Multiple mechanisms for peripheral activation of the peptide-containing radula mechanoafferent neurons B21 and B22 of Aplysia

1996 ◽  
Vol 76 (2) ◽  
pp. 1344-1351 ◽  
Author(s):  
E. C. Cropper ◽  
C. G. Evans ◽  
S. C. Rosen
Keyword(s):  
Central Pattern Generator ◽  
Sensory Neurons ◽  
Sensory Input ◽  
Pattern Generator ◽  
Contractile Properties ◽  
Mechanical Stimuli ◽  
Buccal Ganglion ◽  
Motor Programs ◽  
Peripheral Activation ◽  
Stimulation Of

1. Recently a cluster of sensory neurons (peptidergic radula mechanoafferents) has been identified in the buccal ganglion of Aplysia that is likely to play an important role in influencing the activity of feeding motor programs. All of the neurons of this cluster, which includes the identified cells B21 and B22, send axons via the radula nerve to a layer of tissue that lies under the chitinous radula (the subradula tissue). 2. We show that the subradula tissue has contractile properties. In the absence of the CNS, contractions of the subradula tissue are elicited if the subradula tissue is stretched. Alternatively, contractions are elicited when extracellular suction electrodes are used to stimulate buccal nerve 3 or the radula nerve. 3. Previous studies have shown that neurons of the B21/B22 cluster respond to peripherally applied mechanical stimuli. We show that these neurons are also activated when the subradula tissue contracts. Axon spikes (A spikes) can be intracellularly recorded from radula mechanoafferent neurons when contractions of the subradula tissue are elicited either by stretch or by extracellular stimulation of buccal nerve 3. 4. Mechanical stimuli that are subthreshold when applied alone elicit A spikes if they are applied while the subradula tissue is contracting. We postulate that this type of interaction may play an important role in gating sensory input to the feeding central pattern generator.

A Newly Identified Buccal Interneuron Initiates and Modulates Feeding Motor Programs in Aplysia

2003 ◽  
Vol 90 (4) ◽  
pp. 2190-2204 ◽  
Author(s):  
N. C. Dembrow ◽  
J. Jing ◽  
A. Proekt ◽  
A. Romero ◽  
F. S. Vilim ◽  
...  
Keyword(s):  
Central Pattern Generator ◽  
Pattern Generator ◽  
Considerable Progress ◽  
Buccal Ganglion ◽  
Motor Programs ◽  
Cerebral Ganglia ◽  
Full Complement ◽  
Electrophysiological Characterization

Despite considerable progress in characterizing the feeding central pattern generator (CPG) in Aplysia, the full complement of neurons that generate feeding motor programs has not yet been identified. The distribution of neuropeptide-containing neurons in the buccal and cerebral ganglia can be used as a tool to identify additional elements of the feeding circuitry by providing distinctions between otherwise morphologically indistinct neurons. For example, our recent study revealed a unique and potentially interesting unpaired PRQFVamide (PRQFVa)-containing neuron in the buccal ganglion. In this study, we describe the morphological and electrophysiological characterization of this novel neuron, which we designate as B50. We found that activation of B50 is capable of producing organized rhythmic output of the feeding CPG. The motor programs elicited by B50 exhibit some similarities as well as differences to motor programs elicited by the command-like cerebral-to-buccal interneuron CBI-2. In addition to activating the feeding CPG, B50 may act as a program modulator.

Behavior-Dependent Activities of a Central Pattern Generator in Freely Behaving Lymnaea stagnalis

1997 ◽  
Vol 78 (6) ◽  
pp. 3415-3427 ◽  
Author(s):  
Rene F. Jansen ◽  
Anton W. Pieneman ◽  
Andries ter Maat
Keyword(s):  
Electrical Activity ◽  
Central Pattern Generator ◽  
Lymnaea Stagnalis ◽  
Central Pattern Generators ◽  
Pattern Generator ◽  
Egg Laying ◽  
Buccal Ganglion ◽  
Level Of Activity ◽  
Freely Behaving ◽  
Pattern Generators

Jansen, Rene F., Anton W. Pieneman, and Andries ter Maat. Behavior-dependent activities of a central pattern generator in freely behaving Lymnaea stagnalis. J. Neurophysiol. 78: 3415–3427, 1997. Cyclic or repeated movements are thought to be driven by networks of neurons (central pattern generators) that are dynamic in their connectivity. During two unrelated behaviors (feeding and egg laying), we investigated the behavioral output of the buccal pattern generator as well as the electrical activity of a pair of identified interneurons that have been shown to be involved in setting the level of activity of this pattern generator (PG). Analysis of the quantile plots of the parameters that describe the behavior (movements of the buccal mass) reveals that during egg laying, the behavioral output of the PG is different compared with that during feeding. Comparison of the average durations of the different parts of the buccal movements showed that during egg laying, the duration of one specific part of buccal movement is increased. Correlated with these changes in the behavioral output of the PG were changes in the firing rate of the cerebral giant neurons (CGC), a pair of interneurons that have been shown to modulate the activity of the PG by means of multiple synaptic contacts with neurons in the buccal ganglion. Interval- and autocorrelation histograms of the behavioral output and CGC spiking show that both the PG output and the spiking properties of the CGCs are different when comparing egg-laying animals with feeding animals. Analysis of the timing relations between the CGCs and the behavioral output of the PG showed that both during feeding and egg laying, the electrical activity of the CGCs is largely in phase with the PG output, although small changes occur. We discuss how these results lead to specific predictions about the kinds of changes that are likely to occur when the animal switches the PG from feeding to egg laying and how the hormones that cause egg laying are likely to be involved.

Entrainment of the Swimmeret Rhythm of the Crayfish to Controlled Movements of Some of the Appendages

1989 ◽  
Vol 144 (1) ◽  
pp. 257-278
Author(s):  
SIMON R. T. DELLER ◽  
DAVID L. MACMILLAN
Keyword(s):  
Central Pattern Generator ◽  
Small Proportion ◽  
Nerve Cord ◽  
Sensory Input ◽  
Pattern Generator ◽  
Nerve Cords

Please send reprint requests and enquiries to this author A machine was used to impose controlled movements, closely resembling natural movements, on some of the swimmerets of crayfish with their ventral nerve cords cut between thorax and abdomen. The rhythm of the unrestrained swimmerets could be entrained to the imposed frequency. Full entrainment occurred most readily when three or four swimmerets were controlled and was uncommon with two. When one was controlled, only partial entrainment was seen. A small proportion of preparations could not be entrained irrespective of the number of swimmerets controlled. Entrainment of the neural rhythm also occurred when movement was imposed on one or more swimmerets attached to an otherwise isolated nerve cord. This is the first demonstration that sensory input affects the periodicity of the swimmeret rhythm. In the light of this result, the hypothesis that swimmeret rhythm is largely controlled by a central pattern generator should be viewed with caution. It now appears that there is also an influential sensory component responsible for stabilizing and adjusting the timing of the swimmeret rhythm.

Gating of Afferent Input by a Central Pattern Generator

1999 ◽  
Vol 81 (2) ◽  
pp. 950-953 ◽  
Author(s):  
Ralph A. DiCaprio
Keyword(s):  
Central Pattern Generator ◽  
Sensory Input ◽  
Motor Pattern ◽  
Pattern Generator ◽  
Afferent Input ◽  
Inhibitory Input ◽  
Cycle Period ◽  
Intracellular Recordings ◽  
Afferent Fibers ◽  
Sufficient Magnitude

Gating of afferent input by a central pattern generator. Intracellular recordings from the sole proprioceptor (the oval organ) in the crab ventilatory system show that the nonspiking afferent fibers from this organ receive a cyclic hyperpolarizing inhibition in phase with the ventilatory motor pattern. Although depolarizing and hyperpolarizing current pulses injected into a single afferent will reset the ventilatory motor pattern, the inhibitory input is of sufficient magnitude to block afferent input to the ventilatory central pattern generator (CPG) for ∼50% of the cycle period. It is proposed that this inhibitory input serves to gate sensory input to the ventilatory CPG to provide an unambiguous input to the ventilatory CPG.

Brain-derived neurotrophic factor stimulation of T-type Ca2+ channels in sensory neurons contributes to increased peripheral pain sensitivity

2019 ◽  
Vol 12 (600) ◽  
pp. eaaw2300 ◽  
Author(s):  
Hua Wang ◽  
Yuan Wei ◽  
Yichen Pu ◽  
Dongsheng Jiang ◽  
Xinghong Jiang ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Sensory Neurons ◽  
Neurotrophic Factor ◽  
Pain Sensitivity ◽  
Neuronal Excitability ◽  
Brain Derived Neurotrophic Factor ◽  
Mitogen Activated Protein Kinase ◽  
Mechanical Stimuli ◽  
Action Potential Firing ◽  
Stimulation Of

Although brain-derived neurotrophic factor (BDNF) is implicated in the nociceptive signaling of peripheral sensory neurons, the underlying mechanisms remain largely unknown. Here, we elucidated the effects of BDNF on the neuronal excitability of trigeminal ganglion (TG) neurons and the pain sensitivity of rats mediated by T-type Ca2+ channels. BDNF reversibly and dose-dependently enhanced T-type channel currents through the activation of tropomyosin receptor kinase B (TrkB). Antagonism of phosphatidylinositol 3-kinase (PI3K) but not of its downstream target, the kinase AKT, abolished the BDNF-induced T-type channel response. BDNF application activated p38 mitogen-activated protein kinase (MAPK), and this effect was prevented by inhibition of PI3K but not of protein kinase A (PKA). Antagonism of either PI3K or p38 MAPK prevented the BDNF-induced stimulation of PKA activity, whereas PKA inhibition blocked the BDNF-mediated increase in T-type currents. BDNF increased the rate of action potential firing in TG neurons and enhanced the pain sensitivity of rats to mechanical stimuli. Moreover, inhibition of TrkB signaling abolished the increased mechanical sensitivity in a rat model of chronic inflammatory pain, and this effect was attenuated by either T-type channel blockade or knockdown of the channel Cav3.2. Together, our findings indicate that BDNF enhances T-type currents through the stimulation of TrkB coupled to PI3K-p38-PKA signaling, thereby inducing neuronal hyperexcitability of TG neurons and pain hypersensitivity in rats.

Fast Synaptic Connections From CBIs to Pattern-Generating Neurons in Aplysia: Initiation and Modification of Motor Programs

2003 ◽  
Vol 89 (4) ◽  
pp. 2120-2136 ◽  
Author(s):  
Itay Hurwitz ◽  
Irving Kupfermann ◽  
Klaudiusz R. Weiss
Keyword(s):  
Central Pattern Generator ◽  
Motor Pattern ◽  
Aplysia Californica ◽  
Pattern Generator ◽  
Synaptic Connections ◽  
Motor Patterns ◽  
Motor Programs ◽  
Postsynaptic Potentials ◽  
Buccal Ganglia ◽  
Very High

Consummatory feeding movements in Aplysia californica are organized by a central pattern generator (CPG) in the buccal ganglia. Buccal motor programs similar to those organized by the CPG are also initiated and controlled by the cerebro-buccal interneurons (CBIs), interneurons projecting from the cerebral to the buccal ganglia. To examine the mechanisms by which CBIs affect buccal motor programs, we have explored systematically the synaptic connections from three of the CBIs (CBI-1, CBI-2, CBI-3) to key buccal ganglia CPG neurons (B31/B32, B34, and B63). The CBIs were found to produce monosynaptic excitatory postsynaptic potentials (EPSPs) with both fast and slow components. In this report, we have characterized only the fast component. CBI-2 monosynaptically excites neurons B31/B32, B34, and B63, all of which can initiate motor programs when they are sufficiently stimulated. However, the ability of CBI-2 to initiate a program stems primarily from the excitation of B63. In B31/B32, the size of the EPSPs was relatively small and the threshold for excitation was very high. In addition, preventing firing in either B34 or B63 showed that only a block in B63 firing prevented CBI-2 from initiating programs in response to a brief stimulus. The connections from CBI-2 to the buccal ganglia neurons showed a prominent facilitation. The facilitation contributed to the ability of CBI-2 to initiate a BMP and also led to a change in the form of the BMP. The cholinergic blocker hexamethonium blocked the fast EPSPs induced by CBI-2 in buccal ganglia neurons and also blocked the EPSPs between a number of key CPG neurons within the buccal ganglia. CBI-2 and B63 were able to initiate motor patterns in hexamethonium, although the form of a motor pattern was changed, indicating that non-hexamethonium-sensitive receptors contribute to the ability of these cells to initiate bursts. By contrast to CBI-2, CBI-1 excited B63 but inhibited B34. CBI-3 excited B34 and not B63. The data indicate that CBI-1, -2, and -3 are components of a system that initiates and selects between buccal motor programs. Their behavioral function is likely to depend on which combination of CBIs and CPG elements are activated.

Multiple Contributions of an Input-Representing Neuron to the Dynamics of the Aplysia Feeding Network

2007 ◽  
Vol 97 (4) ◽  
pp. 3046-3056 ◽  
Author(s):  
Alex Proekt ◽  
Jian Jing ◽  
Klaudiusz R. Weiss
Keyword(s):  
Central Pattern Generator ◽  
Motor Program ◽  
Pattern Generator ◽  
Higher Order ◽  
Motor Output ◽  
Slow Dynamics ◽  
Motor Programs ◽  
The Future

In Aplysia, mutually antagonistic ingestive and egestive behaviors are produced by the same multifunctional central pattern generator (CPG) circuit. Interestingly, higher-order inputs that activate the CPG do not directly specify whether the resulting motor program is ingestive or egestive because the slow dynamics of the network intervene. One input, the commandlike cerebral–buccal interneuron 2 (CBI-2), slowly drives the motor output toward ingestion, whereas another input, the esophageal nerve (EN), drives the motor output toward egestion. When the input is switched from EN to CBI-2, the motor output does not switch immediately and remains egestive. Here, we investigated how these slow dynamics are implemented on the interneuronal level. We found that activity of two CPG interneurons, B20 and B40, tracked the motor output regardless of the input, whereas activity of another CPG interneuron, B65, tracked the input regardless of the motor output. Furthermore, we show that the slow dynamics of the network are implemented, at least in part, in the slow dynamics of the interaction between the input-representing and the output-representing neurons. We conclude that 1) a population of CPG interneurons, recruited during a particular motor program, simultaneously encodes both the input that is used to elicit the motor program and the output elicited by this input; and 2) activity of the input-representing neurons may serve to bias the future motor programs.

B64, a newly identified central pattern generator element producing a phase switch from protraction to retraction in buccal motor programs of Aplysia californica

1996 ◽  
Vol 75 (4) ◽  
pp. 1327-1344 ◽  
Author(s):  
I. Hurwitz ◽  
A. J. Susswein
Keyword(s):  
Phase Shift ◽  
Central Pattern Generator ◽  
Motor Program ◽  
Pattern Generator ◽  
Synaptic Activity ◽  
Excitatory Postsynaptic Potential ◽  
Motor Programs ◽  
Identified Neuron ◽  
Protraction Phase ◽  
Two Phases

1. Buccal motor programs in Aplysia are characterized by two phases of activity, which represent protraction and retraction of the radula in intact animals. The shift from protraction to retraction is caused by synaptic activity inhibiting neurons that are active during protraction and exciting neurons that are active during retraction. 2. B64, a newly identified neuron present bilaterally in the buccal ganglia, is partially responsible for the phase shift. Stimulating a single B64 causes bilateral inhibition of neurons B31/B32 and other neurons active during protraction and cause bilateral excitation of neurons B4/B5 and other neurons active during retraction. B64 is active throughout retraction. The amplitude and waveforms of the synaptic potentials caused by firing B64 are similar, but not identical, to those seen during retraction. 3. Some of the effects of B64 on B31/B32 and on B4/B5 are monosynaptic, as shown by their maintained presence in high divalent cation seawater, which blocks polysynaptic activity. 4. A brief depolarization of B64 leads to a long-lasting depolarization and firing. The ability of B64 to respond in this way is at least partially caused by an endogenous plateau potential, as this property is still seen after synaptic transmission is blocked. 5. Hyperpolarization of B64 bilaterally and preventing the somata from firing unmasks a large excitatory postsynaptic potential in B64. This procedure does not block the shift from protraction to retraction, indicating that spiking in the B64 somata is not necessary for the phase shift. 6. The firing pattern and synaptic connections of B64 are consistent with the hypothesis that the neuron is part of a central pattern generator underlying buccal motor programs. B64 is monosynaptically inhibited by neurons that are active along with B31/B32, which are responsible for producing the protraction phase of a buccal motor program. During the later portion of the protraction phase B64 is excited. In addition, firing B64 can phase advance and phase delay buccal motor programs. 7. Regulating the firing of B64 can regulate the expression of buccal motor programs. Stimulation of B64 at frequencies of 0.5-1.0 Hz leads to complete inhibition of buccal motor programs, whereas steady-state depolarization of B64 can lead to repetitive bursts of activity.

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