Suppression of gill withdrawal reflex behaviours in Aplysia: the role of acetylcholine

1990 ◽  
Vol 68 (11) ◽  
pp. 1407-1413
Author(s):  
David Cawthorpe ◽  
Ken Lukowiak
Keyword(s):  
Tactile Stimulation ◽  
Aplysia Californica ◽  
Withdrawal Reflex ◽  
Stimulation Of

Acetylcholine (ACh) dissolved in seawater and perfused through the isolated gill of the Aplysia californica produced suppression of the gill withdrawal reflex (GWR) evoked by tactile stimulation of the gill. This suppression was reversible upon washout and was blocked by co-perfusion of curare and α-bungarotoxin. Co-perfusion of atropine did not block the suppression of the GWR produced by ACh. We concluded that the suppressive effects produced by perfusion of ACh through the gill occur as a result of the action of ACh at the nicotinic-like receptors. The role of ACh suppression in the mediation of gill reflex behaviours is discussed.Key words: Aplysia, gill withdrawal reflex, suppression, acetylcholine.

Transfer of Habituation Shows an Interaction Between Neuronal Circuits of the Gill Withdrawal Reflex in Aplysia Californica

1982 ◽  
Vol 96 (1) ◽  
pp. 107-124
Author(s):  
JEFF GOLDBERG ◽  
KEN LUKOWIAK
Keyword(s):  
Tactile Stimulation ◽  
Neural Circuits ◽  
Repetitive Stimulation ◽  
Integrated System ◽  
Neuronal Circuits ◽  
Withdrawal Reflex ◽  
Motor Neurones ◽  
Excitatory Responses ◽  
Lines Of Evidence ◽  
Stimulation Of

The gill withdrawal reflex (GWR) and its subsequent habituation can be evoked by tactile stimulation of the siphon or gill when the CNS is either intact or removed. It has been suggested that the neural circuits that mediate the GWR evoked at these two loci are parallel and independent. We provide three lines of evidence which show that these circuits interact and, therefore, comprise a single integrated system. Firtly, siphon and gill stimulation evoked similar excitatory responses in the central gill motor neurones. Secondly, the GWR habituated by repetitive stimulation at one locus was dishabituated by stimulation of the other locus. Thirdly, transfer of habituation occurred. Although the transfer was seen neurally at the level of central gill motor neurones, transfer of habituation also occurred after the CNS was removed. Therefore, the neuronal circuits mediating the reflexes evoked at the siphon and gill interact within both the CNS and PNS. The PNS is largely responsible for mediating this gill behaviour that is based on such interactions, while the CNS provides suppressive and facilitatory plasticity to these responses to enable Aplysia to better adapt to a changing environment.

Tactile stimulation of adult rats modulates hormonal responses, depression-like behaviors, and memory impairment induced by chronic mild stress: Role of angiotensin II

2020 ◽  
Vol 379 ◽  
pp. 112250 ◽  
Author(s):  
Rafaela Costa ◽  
Mariana Leite Tamascia ◽  
Andrea Sanches ◽  
Roseli Peres Moreira ◽  
Tatiana Sousa Cunha ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Memory Impairment ◽  
Tactile Stimulation ◽  
Chronic Mild Stress ◽  
Mild Stress ◽  
Adult Rats ◽  
Hormonal Responses ◽  
Stimulation Of

Picrotoxin prevents habituation of the gill withdrawal reflex in Aplysia

1978 ◽  
Vol 56 (6) ◽  
pp. 1079-1082 ◽  
Author(s):  
Ken Lukowiak
Keyword(s):  
Tactile Stimulation ◽  
Aminobutyric Acid ◽  
Adaptive Behaviour ◽  
Repeated Presentation ◽  
Reflex Amplitude ◽  
Repeated Stimulation ◽  
Withdrawal Reflex ◽  
Reflex Latency ◽  
Cns Control ◽  
Stimulation Of

The gill withdrawal reflex evoked by tactile stimulation of the siphon in Aplysia habituates with repeated presentation of the stimulus. This adaptive behaviour is mediated by the integrated activity of the central (CNS) and peripheral (PNS) nervous systems. The PNS mediates the basic reflex and its habituation while the CNS exerts both suppressive and facilitatory control over the PNS. This results in greater adaptability of the reflex behaviours. In young Aplysia the CNS control is absent and this is due to the incomplete development of pathways in the CNS. In an attempt to identify the pathway an attempt was made to manipulate the CNS's suppressive influence by agents which antagonize putative neurotransmitters. The application of picrotoxin-containing seawater over the CNS removed the CNS's suppressive influence but not its facilitatory influence. Thus the reflex amplitude was increased, the reflex latency decreased, and repeated stimulation did not result in habituation. This effect of picrotoxin was completely reversible. It is thus proposed that γ-aminobutyric acid, a putative neurotransmitter, plays an important rote in the mediation of the CNS's suppressive influence.

Contribution of individual mechanoreceptor sensory neurons to defensive gill-withdrawal reflex in Aplysia

1978 ◽  
Vol 41 (2) ◽  
pp. 418-431 ◽  
Author(s):  
J. H. Byrne ◽  
V. F. Castellucci ◽  
E. R. Kandel
Keyword(s):  
Motor Neuron ◽  
Sensory Neuron ◽  
Sensory Neurons ◽  
Motor Neurons ◽  
Tactile Stimulation ◽  
Sensory Cell ◽  
Divalent Cations ◽  
Plastic Properties ◽  
Withdrawal Reflex ◽  
Stimulation Of

1. To evaluate the contribution which mechanoreceptor sensory neurons make to the defensive gill-withdrawal reflex we developed an isolated reflex preparation. We then reduced this isolated reflex to a microcircuit (consisting of a single sensory cell and single motor cell) so as to causally relate the contribution of individual cells to the expression and plastic properties of the behavior. 2. Mechanoreceptor neurons make significant contributions to the amplitude and duration of the complex PSP in the motor neurons. A single spike in a sensory neuron produces an EPSP in the motor neuron which accounts for 7-36% of the complex EPSP produced by weak tactile stimulation of the skin. 3. More than 50% of the synaptic input to the gill motor neurons appears to be monosynaptic. Perfusing the ganglion with solutions of high divalent cations reduced the motor neurons' complex PSP by only 40%. 4. The population response of the mechanoreceptors to a point stimulus can be simulated by repetitively firing a single sensory neuron. Firing a single sensory cell discharges the motor neuron and produces a gill contraction similar to that produced by a natural stimulus. 5. Mechanoreceptors make monosynaptic connections onto gill motor neurons which decrement with repeated stimulation paralleling the decrement of the complex PSP to punctate tactile stimulation of the skin. 6. The results indicate that the known neural elements may quantitatively account for most of the expression of the behavior and its short-term habituation.

scholarly journals Operant conditioning of aerial respiratory behaviour in Lymnaea stagnalis

1996 ◽  
Vol 199 (3) ◽  
pp. 683-691 ◽  
Author(s):  
K Lukowiak ◽  
E Ringseis ◽  
G Spencer ◽  
W Wildering ◽  
N Syed
Keyword(s):  
Operant Conditioning ◽  
Tactile Stimulation ◽  
Direct Evidence ◽  
Lymnaea Stagnalis ◽  
Freshwater Snail ◽  
Withdrawal Reflex ◽  
Before And After ◽  
Opening And Closing ◽  
Stimulation Paradigm ◽  
Stimulation Of

In this study, we operantly conditioned the aerial respiratory behaviour of the freshwater snail Lymnaea stagnalis. Aerial respiration in Lymnaea stagnalis is accomplished by the spontaneous opening and closing of its respiratory orifice, the pneumostome, at the water surface. Weak tactile stimulation of the pneumostome area, when the pneumostome is open, evoked only the pneumostome closure response, which is one aspect of the escape-withdrawal reflex. Pneumostome stimulation resulted in its closure and the termination of aerial respiratory activity. A contingent tactile stimulation paradigm was used to operantly condition the animals. Stimulation of the pneumostome whenever the animal attempted to breathe resulted in significantly fewer attempts to open the pneumostome as training progressed. The latency of the first breath (subsequent to stimulation), the number of breaths and the total breathing time were measured before and after each training period. Significant, quantifiable changes in these behavioural parameters were observed only in the operant conditioning group animals. Control animals receiving tactile stimulation to their pneumostome not contingent upon pneumostome opening movements (yoked controls) or those that were physically prevented from surfacing to breathe (hypoxic controls), did not exhibit significant changes in these behavioural parameters. Our data provide the first direct evidence for operant conditioning of respiration in any animal.

Stimulation of Ca(2+)-dependent exocytosis of the sperm acrosome by cAMP acting downstream of phospholipase A2

Reproduction ◽  
2000 ◽  
pp. 57-68 ◽  
Author(s):  
J Garde ◽  
ER Roldan
Keyword(s):  
Arachidonic Acid ◽  
Phospholipase A2 ◽  
Phospholipase C ◽  
Phosphodiesterase Inhibitors ◽  
Dibutyryl Camp ◽  
Camp Phosphodiesterase ◽  
Ram Sperm ◽  
Camp Formation ◽  
Stimulation Of

Spermatozoa undergo exocytosis in response to agonists that induce Ca2+ influx and, in turn, activation of phosphoinositidase C, phospholipase C, phospholipase A2, and cAMP formation. Since the role of cAMP downstream of Ca2+ influx is unknown, this study investigated whether cAMP modulates phospholipase C or phospholipase A2 using a ram sperm model stimulated with A23187 and Ca2+. Exposure to dibutyryl-cAMP, phosphodiesterase inhibitors or forskolin resulted in enhancement of exocytosis. However, the effect was not due to stimulation of phospholipase C or phospholipase A2: in spermatozoa prelabelled with [3H]palmitic acid or [14C]arachidonic acid, these reagents did not enhance [3H]diacylglycerol formation or [14C]arachidonic acid release. Spermatozoa were treated with the phospholipase A2 inhibitor aristolochic acid, and dibutyryl-cAMP to test whether cAMP acts downstream of phospholipase A2. Under these conditions, exocytosis did not occur in response to A23187 and Ca2+. However, inclusion of dibutyryl-cAMP and the phospholipase A2 metabolite lysophosphatidylcholine did result in exocytosis (at an extent similar to that seen when cells were treated with A23187/Ca2+ and without the inhibitor). Inclusion of lysophosphatidylcholine alone, without dibutyryl-cAMP, enhanced exocytosis to a lesser extent, demonstrating that cAMP requires a phospholipase A2 metabolite to stimulate the final stages of exocytosis. These results indicate that cAMP may act downstream of phospholipase A2, exerting a regulatory role in the exocytosis triggered by physiological agonists.

scholarly journals Pre-motor versus motor cerebral cortex neuromodulation for chronic neuropathic pain

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Igor Lavrov ◽  
Timur Latypov ◽  
Elvira Mukhametova ◽  
Brian Lundstrom ◽  
Paola Sandroni ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Cerebral Cortex ◽  
Motor Cortex ◽  
Initial Assessment ◽  
Motor Cortex Stimulation ◽  
Chronic Neuropathic Pain ◽  
Long Term Effect ◽  
Stimulation Of

AbstractElectrical stimulation of the cerebral cortex (ESCC) has been used to treat intractable neuropathic pain for nearly two decades, however, no standardized approach for this technique has been developed. In order to optimize targeting and validate the effect of ESCC before placing the permanent grid, we introduced initial assessment with trial stimulation, using a temporary grid of subdural electrodes. In this retrospective study we evaluate the role of electrode location on cerebral cortex in control of neuropathic pain and the role of trial stimulation in target-optimization for ESCC. Location of the temporary grid electrodes and location of permanent electrodes were evaluated in correlation with the long-term efficacy of ESCC. The results of this study demonstrate that the long-term effect of subdural pre-motor cortex stimulation is at least the same or higher compare to effect of subdural motor or combined pre-motor and motor cortex stimulation. These results also demonstrate that the initial trial stimulation helps to optimize permanent electrode positions in relation to the optimal functional target that is critical in cases when brain shift is expected. Proposed methodology and novel results open a new direction for development of neuromodulation techniques to control chronic neuropathic pain.

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