the first time that load signals from the leg affect the processing of movement-related feedback in controlling motor output.

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