A System of Electrically Coupled Small Cells in the Buccal Ganglia of the Pond Snail Planorbis Corneus

1972 ◽  
Vol 56 (3) ◽  
pp. 621-637
Author(s):  
MICHAEL S. BERRY
Keyword(s):  
Synaptic Input ◽  
Action Potentials ◽  
Burst Activity ◽  
Small Cells ◽  
Pond Snail ◽  
Trigger System ◽  
Buccal Ganglia ◽  
Large Numbers ◽  
Planorbis Corneus

1. The buccal ganglia of Planorbis contain a population of electrically coupled small cells. This has been studied, in preparations of isolated ganglia, by recording intracellularly from the cells two at a time. 2. The population is usually silent but activity initiated in any one of its members tends to spread to the rest of the population in both ganglia. Failure of spread, or fatigue, gradually occurs on repetition. 3. The group has the properties of a trigger system, initiating prolonged patterned activity in large numbers of neurones in the buccal ganglia. This may normally initiate feeding. 4. In addition to central processes, both in the buccal ganglia and to the rest of the CNS, the system has peripheral axons in most of the buccal nerves. No synaptic input could be demonstrated. 5. Action potentials in some of the cells increase greatly in duration with repetition. The resulting electrotonic EPSP's, recorded in closely coupled trigger cells, correspondingly increase in size. The possible integrative significance of this is discussed, especially its effect in offsetting fatigue. 6. In some preparations spontaneous bursting occurred in trigger cells and this elicited burst activity in large neurones, including motoneurones. The system may have an intrinsic pacemaker.

Esophageal mechanoreceptors in the feeding system of the pond snail, Lymnaea stagnalis

1989 ◽  
Vol 61 (4) ◽  
pp. 727-736 ◽  
Author(s):  
C. J. Elliott ◽  
P. R. Benjamin
Keyword(s):  
Feeding Behavior ◽  
Synaptic Input ◽  
Lymnaea Stagnalis ◽  
Esophageal Wall ◽  
Pond Snail ◽  
Feeding System ◽  
Buccal Ganglia ◽  
Feeding Rhythm ◽  
Feeding Cycle ◽  
Stimulation Of

1. We identify esophageal mechanoreceptor (OM) neurons of Lymnaea with cell bodies in the buccal ganglia and axons that branch repeatedly to terminate in the esophageal wall. 2. The OM cells respond phasically to gut distension. Experiments with a high magnesium/low calcium solution suggest that the OM neurons are primary mechanoreceptors. 3. In the isolated CNS preparation, the OM cells receive little synaptic input during the feeding cycle. 4. The OM cells excite the motoneurons active in the rasp phase of the feeding cycle. 5. The OM cells inhibit each of the identified pattern-generating and modulatory interneurons in the buccal ganglia. Experiments with a saline rich in magnesium and calcium suggest that the connections are monosynaptic. 6. Stimulation of a single OM cell to fire at 5-15 Hz is sufficient to terminate the feeding rhythm in the isolated CNS preparation. 7. We conclude that these neurons play a role in terminating feeding behavior.

Synaptic relationships of the cerebral giant cells with motoneurones in the feeding system of Lymnaea stagnalis

1980 ◽  
Vol 85 (1) ◽  
pp. 169-186
Author(s):  
C. R. McCrohan ◽  
P. R. Benjamin
Keyword(s):  
Synaptic Input ◽  
Lymnaea Stagnalis ◽  
Giant Cells ◽  
Burst Activity ◽  
Feeding System ◽  
Postsynaptic Potentials ◽  
Buccal Ganglia ◽  
Long Latency ◽  
Burst Intensity ◽  
Feeding Cycle

1.The cerebral giant cells (CGCs) of Lymnaea have a tonic, modulatory effect on the intensity of output from feeding motoneurones in the buccal ganglia. 2. Short latency, excitatory and probably monosynaptic connexions occur between the CGCs and three identified feeding motoneurones. Unitary excitatory postsynaptic potentials in these motoneurones, following CGC spikes, are of different sizes and durations, and hence have different summation properties. 3. The CGCs make long latency, excitatory polysynaptic connexions with four other feeding motoneurone types. 4. Bursts of spikes in the CGCs, resulting from phasic synaptic input, synchronous with the feeding cycle, amplify their modulatory effect on burst intensity in feeding motoneurones. 5. Thte for reinforcing their cyclic burst activity.

Optical mapping of atrioventricular node reveals a conduction barrier between atrial and nodal cells

1998 ◽  
Vol 274 (3) ◽  
pp. H829-H845 ◽  
Author(s):  
Bum-Rak Choi ◽  
Guy Salama
Keyword(s):  
Action Potentials ◽  
Imaging Techniques ◽  
Atrioventricular Node ◽  
Small Cells ◽  
Av Node ◽  
Propagation Pattern ◽  
Voltage Sensitive Dyes ◽  
Decremental Conduction ◽  
Microelectrode Techniques ◽  
Av Delay

The mechanisms responsible for atrioventricular (AV) delay remain unclear, in part due to the inability to map electrical activity by conventional microelectrode techniques. In this study, voltage-sensitive dyes and imaging techniques were refined to detect action potentials (APs) from the small cells comprising the AV node and to map activation from the “compact” node. Optical APs (124) were recorded from 5 × 5 mm (∼0.5-mm depth) AV zones of perfused rabbit hearts stained with a voltage-sensitive dye. Signals from the node exhibited a set of three spikes; the first and third ( peaks I and III) were coincident with atrial (A) and ventricular (V) electrograms, respectively. The second spike ( peak II) represented the firing of midnodal (N) and/or lower nodal (NH) cell APs as indicated by their small amplitude, propagation pattern, location determined from superimposition of activation maps and histological sections of the node region, dependence on depth of focus, and insensitivity to tetrodotoxin (TTX). AV delays consisted of τ1 (49.5 ± 6.59 ms, 300-ms cycle length), the interval between peaks I and II (perhaps AN to N cells), and τ2 (57.57 ± 5.15 ms), the interval between peaks II and III (N to V cells). The conductance time across the node was 10.33 ± 3.21 ms, indicating an apparent conduction velocity (ΘN) of 0.162 ± 0.02 m/s ( n = 9) that was insensitive to TTX. In contrast, τ1 correlated with changes in AV node delays (measured with surface electrodes) caused by changes in heart rate or perfusion with acetylcholine. The data provide the first maps of activation across the AV node and demonstrate that ΘN is faster than previously presumed. These findings are inconsistent with theories of decremental conduction and prove the existence of a conduction barrier between the atrium and the AV node that is an important determinant of AV node delay.

Cholinergic interneurons in the feeding system of the pond snail lymnaea stagnalis. I. cholinergic receptors on feeding neurons

1992 ◽  
Vol 336 (1277) ◽  
pp. 157-166 ◽  
Keyword(s):  
Synaptic Input ◽  
Lymnaea Stagnalis ◽  
Cholinergic Receptors ◽  
Pond Snail ◽  
Feeding System ◽  
Inhibitory Receptor ◽  
Excitatory Response ◽  
Cholinergic Interneurons ◽  
Feeding Rhythm ◽  
Cholinergic Response

All the identified feeding motoneurons of Lymnaea respond to bath or iontophoretically applied acetylcholine (ACh). Three kinds of receptors (one excitatory, one fast inhibitory and one slow inhibitory) were distinguished pharmacologically. The agonist TMA (tetram ethylam m onium ) activates all three receptors, being weakest at the slow inhibitory receptor. PTMA (phenyltrim ethylam monium ) is less potent than TMA and is ineffective at the slow inhibitory receptor, which is the only receptor sensitive to arecoline. At 0.5 mM the antagonists HMT (hexamethonium) and ATR (atropine) selectively block the excitatory response, while PTMA reduces the response to ACh at all three receptors. d-TC (curare) antagonizes only the fast excitatory and the fast inhibitory responses, but MeXCh (methylxylocholine) blocks the fast excitatory and slow inhibitory responses solely. For each of the feeding motoneurons, the sign of the cholinergic response (excitation or inhibition) is the same as the synaptic input received in the N1 phase of the feeding rhythm .

Interneuronal Control of Feeding in the Pond Snail Lymnaea Stagnalis: II. The Interneuronal Mechanism Generating Feeding Cycles

1981 ◽  
Vol 92 (1) ◽  
pp. 203-228
Author(s):  
R. M. ROSE ◽  
P. R. BENJAMIN
Keyword(s):  
Cell Population ◽  
Synaptic Input ◽  
Lymnaea Stagnalis ◽  
Pond Snail ◽  
Feeding Cycle ◽  
Interneuronal Network

The feeding cycle of Lymnaea is generated by a network of three types of interneurone, N1, N2 and N3. This network is driven by the slow oscillator (SO) interneurone described in the previous paper. Interaction between the different interneurones is dependent on both connectivity and endogenous properties, and utilizes such properties as post-inhibitory rebound and self-feedback within electrically-coupled populations. Each of the four components of the interneuronal network (SO, N1, N2 and N3) is responsible for a different phase of synaptic input to the follower cell population which was previously shown to directly control feeding movements.

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.

Peripheral neural input to neurons of the middle cervical ganglion in the cat

1984 ◽  
Vol 246 (3) ◽  
pp. R354-R358
Author(s):  
Z. J. Bosnjak ◽  
J. P. Kampine
Keyword(s):  
Electrical Stimulation ◽  
Synaptic Input ◽  
Action Potentials ◽  
Efferent Nerve ◽  
Neural Input ◽  
Central Origin ◽  
Cervical Ganglion ◽  
Intracellular Action ◽  
Peripheral Origin

In vitro studies were conducted on the middle cervical ganglion (MCG) of the cat by recording intracellular action potentials from its neurons. The purpose of this study was to examine the possibility of a peripheral synaptic input to the MCG. Preganglionic electrical stimulation, via the ventral ansa (VA) and dorsal ansa (DA) subclavia, and post-ganglionic electrical stimulation, via the ventrolateral cardiac nerve (VCN), evoked graded synaptic responses that led to the discharge of one or more action potentials in the 14 ganglia studied. The conduction velocity of these pathways ranged from 0.4 to 0.9 m/s. Ten percent of the cells impaled were inexcitable, even with direct intracellular depolarizing current, whereas 80% of the neurons studied received a synaptic input from fibers of both central and peripheral origin. In addition, subthreshold synaptic inputs from peripheral and central origin sum to discharge the cell, suggesting an integration of neural inputs in the MCG. These responses were blocked by d-tubocurarine chloride. This evidence indicates that sympathetic efferent nerve activity can be modified by peripheral excitatory inputs and that these inputs may function as pathways for a peripheral reflex at the level of the MCG.

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.

Spontaneous Subthreshold Membrane Potential Fluctuations and Action Potential Variability of Rat Corticostriatal and Striatal Neurons In Vivo

1997 ◽  
Vol 77 (4) ◽  
pp. 1697-1715 ◽  
Author(s):  
Edward A. Stern ◽  
Anthony E. Kincaid ◽  
Charles J. Wilson
Keyword(s):  
Membrane Potential ◽  
Synaptic Input ◽  
High Frequency ◽  
Action Potentials ◽  
State Transitions ◽  
Striatal Neurons ◽  
Interspike Intervals ◽  
Potential Fluctuations ◽  
Membrane Potential Fluctuations

Stern, Edward A., Anthony E. Kincaid, and Charles J. Wilson. Spontaneous subthreshold membrane potential fluctuations and action potential variability of rat corticostriatal and striatal neurons in vivo. J. Neurophysiol. 77: 1697–1715, 1997. We measured the timing of spontaneous membrane potential fluctuations and action potentials of medial and lateral agranular corticostriatal and striatal neurons with the use of in vivo intracellular recordings in urethan-anesthetized rats. All neurons showed spontaneous subthreshold membrane potential shifts from 7 to 32 mV in amplitude, fluctuating between a hyperpolarized down state and depolarized up state. Action potentials arose only during the up state. The membrane potential state transitions showed a weak periodicity with a peak frequency near 1 Hz. The peak of the frequency spectra was broad in all neurons, indicating that the membrane potential fluctuations were not dominated by a single periodic function. At frequencies >1 Hz, the log of magnitude decreased linearly with the log of frequency in all neurons. No serial dependence was found for up and down state durations, or for the time between successive up or down state transitions, showing that the up and down state transitions are not due to superimposition of noisy inputs onto a single frequency. Monte Carlo simulations of stochastic synaptic inputs to a uniform finite cylinder showed that the Fourier spectra obtained for corticostriatal and striatal neurons are inconsistent with a Poisson-like synaptic input, demonstrating that the up state is not due to an increase in the strength of an unpatterned synaptic input. Frequency components arising from state transitions were separated from those arising from the smaller membrane potential fluctuations within each state. A larger proportion of the total signal was represented by the fluctuations within states, especially in the up state, than was predicted by the simulations. The individual state spectra did not correspond to those of random synaptic inputs, but reproduced the spectra of the up and down state transitions. This suggests that the process causing the state transitions and the process responsible for synaptic input may be the same. A high-frequency periodic component in the up states was found in the majority of the corticostriatal cells in the sample. The average size of the component was not different between neurons injected with QX-314 and control neurons. The high-frequency component was not seen in any of our sample of striatal cells. Corticostriatal and striatal neurons' coefficients of variation of interspike intervals ranged from 1.0 to 1.9. When interspike intervals including a down state were subtracted from the calculation, the coefficient of variation ranged from 0.4 to 1.1, indicating that a substantial proportion of spike interval variance was due to the subthreshold membrane potential fluctuations.

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