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K Lukowiak

Publications and source records attributed to K Lukowiak.

At least 91 records · Page 5Linked to original sources
PubMed1984

Cholinergic receptors in the Aplysia gill.

Acetylcholine has been suggested as a neurotransmitter released in the Aplysia gill by peripheral afferents of central neurons and by peripheral neurons within the gill. The perfused gill, isolated from the abdominal ganglion, was examined. At concentrations greater than 1 microM, acetylcholine elicited a slowly developing tonic contraction of the afferent vein that reversed upon washout. This effect was observed on both quiescent and active preparations. At concentrations less than 1 microM, acetylcholine perfusion resulted in a reduction of gill tone. The excitatory effect of acetylcholine was reduced 80 and 60% by the cholinergic antagonists atropine and hexamethonium, respectively. The acetylcholine-evoked contraction was potentiated 2.5-fold when curare was coinfused. Carbachol did not mimic the excitatory effects of acetylcholine. At all concentrations examined (1-100 microM), carbachol infusion reduced baseline tension, the amplitude of spontaneous contractions and contractions evoked by FMRFamide and dopamine. Contractions evoked by perfusion of p-chlorophenylthiocyclic AMP were greatly reduced when carbachol was added to the perfusate. Further addition of curare reversibly blocked carbachol inhibition of the cyclic AMP-evoked contractions. These findings suggest that excitatory and inhibitory cholinergic receptors are involved in the regulation of gill contractile behavior by acetylcholine.

Acetylcholine↗
PubMed1984

Transfer of habituation in Aplysia: contribution of heterosynaptic pathways in habituation of the gill-withdrawal reflex.

Habituation of the Aplysia gill-withdrawal reflex (and siphon-withdrawal reflex) has been attributed to low-frequency homosynaptic depression at central sensory-motor synapses. The recent demonstration that transfer of habituation between stimulation sites occurs in this model system has prompted the hypothesis that heterosynaptic inhibitory pathways also play a role in the mediation of habituation behavior. To test this hypothesis, the sites and mechanisms of neural plasticity which underlie transfer of habituation in Aplysia were examined. Transfer of habituation is a reduction in the reflex evoked at one stimulation site (siphon) due to repeated presentation of a stimulus to a second site (gill). Centrally mediated transfer of habituation, measured in a preparation lacking the siphon-gill peripheral nervous system (PNS), was associated with a reduced excitatory response in central motor neurons. Repeated tactile stimulation of the gill did not attenuate the gill response evoked by electrical stimulation of the branchial nerve nor the mechanoreceptor response recorded in LE sensory neurons. In contrast, repeated stimulation of siphon or gill at a site which was "off" the sensory field of a specific mechanoreceptor led to a diminution in synaptic transmission between that sensory neuron and its followers (motor neurons and inter-neurons). These data demonstrate that centrally mediated transfer of habituation results from heterosynaptic modulation of synaptic transmission at the sensory-motor (and sensory-interneuron) synapses. Therefore, habituation behavior in Aplysia is mediated through the conjoint action of homosynaptic and heterosynaptic inhibitory processes.

Animals↗
PubMed1984

Long-lasting inhibition of neuron R15 of Aplysia: role of the interneuron II network.

Stimulation of the branchial or either connective nerve of the abdominal ganglion of Aplysia californica evokes simultaneous responses in cells R15, L8, L9, and L11 which are indistinguishable from those arising from spontaneous interneuron II (INT II) activity. Threshold for the INT II-like response in all cells is identical, suggesting that the response is mediated by INT II activity. The magnitude of the response in each cell increases with stimulus intensity and is subject to both temporal and spatial summation, implying the existence of multiple fibres in each nerve which converge on INT II. Repetitive stimulation evokes long-lasting inhibition in R15. The onset of this phenomenon is always accompanied by an INT II burst in the other follower cells. Long-lasting inhibition in R15 is not accompanied by prolonged INT II activity, suggesting an endogenous mechanism of inhibition. The phosphodiesterase inhibitor, IBMX, potentiates the response of R15 to nerve stimulation without affecting threshold for the response. This is consistent with inhibition by a mechanism endogenous to R15.

1-Methyl-3-isobutylxanthine↗
PubMed1984

Evidence for FMRF-amide as a neurotransmitter in the gill of Aplysia californica.

In Aplysia californica, multiple regulatory mechanisms are involved in the actions of neurotransmitters on the gill. Neurotransmitter receptors and adenylate cyclase were examined in a particulate fraction of gill homogenates. The neuropeptide FMRF-amide stimulated enzyme activity 7- to 8-fold (EC50, 1 microM) via receptors that were pharmacologically distinct from those for dopamine and serotonin. FMRF-amide augmented cyclic AMP levels in slices of gill tissue with a time course similar to that for adenylate cyclase activation. Increases in cyclic AMP levels produced by the neuropeptide were potentiated by the phosphodiesterase inhibitor theophylline. Physiological responses to neuropeptides and cyclic AMP analogues were examined in a perfused, isolated gill preparation. Phasic contractions evoked by FMRF-amide (EC50, 0.1 microM) were mimicked by membrane-permeable analogues of cyclic AMP. Comparison of FMRF-amide effects on adenylate cyclase and gill behavior suggests an association between cyclic AMP and phasic contractions. In addition, FMRF-amide-like immunoreactivity, detected by antisera raised against the neuropeptide, was found in nerve fibers innervating the gill. These findings indicate that in Aplysia, FMRF-amide or a closely related peptide neurotransmitter may be involved in the physiological regulation of gill behavior.

Adenylyl Cyclases↗
PubMed1983

Modulation of the Aplysia gill withdrawal reflex by dopamine.

The ability of dopamine to modulate gill contractions was tested in Aplysia. When dopamine was perfused through the gill vasculature, gill contractions caused by siphon stimulation (gill withdrawal reflex) and by depolarization of the gill motor neuron L7 were increased in amplitude, as compared with those evoked during seawater perfusion. Habituation of gill movements, brought about by repetitive stimulation of the siphon or of L7, was prevented by dopamine. Despite the absence of reflex habituation, the number of action potentials in central gill motor neurons, evoked by siphon stimulation, showed normal decrement. Dopamine's effects were blocked when the ctenidial nerve was cut or when L7 hyperpolarized. These data suggest that dopamine acts peripherally to increase the efficacy of L7's synaptic transmission onto gill muscle or elements of the gill neural plexus.

Animals↗
PubMed1983

The gill withdrawal reflex is suppressed in sexually active Aplysia.

In Aplysia, the central nervous system and peripheral nervous system interact and form an integrated system that mediates adaptive gill withdrawal reflex behaviours evoked by tactile stimulation of the siphon. The central nervous system (CNS) exerts suppressive and facilitatory control over the peripheral nervous system (PNS) in the mediation of these behaviours. We found that the CNS's suppressive control over the PNS was increased significantly in animals engaged in sexual activity as either a male or female. In control animals, the evoked gill withdrawal reflex met a minimal response amplitude criterion, while in sexually active animals the reflex did not meet this criterion. At the neuronal level, the increased CNS suppressive control was manifested as a decrease in excitatory input to the central gill motor neurons.

Action Potentials↗
PubMed1983

Transfer of habituation between stimulation sites of the siphon withdrawal reflex in Aplysia californica.

Habituation of the siphon withdrawal reflex (SWR) can be evoked by iterative tactile stimuli presented to one of several sites, including the siphon and gill. The SWR evoked at an arbitrary "test" site did not habituate when stimuli were presented at 20-min intervals. However, there was a large decrease in the reflex evoked at the test site when the trial was preceded by 10 repetitive stimuli (interstimuli interval = 30 s) presented to the opposite "habituation" site. Transfer of habituation occurred from gill to siphon stimulation sites, and vice versa. There was a concomitant decrease in the excitatory input evoked in the central siphon motor neurons LDS1 and LDS3. Moreover, transfer of habituation occurred after the abdominal ganglion (central nervous system) was removed. There was little change in the magnitude of the control responses or transfer of habituation after deganglionation. Since transfer of habituation between stimulation sites of the SWR was similar to that reported previously for the gill withdrawal reflex, it was suggested that a common mechanism may underlie the two behaviors.

Animals↗
PubMed1983

FMRFamide effects on spontaneous and induced contractions of the anterior gizzard in Aplysia.

The effects of FMRFamide (Phe-Met-Arg-Phe-NH2), YGG-FMRFamide (Tyr-Gly-Gly-Phe-Met-Arg-Phe-NH2), and Met-enkephalin (Tyr-Gly-Gly-Phe-Met) on the isolated Aplysia anterior gizzard were examined. (i) FMRFamide inhibits spontaneous gut activity. While YGG-FMRFamide also inhibits spontaneous activity it is less potent than FMRFamide. Met-enkephalin does not affect spontaneous gut activity. (ii) FMRFamide inhibits the excitatory response of acetylcholine on both the anterior gizzard of Aplysia and the isolated stomach region of Navanax. (iii) Neither FMRFamide, YGG-FMRFamide, Met-enkephalin, nor acetylcholine stimulated the activity of adenylate cyclase in the Aplysia anterior gizzard.

Acetylcholine↗
PubMed1982

Methionine enkephalin increases CNS suppressive control exerted over gill reflex behaviours and associated neural activity in Aplysia california.

Suprafusion of methionine (Met) enkephalin (10(-9) to 10(-12) M) over the abdominal ganglion of Aplysia californica suppressed the amplitude of the siphon-evoked gill withdrawal reflex (GWR), increased the rate at which the GWR habituated and decreased the number of action potentials evoked in identified central gill motor neurons. The suppressive effects of Met-enkephalin could be blocked by pretreatment with naloxone; in addition, the presentation of a sensitizing stimulus immediately but transiently reversed the effects induced by the peptide. Met-Enkephalin did not affect the passive membrane properties of the gill motor neurons and thus it may act by affecting the activity of neurons which exert suppressive control over both gill reflex behaviours and afferent activity to the gill motor neurons.

Action Potentials↗
PubMed1981

An arginine vasotocin-like neuropeptide is present in the nervous system of the marine mollusc Aplysia californica.

Radioimmunoassays and high pressure liquid chromatography have been used to demonstrate the presence of an arginine-vasotocin-like peptide (AVT) in the anterior ganglia of Aplysia. Previously, AVT, using similar methods, was found to be present only in vertebrates. AVT when perfused over the abdominal ganglion (10(-6)-10(-12)M) was found to increase the bursting activity of R15, to decrease the bursting activity of L3-L6 and to increase the CNS's suppressive influence over the gill withdrawal reflex evoked by siphon stimulation. The AVT present in the nervous system of Aplysia may mediate long-term suppression of gill reflex behaviors induced by factors such as satiation and, as well, regulate the activity of certain neurosecretory neurons.

Animals↗
PubMed1981

Arginine vasotocin, an endogenous neuropeptide of Aplysia, suppresses the gill withdrawal reflex and reduces the evoked synaptic input to central gill motor neurons.

The superfusion (15 min) of arginine vasotocin (AVT; 10(-9)--10(-12) M) over the abdominal ganglion of Aplysia californica suppressed the amplitude of the gill withdrawal reflex evoked by tactile stimulation of the siphon, increased the rate of gill reflex habituation, and decreased the evoked synaptic activity to central gill motor neurons. The suppressive effects of AVT on gill reflex behaviors were not due to toxic effects of the hormone since the effects were completely reversible following washout and 3 h rest. The results obtained with AVT were similar to those previously found using the mammalian neuropeptide arginine vasopressin. AVT may act by increasing the activity of central neurons which exert suppressive control over both gill reflex behaviors and evoked activity to central gill motor neurons.

Animals↗
PubMed1980

CNS control over gill reflex behaviors in Aplysia: satiation causes an increase in the suppressive control in older but not young animals.

The CNS and PNS interact and form an integrated system which mediates adaptive gill withdrawal reflex behaviors evoked by tactile stimulation of the siphon. The CNS exerts suppressive and facilitatory control over the PNS in the mediation of these behaviors. It was found that in Aplysia the CNS's supressive control over the PNS was significantly greater than in nonsatiated control animals. In the controls, the evoked gill reflex met a mimimal response amplitute criterion with the CNS and PNS present, while in the satiated group the reflex did not meet this criterion. In the control group, the relflex amplitute and the subsequent habituation were the same following removal of the CNS, while in satiated animals the reflex amplitude was larger and the rate of habituation slower with only the PNS intact. Satiation had no effect on young Aplysia since CNS control was not yet operable. It is thus of prime importance to take the "state" of the preparation into consideration in the analysis of the neural mechanisms that underlie adaptive gill reflex behaviors. The gill withdrawal reflex and its subsequent habituation evoked by repeated tactile stimulation of the siphon in Aplysia has been studied extensively in an attempt to gain an understanding of the neuronal mechanisms that underlie adaptive behavior (Jacklet and Lukowiak, 1975; Kandel, 1976). It has been found that the central (CNS) and peripheral(PNS) nervous systems in Aplysia interact and form an integrated system which normally mediates both the reflex and its subsequent habituation (Peretz, Jacklet, and Lukowaik, 1976; Lukowiak and Peretz, 1977). Further, it was found that in the integrated system the CNS exerted both suppressive and facilitatory control over the PNS in the mediation of gills reflex behaviors (Lukowiak, 1977a). Removal of only the CNS's suppressive control over the PNS, while leaving intact its facilitatory influence, resulted in a significant reduction in reflex latency, a significant increase in reflex amplitude, and a reflex that is resistant to habituation with repeated stimulation (Lukowiak, 1977a). In addition, it was found that an identifiable neuron, Ld9, could modulate the ability of the reflex to habituate (Lukowiak, 1979a). With induced tonic low-level activity in L9 the reflex evoked by repeated siphon stimulation did not habituate even though the synaptic decremental process which occurs in gill motor neurons such as L7 and accompanies gill reflex habituation (Castellucci et al., 1970) continued to occur. The neurons in abdominal ganglion, which by their activity exert control over the PNS and thus the reflex, have not yet been identified but it is known that these same neutrons apparently exert control over the synaptic input received by gill motor neurons such as L7 from the central sensory neurons (Byrne, Castellucci, and Kandel, 1974) as a result of siphon stimulation (Peretz and Lukowiak, 1975; Lukowiak and Peretz, 1980).

Adaptation, Physiological↗
PubMed1980

Vasopressin increases the central nervous system suppressive control over gill reflex behaviours and associated neural activity in Aplysia.

Exposure of the abdominal ganglion of Aplysia to arginine vasopressin (10(-12) M) reduces the amplitude of the gill withdrawal reflex, accelerates its rate of habituation, and causes a concomitant decrease in the number of action potentials evoked in gill motor neuron L7. The effects of vasopressin on both the reflex and the concomitant neural activity evoked in L7 were completely reversible. Vasopressin did not affect the passive membrane properties of L7. The results indicate that a vertebrate neurohypophyseal hormone can affect behavioural responses as well as modify the synaptic efficacy of the reflex pathway.

Animals↗
PubMed1979

L9 modulation of L7's elicited gill withdrawal response in Aplysia.

The effects of induced L9 activity on gill motor neuron L7's ability to elicit a gill withdrawal response were studied. It was found that L9 was a modulator of L7's effectiveness to elicit gill movements. Following L9 activity, L7's ability to elicit a gill withdrawal response was significantly potentiated by up to 240% of control. L9 activity potentiated L7's elicited gill withdrawal response when frequencies of L7 activity were used which would result in decrement of the response or when frequencies were used in which decrement does not occur. Induced L9 activity may also have a minor potentiating effect on LDG1's ability to elicit gill movements. L9 was the only neuron found to possess these modulatory abilities. The interposition of the activity in the other gill motor neurons failed to have any effect. L9's modulatory role is separate and independent from its role as a gill motor neuron. L9's modulation of L7 is mediated peripherally in the gill and not in the CNS.

Animals↗
PubMed1979

L9 modulation of gill withdrawal reflex habituation in Aplysia.

Repeated tactile stimulation of the siphon in Aphysia normally results in habituation of the gill withdrawal reflex and a concomitant decrease in the amplitude of the excitatory synaptic input ot gill motor neurons in the abdominal ganglion. It was found, however, that induced low-level tonic activity in motor neuron L9, which does not itself elicit a gill withdrawal movement, prevented habituation of the reflex from occurring. Further, in preparations already habituated, this tonic low-level activity brought about a reversal of habituation. Although tonic L9 activity prevented the occurrence of habituation or brought about its reversal, it did not interfere with the synaptic decremental process which normally accompanies gill reflex habituation. Motor neurons L7 and LDG1 were found not to possess this ability of L9 to modulate gill reflex habituation. Evidence suggests that L9's modulatory effect is mediated in the periphery, in the gill and not centrally in the abdominal ganglion.

Animals↗
PubMed1979

Dopamine modulation of gill reflex behavior in Aplysia.

We have studied the effects of dopamine on the gill withdrawal reflex evoked by tactile siphon stimulation in the margine mollusc Aplysia. Physiological concentrations of dopamine (diluted in seawater) were perfused through the gill during siphon stimulation series. The amplitude of the reflex was potentiated by dopamine and habituation of the reflex was prevented. This occurred with no change in the activity evoked in central motor neurons. These results lead us to conclude that the dopaminergic motor neuron L9 is modulating habituation in the periphery and that the central nervous system facilitatory control of the peripheral nervous system may act via a dopaminergic pathway.

Animals↗
PubMed1979

The development of central nervous system control of the gill withdrawal reflex evoked by siphon stimulation in Aplysia.

In older Aplysia, the central nervous system (CNS) (abdominal ganglion) exerts suppressive and facilitatory control over the peripheral nervous system (PNS) which initially mediates the gill withdrawal reflex and its subsequent habituation evoked by tactile stimulation of the siphon. In young animals, both the suppressive and facilitatory CNS control were found to be absent. In older animals, removal of branchial nerve (Br) input to the gill resulted in a significantly reduced reflex latency and, with ctenidial (Ct) and siphon (Sn) nerves intact, a significantly increased reflex amplitude and an inability of the reflex to habituate with repeated siphon stimulation. In young animals, removal of Br had no effect on reflex latency and with Ct and Sn intact, the reflex amplitude latency was not increased and the reflex habituated. Older animals can easily discriminate between different intensity stimuli applied to the siphon as evidenced by differences in reflex amplitude, rates of habituation, and evoked neural activity. On the other hand, young animals cannot discriminate well between different stimulus intensities. The lack of CNS control in young animals was found to be due to incompletely developed neural processes within the abdominal ganglion and not the PNS. The lack of CNS control in young Aplysia results in gill reflex behaviours being less adaptive in light of changing stimulus conditions, but may be of positive survival value in that the young will not habituate as easily. The fact that CNS control is present in older animals strengthens the idea that in any analysis of the underlying neural mechanisms of habituation the entire integrated CNS-PNS must be taken into account.

Animals↗