Synaptic Modulation Contributes to Firing Pattern Generation in Jaw Motor Neurons During Rejection of Seaweed in Aplysia kurodai

1999 ◽  
Vol 82 (5) ◽  
pp. 2579-2589 ◽  
Author(s):  
Tatsumi Nagahama ◽  
Kenji Narusuye ◽  
Hidekazu Arai
Keyword(s):  
Motor Neurons ◽  
Firing Frequency ◽  
Pattern Generation ◽  
Jaw Movements ◽  
Japanese Species ◽  
Initial Portion ◽  
Synaptic Modulation ◽  
Buccal Ganglia ◽  
Cerebral Neurons ◽  
Protraction Phase

Japanese species, Aplysia kurodai, feeds well on Ulva but rejects Gelidium ( Geli.) or Pachydictyon ( Pach.) with different rhythmic patterned movements of the jaws and radula. During ingestion the jaws open at the radula-protraction phase and remain half open at the initial phase of the radula-retraction, whereas during rejection the jaws open similarly but start to close immediately after the onset of the radula-retraction. These can be induced not only by the natural seaweed but by the extract solutions. We previously showed that the change of the patterned jaw movements from the ingestion to the rejection may result from the decrease in the delay of the firing onset of the jaw-closing (JC) motor neurons during their depolarization. This diminished delay produces a phase advance relative to the radula-retraction phase. In that study, we showed that during ingestion the buccal multiaction (MA) neurons may generate the delay of firing onset of the JC motor neurons by producing monosynaptic inhibitory postsynaptic potentials (IPSPs) during the initial portion of their depolarization. In the present experiments, the firing patterns in the MA neurons induced by application of the Geli. or Pach. extract to the lips were explored in the semi-intact preparations. During the Pach. response the duration and the firing frequency of the MA firing at each depolarizing phase were decreased in comparison with the Ulvaresponse. No decreases in the MA firing were observed during the Geli. response, suggesting that the similar patterned jaw movements during rejection of Geli. and Pach. may be generated by different neural mechanisms. Moreover, the size of the MA-induced IPSP in the JC motor neurons was largely decreased by application of the Geli. or Pach. extract to the lips in the reduced preparations consisting of the tentacle-lips and the cerebral-buccal ganglia. Voltage-clamp experiments on the JC motor neurons showed that the size of synaptic current induced by the MA spikes was decreased by application of these solutions to the lips. The decrease was induced when the buccal ganglia were bathed in a solution to block polysynaptic pathways. These results suggest that the advance of the onset of the JC firing at each depolarizing phase during the Geli. or Pach. response may be mainly or partly caused by the decrease in the size of the MA-induced IPSP in the motor neurons. Modulatory action of cerebral neurons or peripheral afferent neurons in the lip region may contribute to this synaptic plasticity.

Cerebral CBm1 Neuron Contributes to Synaptic Modulation Appearing During Rejection of Seaweed in Aplysia kurodai

2002 ◽  
Vol 88 (5) ◽  
pp. 2778-2795 ◽  
Author(s):  
Kenji Narusuye ◽  
Tatsumi Nagahama
Keyword(s):  
Motor Neurons ◽  
Spike Activity ◽  
Firing Frequency ◽  
Japanese Species ◽  
Synaptic Modulation ◽  
Seaweed Extracts ◽  
Cerebral Neurons ◽  
A Cell ◽  
Taste Stimulation ◽  
Calcium Green

The Japanese species Aplysia kurodai feeds well on Ulva but rejects Gelidium with distinctive rhythmic patterned movements of the jaws and radula. We have previously shown that the patterned jaw movements during the rejection of Gelidium might be caused by long-lasting suppression of the monosynaptic transmission from the multiaction MA neurons to the jaw-closing (JC) motor neurons in the buccal ganglia and that the modulation might be directly produced by some cerebral neurons. In the present paper, we have identified a pair of catecholaminergic neurons (CBm1) in bilateral cerebral M clusters. The CBm1, probably equivalent to CBI-1 in A. californica, simultaneously produced monosynaptic excitatory postsynaptic potentials (EPSPs) in the MA and JC neurons. Firing of the CBm1 reduced the size of the inhibitory postsynaptic currents (IPSCs) in the JC neuron, evoked by the MA spikes, for >100 s. Moreover, the application of dopamine mimicked the CBm1 modulatory effects and pretreatment with a D1 antagonist, SCH23390, blocked the modulatory effects induced by dopamine. It could also largely block the modulatory effects induced by the CBm1 firing. These results suggest that the CBm1 may directly modulate the synaptic transmission by releasing dopamine. Moreover, we explored the CBm1 spike activity induced by taste stimulation of the animal lips with seaweed extracts by the use of calcium imaging. The calcium-sensitive dye, Calcium Green-1, was iontophoretically loaded into a cell body of the CBm1 using a microelectrode. Application of either Ulva or Gelidium extract to the lips increased the fluorescence intensity, but the Gelidium extract always induced a larger change in fluorescence compared with the Ulva extract, although the solution used induced the maximum spike responses of the CBm1 for each of the seaweed extracts. When the firing frequency of the CBm1 activity after taste stimulation was estimated, the Gelidium extract induced a spike activity of ∼30 spikes/s while the Ulva extract induced an activity of ∼20 spikes/s, consistent with the effective firing frequency (>25 spikes/s) for the synaptic modulation. These results suggest that the CBm1 may be one of the cerebral neurons contributing to the modulation of the basic feeding circuits for rejection induced by the taste of seaweeds such as Gelidium.

Premotor neurons B51 and B52 in the buccal ganglia of Aplysia californica: synaptic connections, effects on ongoing motor rhythms, and peptide modulation

1990 ◽  
Vol 63 (3) ◽  
pp. 539-558 ◽  
Author(s):  
M. R. Plummer ◽  
M. D. Kirk
Keyword(s):  
Cell Body ◽  
Motor Neurons ◽  
Firing Frequency ◽  
Inhibitory Synapses ◽  
Adjacent Cell ◽  
Synaptic Connections ◽  
Synaptic Potentials ◽  
Buccal Ganglia ◽  
Premotor Neurons ◽  
Electrical Connections

1. Two buccal ganglia interneurons, labeled here as B51 and B52, have been identified on the basis of morphological and physiological criteria. 2. These neurons have multipolar cell bodies. B51 extends a major neurite, which arborizes in the neuropil ipsilateral to the soma; extends into the buccal commissure, where it branches profusely; and projects an axon out the radular nerve (n1); other processes emanating from the soma arborize in the adjacent cell body layer. B52 arborizes ipsilateral to its cell body and sends a major process out of the ipsilateral hemiganglion into the sheath that attaches the buccal ganglia to the buccal mass proper. Here the B52 axon projects through a previously undescribed structure, which forms an arch over the buccal commissure that we designate the commissural arch. The extraganglionic B52 axon sends several branches into the connective tissue and then returns to the contralateral hemiganglion, where it again branches. 3. Each neuron exhibits a unique set of physiological properties. B51 frequently produces plateau potentials, which persist and are even enhanced in solutions where Ca2+ is replaced with Co2+. On the other hand, B52 shows a powerful posthyperpolarization rebound that contributes to its burst formation during spontaneous and nerve-elicited cyclic motor output. 4. B51 and B52 display distinctive rhythmic bursting on stimulation of the radular nerve or esophageal nerve. Their burst-firing tended to occur at certain phase relationships with respect to firing in other buccal premotor and motor neurons. 5. When firing frequency is measured as a function of intracellularly injected current, B51 shows a steplike increase in firing with increasing current, whereas B52 firing frequency is continuously graded. 6. B51 and B52 were found to make extensive synaptic connections within the buccal ganglia. B51 exhibited primarily excitatory electrical connections with known premotor and motor neurons, including an electrotonic synapse with its contralateral homologue. 7. In contrast, B52 made bilateral inhibitory synapses with nearly all of the premotor and motor neurons of the ventral motor cluster. Most of these connections appeared to be monosynaptic, producing synaptic potentials with short and fixed latencies that persisted when the ganglia were bathed in solutions containing elevated concentrations of Ca2+ and Mg2+. 8. Other synaptic potentials produced by B52 were more variable in size and latency; these included slow inhibition of the B4 and B5 neurons and excitation of an identifiable neuron that projected out the radular nerve.(ABSTRACT TRUNCATED AT 400 WORDS)

Activity patterns of the B31/B32 pattern initiators innervating the I2 muscle of the buccal mass during normal feeding movements in Aplysia californica

1996 ◽  
Vol 75 (4) ◽  
pp. 1309-1326 ◽  
Author(s):  
I. Hurwitz ◽  
D. Neustadter ◽  
D. W. Morton ◽  
H. J. Chiel ◽  
A. J. Susswein
Keyword(s):  
Feeding Behavior ◽  
Motor Neurons ◽  
Activity Patterns ◽  
Aplysia Californica ◽  
Motor Programs ◽  
Physiological Functions ◽  
Rest Position ◽  
Buccal Ganglia ◽  
Normal Feeding ◽  
Protraction Phase

1. B31 and B32 are pattern-initiator neurons in the buccal ganglia of Aplysia. Along with the B61/B62 neurons, B31/B32 are also motor neurons that innervate the 12 buccal muscle via the I2 nerve. This research was aimed at determining the physiological functions of the B31/B32 and B61/B62 neurons, and of the I2 muscle. 2. Stimulating the I2 muscle in the radula rest position produces radula protraction. In addition, in behaving animals lesioning either the muscle or the I2 nerve greatly reduces radula protraction. 3. During buccal motor programs in reduced preparations, B31/B32 and B61/62 fire preceding activity in neuron B4, whose firing indicates the onset of radula retraction. In addition, during both ingestion-like and rejection-like patterns the activity in the I2 nerve is correlated with protraction. 4. B31/B32 fire at frequencies of 15-25 Hz. Neither B31/B32 nor B61/B62 elicit facilitating end-junction potentials (EJPs) and electromyograms (EMGs) in the I2 muscle. EMGs from B31/B32 are smaller than those from B61/B62. B31/B32 and B61/B62 innervate all areas of the muscle approximately uniformly. 5. In behaving animals, EMGs consistent with B31/B32 activity are seen in the I2 muscle during the protraction phase of biting, swallowing, and rejection movements. In addition, the I2 muscle receives inputs that cannot be attributed to either the B31/B32 or B61/B62 neurons, either because the potentials are too large, firing frequencies are too low, or a prominent facilitation is seen. Such potentials are associated with lip movements, and also with radula retraction. 6. EMGs were recorded from the I2 muscle during feeding behavior after a lesion of the I2 nerve. Animals that had severe deficits in protraction showed no activity consistent with B31/B32 or B61/B62, but did show activity during retraction. 7. Our data indicate that the I2 muscle and the B31/B32 motor neurons are essential constituents contributing to protraction movements. Activity in these neurons is associated with radula protraction, which occurs as a component of a number of different feeding movements. The I2 muscle may also contribute to retraction, via activation by other motor neurons.

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.

Synaptic Actions of Oesophageal Proprioceptors in the Mollusc, Philine

1981 ◽  
Vol 94 (1) ◽  
pp. 95-104
Author(s):  
J. N. SIGGER ◽  
D. A. DORSETT
Keyword(s):  
Receptive Fields ◽  
Large Cell ◽  
The Other ◽  
Small Cells ◽  
Sensory Cells ◽  
Periodic Activity ◽  
Buccal Ganglia ◽  
Excitatory Synaptic Input ◽  
Feeding Cycle ◽  
Protraction Phase

The buccal ganglia of Philine each contain a group of mechanoreceptors, consisting of 1 large and 3 small cells, with receptive fields in the oesophagus. Synaptic contacts occur between the receptors; the large cell providing an EIPSP input to its contralateral partner and to the two groups of smaller receptors. The small receptors make weak excitatory contacts with both the large receptors. The sensory cells synapse with other buccal motoneurones and interneurones, some of which show periodic activity associated with the feeding movements. Protraction phase neurones are divisible into two groups, one of which receives EPSPs from the receptors, while the other group receives IPSPs. Retraction phase neurones receive a biphasic EIPSP. The receptors provide excitatory synaptic input to a pair of interneurones which ‘gate’ the feeding cycle. A third class of neurones which are not rhythmically active during feeding receive a predominantly inhibitory EIPSP.

Control of extrinsic feeding muscles in Aplysia

1983 ◽  
Vol 49 (6) ◽  
pp. 1481-1503 ◽  
Author(s):  
B. Jahan-Parwar ◽  
S. M. Fredman
Keyword(s):  
Motor Neuron ◽  
Motor Neurons ◽  
Synaptic Input ◽  
Cerebral Ganglion ◽  
Cyclic Activity ◽  
Buccal Mass ◽  
Buccal Ganglia ◽  
Identified Neuron ◽  
Single Oscillator ◽  
Extrinsic Muscles

The extrinsic buccal muscles in Aplysia are responsible for the overall protraction and retraction of the buccal mass during feeding. The six pairs of extrinsic muscles are organized into two groups, consisting of three protractors and three retractors. Insights into how the extrinsic muscles are controlled were obtained by examining the organization of the motor neurons that innervated them. The extrinsic buccal muscles are innervated by cerebral ganglion nerves and neurons. All the muscles examined appear to be multiply innervated. Identified neurons in the cerebral B, E, and G clusters were found to be motor neurons for individual extrinsic muscles. Some extrinsic muscles had both excitatory and inhibitory innervation. Two synergistic muscles, the extrinsic ventrolateral protractor (ExVLP) and the extrinsic dorsal protractor (ExDP), had common excitatory innervation by identified neuron E5. Two antagonistic muscles, the ExVLP and the extrinsic ventral retractor (ExVR), also had common innervation. Identified neuron E1 appeared to be an inhibitory motor neuron for the ExVLP but an excitatory motor neuron for the ExVR. Common innervation provides a simple mechanism for coordinating synergistic and antagonistic extrinsic muscles. On the basis of these data, a model for the control of buccal mass protraction and retraction is proposed. Bursting by extrinsic buccal muscles was coordinated with cyclic activity in the intrinsic muscles of the buccal mass. Antagonistic extrinsic muscles burst antiphasically and synergistic extrinsic muscles burst in phase when the buccal mass was fully protracted and exhibited a series of rhythmic contractions. Additionally, cerebral E cluster neurons burst in phase with stereotyped rhythmic buccal motor neuron discharges recorded from buccal nerves. The cerebral E cluster motor neurons were coordinated by common synaptic input. No monosynaptic connections were observed; homologous neurons in each E cluster received synaptic input with similar but not identical timing, indicating that the interneurons that coordinate the homologous motor neurons are synchronized. The source of the rhythm that drives synaptically mediated cerebral extrinsic muscle motor neuron bursting was in the buccal ganglia. Cutting one cerebral-buccal connective eliminated E neuron bursting on that side but had no effect on homologous neurons on the intact side. This suggests that a single oscillator in the buccal ganglia may coordinate both the extrinsic and intrinsic buccal muscles during feeding.

Afferent-Induced Changes in Rhythmic Motor Programs in the Feeding Circuitry of Aplysia

2004 ◽  
Vol 92 (4) ◽  
pp. 2312-2322 ◽  
Author(s):  
Avniel N. Shetreat-Klein ◽  
Elizabeth C. Cropper
Keyword(s):  
Sensory Neurons ◽  
Motor Neurons ◽  
Rhythmic Activity ◽  
Motor Program ◽  
Firing Frequency ◽  
Afferent Activity ◽  
Motor Programs ◽  
Rhythmic Motor ◽  
Induced Changes ◽  
The Impact

A manipulation often used to determine whether a neuron plays a role in the generation of a motor program involves injecting current into the cell during rhythmic activity to determine whether activity is modified. We perform this type of manipulation to study the impact of afferent activity on feeding-like motor programs in Aplysia. We trigger biting-like programs and manipulate sensory neurons that have been implicated in producing the changes in activity that occur when food is ingested, i.e., when bites are converted to bite-swallows. Sensory neurons that are manipulated are the radula mechanoafferent B21 and the retraction proprioceptor B51. Data suggest that both cells are peripherally activated during radula closing/retraction when food is ingested. We found that phasic subthreshold depolarization of a single sensory neuron can significantly prolong radula closing/retraction, as determined by recording both from interneurons (e.g., B64), and motor neurons (e.g., B15 and B8). Additionally, afferent activity produces a delay in the onset of the subsequent radula opening/protraction, and increases the firing frequency of motor neurons. These are the changes in activity that are seen when food is ingested. These results add to the growing data that implicate B21 and B51 in bite to bite-swallow conversions and indicate that afferent activity is important during feeding in Aplysia.

Phasic bursts of the antagonistic jaw muscles during REM sleep mimic a coordinated motor pattern during mastication

2013 ◽  
Vol 114 (3) ◽  
pp. 316-328 ◽  
Author(s):  
T. Kato ◽  
N. Nakamura ◽  
Y. Masuda ◽  
A. Yoshida ◽  
T. Morimoto ◽  
...  
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Nrem Sleep ◽  
Pattern Generation ◽  
Burst Duration ◽  
Temporal Association ◽  
Rapid Eye Movement ◽  
Jaw Movements ◽  
Motor Patterns ◽  
Jaw Muscles

Sleep-related movement disorders are characterized by the specific phenotypes of muscle activities and movements during sleep. However, the state-specific characteristics of muscle bursts and movement during sleep are poorly understood. In this study, jaw-closing and -opening muscle electromyographic (EMG) activities and jaw movements were quantified to characterize phenotypes of motor patterns during sleep in freely moving and head-restrained guinea pigs. During non-rapid eye movement (NREM) sleep, both muscles were irregularly activated in terms of duration, activity, and intervals. During rapid eye movement (REM) sleep, clusters of phasic bursts occurred in the two muscles. Compared with NREM sleep, burst duration, activity, and intervals were less variable during REM sleep for both muscles. Although burst activity was lower during the two sleep states than during chewing, burst duration and intervals during REM sleep were distributed within a similar range to those during chewing. A trigger-averaged analysis of muscle bursts revealed that the temporal association between the bursts of the jaw-closing and -opening muscles during REM sleep was analogous to the temporal association during natural chewing. The burst characteristics of the two muscles reflected irregular patterns of jaw movements during NREM sleep and repetitive alternating bilateral movements during REM sleep. The distinct patterns of jaw muscle bursts and movements reflect state-specific regulations of the jaw motor system during sleep states. Phasic activations in the antagonistic jaw muscles during REM sleep are regulated, at least in part, by the neural networks involving masticatory pattern generation, demonstrating that waking jaw motor patterns are replayed during sleep periods.

Pharmacologically induced elements of the hunting and feeding behavior in the pteropod mollusk Clione limacina. I. Effects of GABA

1993 ◽  
Vol 69 (2) ◽  
pp. 512-521 ◽  
Author(s):  
Y. I. Arshavsky ◽  
T. G. Deliagina ◽  
G. N. Gamkrelidze ◽  
G. N. Orlovsky ◽  
Y. V. Panchin ◽  
...  
Keyword(s):  
Feeding Behavior ◽  
Motor Neurons ◽  
Gabab Receptors ◽  
Gamma Aminobutyric Acid ◽  
Rhythmic Movements ◽  
Rhythm Generator ◽  
Buccal Ganglia ◽  
Gabaa Receptor Antagonist ◽  
Feeding Rhythm ◽  
Clione Limacina

1. The pteropod mollusk Clione limacina is a predator, feeding on the small pteropod mollusk Limacina helicina. Injection of gamma-aminobutyric acid (GABA) into the hemocoel of the intact Clione evoked some essential elements of the hunting and feeding behavior, i.e., protracting the tentacles, opening the mouth, and triggering the rhythmic movements of the buccal mass. This pattern resembled that evoked by presentation of the prey: Clione grasped the Limacina by its tentacles, extracted the prey's body from the shell and then swallowed it. 2. In electrophysiological experiments, several targets of GABA action have been found: 1) direct application of GABA to isolated cerebral motor neurons projecting to the protractor muscles of tentacles resulted in their excitation; 2) GABA activated the feeding rhythm generator located in the buccal ganglia; 3) GABA exerted excitatory or inhibitory effects on the receptor cells of statocysts, the effects being mediated by the efferent input to these cells; 4) GABA suppressed the defense reaction, which is an inhibition of the locomotor activity and of tentacle motor neurons, arising in response to stimulation of the head afferents; and 5) GABA potentiated an excitatory action of the serotoninergic metacerebral cells on the feeding rhythm generator. 3. Effects of GABA on the tentacle motor neurons and the feeding rhythm generator are pharmacologically distinguishable. The action of GABA on the feeding rhythm generator was mimicked by baclofen (which activates the GABAB receptors in mammalian neurons) and was not sensitive to bicuculline (the GABAA receptor antagonist in mammals). On the other hand, bicuculline competitively inhibited the GABA-induced excitation of the tentacle motor neurons. 4. GABAergic neurons have been located in the cerebral, pedal, and buccal ganglia by means of immunohistochemical methods.

Mechanisms of pattern generation underlying swimming in Tritonia. IV. Gating of central pattern generator

1985 ◽  
Vol 53 (2) ◽  
pp. 466-480 ◽  
Author(s):  
P. A. Getting ◽  
M. S. Dekin
Keyword(s):  
Motor Neurons ◽  
Motor Pattern ◽  
Inhibitory Interneuron ◽  
Pattern Generation ◽  
Excitatory Synapses ◽  
Tonic Component ◽  
Inward Current ◽  
Marine Mollusc ◽  
Inward Currents ◽  
Tonic Current

Swimming behavior in the marine mollusc Tritonia diomedea is episodic, consisting of a series of alternating dorsal and ventral flexions initiated by a brief sensory stimulus. The swim motor pattern is generated by a network formed of four groups of premotor interneurons: cerebral cell 2 (C2), dorsal swim interneurons (DSIs), and two types of ventral swim interneurons (VSI-A and VSI-B). The initiation and maintenance of swimming depends on the establishment of a long-lasting ramp depolarization in both the premotor, pattern-generating interneurons, and the motor neurons (i.e., flexion neurons). Voltage clamp was used to measure the membrane current responsible for the ramp depolarization. In all cell classes the current had two components: a tonic inward current, which decayed as the swim progressed, and phasic inward current waves, which provided the synaptic drive during each swim burst. The ramp current in the flexion neurons and in C2 was generated largely by activity within the interneuronal pattern-generating network (PGN). The ramp current could be mimicked by driving activity in the pattern-generating interneurons. In VSI-B, the tonic component of the ramp current was independent of activity within the PGN and appeared to be derived from the long-lasting effect of an extrinsic input. The phasic components of the ramp, however, were dependent on PGN activity. The phasic inward current waves were blocked when pattern generation was prevented. In addition, phasic inward currents similar to those occurring during swimming could be produced by driving the C2. The tonic component of the ramp current in a DSI was dependent both on extrinsic inputs and PGN activity. Extrinsic inputs appeared to control the first 10-15 s of the tonic current. At longer times, activity within the DSI population itself maintained the ramp current. When one DSI was driven in a quiescent preparation, all other DSIs were inhibited, yet the DSIs are known to be coupled by monosynaptic, reciprocal excitatory synapses. This effect could be explained by the action of an unidentified inhibitory interneuron (I-neuron), which was excited by DSIs and in turn inhibited all other DSIs. The DSIs were therefore coupled reciprocally by both monosynaptic excitation and polysynaptic inhibition. Activity in C2 switched the DSI-DSI interaction from inhibition to excitation by inhibiting the I-neuron.(ABSTRACT TRUNCATED AT 400 WORDS)

Sign in / Sign up

Export Citation Format

Share Document