Selective activation of Ca(2+)-activated PKCs in Aplysia neurons by 5- HT

Sossin, WS; Schwartz, JH

doi:10.1523/jneurosci.12-04-01160.1992

Cited by 78 publications

(77 citation statements)

References 23 publications

(34 reference statements)

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“…The PSITE program detected four potential protein kinase C (PKC) sites and numerous casein kinase II sites, but these consensus sequences occur frequently and may not be phosphorylated. Previous studies did not detect an increase in phosphorylation of protein 3 following treatment with phorbol diacetate, an activator of PKC, nor after treatment with 5-HT (Homayouni et al 1995), which also activates PKC in sensory neurons (Sossin and Schwartz 1992). In future studies it will be of interest to determine which sites are phosphorylated.…”

Section: Proteinmentioning

confidence: 84%

Identification of specific mRNAs affected by treatments producing long-term facilitation in Aplysia.

Zwartjes

West

Hattar³

et al. 1998

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Neural correlates of long-term sensitization of defensive withdrawal reflexes in Aplysia occur in sensory neurons in the pleural ganglia and can be mimicked by exposure of these neurons to serotonin (5-HT). Studies using inhibitors indicate that transcription is necessary for production of long-term facilitation by 5-HT. Several mRNAs that change in response to 5-HT have been identified, but the molecular events responsible for long-term facilitation have not yet been fully described. To detect additional changes in mRNAs, we investigated the effects of 5-HT (1.5 hr) on levels of mRNA in pleural-pedal ganglia using in vitro translation. Four mRNAs were affected by 5-HT, three of which were identified as calmodulin (CaM), phosphoglycerate kinase (PGK), and a novel gene product (protein 3). Using RNase protection assays, we found that 5-HT increased all three mRNAs in the pleural sensory neurons. CaM and protein 3 mRNAs were also increased in the sensory neurons 4Corresponding author.by sensitization training. Furthermore, stimulation of peripheral nerves of pleural-pedal ganglia, an in vitro analog of sensitization training, increased the incorporation of labeled amino acids into CaM, PGK, and protein 3. These results indicate that increases in CaM, PGK, and protein 3 are part of the early response of sensory neurons to stimuli that produce long-term facilitation, and that CaM and protein 3 could have a role in the generation of long-term sensitization.

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Section: Proteinmentioning

confidence: 84%

Identification of specific mRNAs affected by treatments producing long-term facilitation in Aplysia.

Zwartjes

West

Hattar³

et al. 1998

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“…As in mammals, PKC in Aplysia has three isoforms: a conventional form (Apl I) that requires diacylglycerol and Ca 2+ for its activation, a novel form (Apl II) that requires diacylglycerol but not Ca 2+ , and an atypical form (Apl III) that requires neither (Kruger et al 1991;Bougie et al 2009). We injected the pseudosubstrate PKC(19-31), which inhibits conventional and novel but not atypical isoforms (Sossin and Schwartz 1992;Liu et al 2000). Presynaptic injection of PKC(19-31) blocked facilitation by 1-min 5-HT at depressed synapses and facilitation by 10-min 5-HT at rested synapses, whereas postsynaptic injection of PKC(19-31) did not block either.…”

Section: Discussionmentioning

confidence: 99%

Whereas short-term facilitation is presynaptic, intermediate-term facilitation involves both presynaptic and postsynaptic protein kinases and protein synthesis

Jin¹,

Kandel²,

Hawkins³

2011

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Whereas short-term plasticity involves covalent modifications that are generally restricted to either presynaptic or postsynaptic structures, long-term plasticity involves the growth of new synapses, which by its nature involves both pre-and postsynaptic alterations. In addition, an intermediate-term stage of plasticity has been identified that might form a bridge between short-and long-term plasticity. Consistent with that idea, although short-term term behavioral sensitization in Aplysia involves presynaptic mechanisms, intermediate-term sensitization involves both pre-and postsynaptic mechanisms. However, it has not been known whether that is also true of facilitation in vitro, where a more detailed analysis of the mechanisms involved in the different stages and their interrelations is feasible. To address those questions, we have examined preand postsynaptic mechanisms of short-and intermediate-term facilitation at Aplysia sensory-motor neuron synapses in isolated cell culture. Whereas short-term facilitation by 1-min 5-HT involves presynaptic PKA and CamKII, intermediate-term facilitation by 10-min 5-HT involves presynaptic PKC and postsynaptic Ca 2+ and CamKII, as well as both pre-and postsynaptic protein synthesis. These results support the idea that the intermediate-term stage is the first to involve both pre-and postsynaptic molecular mechanisms, which could in turn serve as some of the initial steps in a cascade leading to synaptic growth during long-term plasticity.

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“…The exact mechanism by which 5-HT induces this spike-independent enhancement of release is not known, but it has been termed "mobilization" because of the characteristic increase in EPSP slope it produces, as if the release sites are primed with vesicles to be rapidly released (Hochner et al, 1986b). While CAMP may also play a role in this mobilizing effect of 5-HT (Goldsmith and Abrams, 1991) the second process can be distinguished from the first process in that it involves protein kinase C (Braha et al, 1990;Ghirardi et al, 1992) which is also activated by 5-HT in sensory neurons (Sacktor and Schwartz, 1990;Sossin and Schwartz, 1992).…”

Section: Discussionmentioning

confidence: 99%

“…For example, previous findings do not rule out a role for the second process in pairing-specific facilitation. Because the second process is mediated in large part by protein kinase C, which is also dually activated by 5-HT and intracellular Ca*+ (Sacktor and Schwartz, 1990;Sossin and Schwartz, 1992), this mobilizationlike process seems a good candidate for pairing-specific enhancement. Also, if pairing-specific facilitation requires Ca*+ influx, what is the source of this influx?…”

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confidence: 99%

Pairing-specific, activity-dependent presynaptic facilitation at Aplysia sensory-motor neuron synapses in isolated cell culture

et al. 1994

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Synapses made by Aplysia sensory neurons onto motor- and interneuron followers in the intact nervous system exhibit an associative form of synaptic facilitation that is thought to contribute to classical conditioning of the animal's gill and siphon withdrawal reflex (Hawkins et al., 1983; Walters and Byrne, 1983). Here we demonstrate that a similar associative facilitation can be induced between individual sensory and motor neurons isolated in culture. Pairing tetanic stimulation with either of two facilitatory transmitters, 5-HT or small cardioactive peptide, considerably prolongs facilitation compared to either tetanus or transmitter alone. When corrected for the depression that occurs simply in response to low-frequency testing, the facilitation produced by one pairing trial does not decay for more than 20 min after training. This facilitation requires the temporal pairing (0.5 sec forward interstimulus interval) of the two stimuli, tetanus and 5-HT. Delivering the same two stimuli in an unpaired fashion (1 min forward interval) fails to produce the long-lasting effect. Measurements of spontaneous transmitter release during either paired or unpaired training reveal no changes in unitary mEPSP or mEPSC (“mini”) amplitude, indicating that the facilitation involves a presynaptic mechanism. While both forms of training dramatically increase the initial frequency of spontaneous release, mini frequency does not remain elevated as long as the evoked EPSP following paired training, nor does paired training specifically enhance spontaneous release frequency. Pairing-specific facilitation was not blocked by the protein kinase C inhibitor H7. In contrast, the same training procedure produced pairing-specific increases of sensory neuron excitability and action potential width, suggesting that cAMP-mediated processes are involved in the paired effect. Although Ca2+ influx is necessary for the associative effect (Abrams, 1985), we find that the facilitation does not require influx through L-type voltage-gated Ca2+ channels, since the effect was not blocked by the dihydropyridine antagonist nitrendipine. Together, these findings indicate that the mechanism underlying associative, activity-dependent facilitation is intrinsic to the sensory neuron synapse, that it is presynaptically mediated by processes unique to evoked synaptic transmission, and that it appears to involve a pairing-specific broadening of the presynaptic action potential, allowing enhanced Ca2+ influx through the dihydropyridine- insensitive channels responsible for release.

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Selective activation of Ca(2+)-activated PKCs in Aplysia neurons by 5- HT

Cited by 78 publications

References 23 publications

Identification of specific mRNAs affected by treatments producing long-term facilitation in Aplysia.

Identification of specific mRNAs affected by treatments producing long-term facilitation in Aplysia.

Whereas short-term facilitation is presynaptic, intermediate-term facilitation involves both presynaptic and postsynaptic protein kinases and protein synthesis

Pairing-specific, activity-dependent presynaptic facilitation at Aplysia sensory-motor neuron synapses in isolated cell culture

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