Cerebral neurons underlying prey capture movements in the pteropod mollusc, Clione limacina

1993 ◽  
Vol 172 (2) ◽  
pp. 153-169 ◽  
Author(s):  
T. P. Norekian ◽  
R. A. Satterlie
Keyword(s):  
Prey Capture ◽  
Cerebral Neurons ◽  
Clione Limacina

Whole body withdrawal circuit and its involvement in the behavioral hierarchy of the mollusk Clione limacina

1996 ◽  
Vol 75 (2) ◽  
pp. 529-537 ◽  
Author(s):  
T. P. Norekian ◽  
R. A. Satterlie
Keyword(s):  
Feeding Behavior ◽  
Motor Neurons ◽  
Prey Capture ◽  
The Body ◽  
Whole Body ◽  
High Threshold ◽  
Behavioral Repertoire ◽  
Withdrawal Behavior ◽  
Cerebral Neurons ◽  
Clione Limacina

1. The behavioral repertoire of the holoplanktonic pteropod mollusk Clione limacina includes a few well-defined behaviors organized in a priority sequence. Whole body withdrawal takes precedence over slow swimming behavior, whereas feeding behavior is dominant over withdrawal. In this study a group of neurons is described in the pleural ganglia, which controls whole body withdrawal behavior in Clione. Each pleural withdrawal (Pl-W) neuron has a high threshold for spike generation and is capable of inducing whole body withdrawal in a semi-intact preparation: retraction of the body-tail, wings, and head. Each Pl-W neuron projects axons into the main central nerves and innervates all major regions of the body. 2. Stimulation of Pl-W neurons produces inhibitory inputs to swim motor neurons that terminate swimming activity in the preparation. In turn, Pl-W neurons receive inhibitory inputs from the cerebral neurons involved in the control of feeding behavior in Clione, neurons underlying extrusion of specialized prey capture appendages. Thus it appears that specific inhibitory connections between motor centers can explain the dominance of withdrawal behavior over slow swimming and feeding over withdrawal in Clione.

Cerebral serotonergic neurons reciprocally modulate swim and withdrawal neural networks in the mollusk Clione limacina

1996 ◽  
Vol 75 (2) ◽  
pp. 538-546 ◽  
Author(s):  
T. P. Norekian ◽  
R. A. Satterlie
Keyword(s):  
Neural Networks ◽  
Motor Neurons ◽  
Swimming Behavior ◽  
Whole Body ◽  
Inhibitory Effects ◽  
Serotonergic Neurons ◽  
Serotonin Antagonist ◽  
Cerebral Ganglia ◽  
Cerebral Neurons ◽  
Clione Limacina

1. A pair of serotonin-immunoreactive neurons has been identified in the cerebral ganglia of the pteropod mollusk Clione limacina, which produce coordinated, excitatory/inhibitory effects on neurons controlling two incompatible behaviors, swimming and whole body withdrawal. These cells were designated cerebral serotonergic ventral (Cr-SV) neurons. 2. Activation of Cr-SV neurons produces a prominent inhibition of the pleural withdrawal neurons, which have been previously shown to induce whole body withdrawal in Clione. In addition, the cerebral neurons produce weak excitatory inputs to swim motor neurons, pedal serotonergic neurons involved in the peripheral modulation of swimming, and to the serotonergic heart excitor neuron. 3. Inhibitory and excitatory effects appear to be produced by serotonin because they are mimicked by exogenous serotonin and are blocked by the serotonin antagonist mianserin. 4. All serotonergic neurons identified thus far in the CNS of Clione appear to function in a coordinated manner, altering a variety of neural centers all directed toward the activation of swimming behavior.

scholarly journals Serotonergic modulation of swimming speed in the pteropod mollusc Clione limacina. III. Cerebral neurons.

1995 ◽  
Vol 198 (4) ◽  
pp. 917-930 ◽  
Author(s):  
R A Satterlie ◽  
T P Norekian
Keyword(s):  
Motor Neurons ◽  
Time Course ◽  
Neuron Activity ◽  
Target Cells ◽  
Cellular Mechanisms ◽  
Cycle Frequency ◽  
Course Of Action ◽  
Cell Groups ◽  
Cerebral Neurons ◽  
Clione Limacina

Swim acceleration in Clione limacina can occur via central inputs to pattern generator interneurons and motor neurons and through peripheral inputs to the swim musculature. In the previous paper, peripheral modulation of the swim muscles was shown to increase wing contractility. In the present paper, central inputs are described that trigger an increase in swim frequency and an increase in motor neuron activity. In dissected preparations, spontaneous acceleration from slow to fast swimming included an increase in the cycle frequency, a baseline depolarization in the swim interneurons and an increase in the intensity of motoneuron firing. Similar effects could be elicited by bath application of 10(-5) mol l-1 serotonin. Two clusters of cerebral serotonin-immunoreactive interneurons were found to produce acceleration of swimming accompanied by changes in neuronal activity. Posterior cluster neurons triggered an increase in swim frequency, depolarization of the swim interneurons, an increase in general excitor motoneuron activity and activation of type 12 interneurons and pedal peripheral modulatory neurons. Cells from the anterior cerebral cluster also increased swim frequency, increased activity in the swim motoneurons and activated type 12 interneurons, pedal peripheral modulatory neurons and the heart excitor neuron. The time course of action of the anterior cluster neurons did not greatly outlast the duration of spike activity, while that of the posterior cluster neurons typically outlasted burst duration. It appears that the two discrete clusters of serotonin-immunoreactive neurons have similar, but not identical, effects on swim neurons, raising the possibility that the two serotonergic cell groups modulate the same target cells through different cellular mechanisms.

Coordination of Startle and Swimming Neural Systems in the Pteropod Mollusk Clione limacina: Role of the Cerebral Cholinergic Interneuron

1997 ◽  
Vol 78 (1) ◽  
pp. 308-320 ◽  
Author(s):  
Tigran P. Norekian
Keyword(s):  
Central Pattern Generator ◽  
Prey Capture ◽  
Pattern Generator ◽  
Neural Systems ◽  
Cholinergic Antagonists ◽  
Short Latency Response ◽  
Latency Response ◽  
Cholinergic Interneuron ◽  
Clione Limacina

Norekian, Tigran P. Coordination of startle and swimming neural systems in the pteropod mollusk Clione limacina: role of the cerebral cholinergic interneuron. J. Neurophysiol. 78: 308–320, 1997. The holoplanktonic pteropod mollusk Clione limacina has a unique startle system that provides a very fast, ballistic movement of the animal during escape or prey capture behaviors. The startle system consists of two groups of large pedal motoneurons that control ventral or dorsal flexions of the wings. Although startle motoneurons innervate the same musculature used during normal swimming, they are independent of the swim central pattern generator and swim motoneurons. This study demonstrates that a cerebral startle (Cr-St) interneuron, which provides prominent excitatory inputs to startle motoneurons, plays a very important role in coordination of the startle and swimming neural systems. The Cr-St interneuron produces, simultaneously with monosynaptic excitatory inputs to dorsal startle motoneurons, monosynaptic inhibitory inputs to all types of swim neurons, including interneurons of the central pattern generator, general excitor motoneurons, small motoneurons, and modulatory pedal serotonergic wing neurons. The inhibitory synaptic transmission between the Cr-St interneuron and swim interneurons and motoneurons, as well as excitatory transmission between the Cr-St interneuron and startle motoneurons, appears to be cholinergic because it is blocked by the cholinergic antagonists atropine and d-tubocurarine, mimicked by exogenous acetylcholine in very low concentrations, and enhanced by the cholinesterase inhibitor eserine (physostigmine). The Cr-St-neuron-mediated inhibitory inputs to the swimming system are strong enough to completely terminate swimming activity while the Cr-St interneuron is active. Mechanosensory inputs are capable of triggering Cr-St neuron firing at rates sufficient to suppress fictive swimming in reduced preparations. Thus the Cr-St interneuron can temporally remove the swimming system from the control over the swim musculature while simultaneously activating the startle system to produce a powerful, short-latency response.

Cholinergic Activation of Startle Motoneurons by a Pair of Cerebral Interneurons in the Pteropod Mollusk Clione limacina

1997 ◽  
Vol 77 (1) ◽  
pp. 281-288 ◽  
Author(s):  
Tigran P. Norekian ◽  
Richard A. Satterlie
Keyword(s):  
Synaptic Transmission ◽  
Tactile Stimulation ◽  
Prey Capture ◽  
Escape Behavior ◽  
Dorsal Surface ◽  
Excitatory Postsynaptic Potential ◽  
Neuronal System ◽  
Clione Limacina ◽  
Stimulation Of ◽  
Cholinergic Activation

Norekian, Tigran P. and Richard A. Satterlie. Cholinergic activation of startle motoneurons by a pair of cerebral interneurons in the pteropod mollusk Clione limacina. J. Neurophysiol. 77: 281–288, 1997. The holoplanktonic pteropod mollusk Clione limacina exhibits an active escape behavior that is characterized by fast swimming away from the source of potentially harmful stimuli. The initial phase of escape behavior is a startle response that is controlled by pedal motoneurons whose activity is independent of the normal swim pattern generator. In this study, a pair of cerebral interneurons is described that produces strong activation of the d-phase startle motoneurons, which control dorsal flexion of the wings. These interneurons were designated cerebral startle (Cr-St) interneurons. Each Cr-St neuron has a small cell body on the dorsal surface of the cerebral ganglia and one large axon that runs into the ipsilateral cerebral-pedal connective and the neuropile of the ipsilateral pedal ganglion. Each spike in a Cr-St neuron produces a fast, high-amplitude (up to 50 mV) excitatory postsynaptic potential (EPSP) in the d-phase startle motoneurons. This 1:1 ratio of spikes to EPSPs and the stable short synaptic latencies (2 ms) persist in high-Mg2+, high-Ca2+ seawater, suggesting monosynaptic connections. Synaptic transmission between Cr-St neurons and startle motoneurons exhibits a very slow synaptic depression, because a number of spikes in Cr-St neurons is required to achieve a noticeable decrease in EPSP amplitude. Synaptic transmission between Cr-St interneurons and startle motoneurons appears to be cholinergic. In startle neurons, 20 μM atropine and 50 μM d-tubocurarine reversibly block EPSPs produced by spike activity in Cr-St interneurons. Hexamethonium only partially blocks EPSPs in startle neurons, and much higher concentrations are required. Exogenous acetylcholine (1 μM) produces a dramatic depolarization of startle motoneurons in high-Mg2+ seawater, and this depolarization is reversibly blocked by atropine. Nicotine also has a depolarizing effect on startle motoneurons, although higher concentrations are required. Cr-St interneurons and startle motoneurons are also electrically coupled; however, the coupling is weak. Stimuli that are known to initiate escape responses in intact animals, such as tactile stimulation of the tail or wings, produce excitatory inputs to Cr-St interneurons. In addition, tactile stimulation of the lips and buccal cones, which is known to trigger prey capture reactions in Clione, also produces excitatory inputs to Cr-St interneurons and startle motoneurons, suggesting involvement of the startle neuronal system in prey capture behavior of Clione.

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