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Although we refer to the two compartments as somatic (pleural ganglion) and synaptic (pedal ganglion) because they include the SN somata and their remote synapses, respectively, both compartments also contain interneurons (INTs) that make synapses with the SNs or MNs, and the SNs make synapses onto proximal INTs in the pleural ganglion [Y. Xu, J. P. Pieroni, L. J. Cleary, J. H. Byrne, J. Neurophysiol. 73, 1313 (1995); L. J. Cleary and J. H. Byrne, ibid. 70, 1767 (1993) ].
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Although we refer to the two compartments as somatic (pleural ganglion) and synaptic (pedal ganglion) because they include the SN somata and their remote synapses, respectively, both compartments also contain interneurons (INTs) that make synapses with the SNs or MNs, and the SNs make synapses onto proximal INTs in the pleural ganglion [Y. Xu, J. P. Pieroni, L. J. Cleary, J. H. Byrne, J. Neurophysiol. 73, 1313 (1995); L. J. Cleary and J. H. Byrne, ibid. 70, 1767 (1993) ].
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We made recordings from monosynaptically connected SN-MN pairs. To prevent firing, we hyperpolarized the MN membrane potential to -70 mV. There was no spontaneous activity in SNs in either artificial seawater or 5HT. We used only synapses that (i) did not decrement (<20% decrease in amplitude) during the three pretests (which were averaged for a baseline) and (ii) showed ST responses during 5HT exposure (>75% of preparations). ST responses included STF, increased SN spike width, and decreased SN spike threshold [D. A. Baxter and J. H. Byrne, J. Neurophysiol. 64, 978 (1990); E. T. Walters, J. H. Byrne, T. J. Carew, E. R. Kandel, ibid. 50, 1543 (1983)]. For procedural details, see (3).
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For procedural details, see (3)
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We made recordings from monosynaptically connected SN-MN pairs. To prevent firing, we hyperpolarized the MN membrane potential to -70 mV. There was no spontaneous activity in SNs in either artificial seawater or 5HT. We used only synapses that (i) did not decrement (<20% decrease in amplitude) during the three pretests (which were averaged for a baseline) and (ii) showed ST responses during 5HT exposure (>75% of preparations). ST responses included STF, increased SN spike width, and decreased SN spike threshold [D. A. Baxter and J. H. Byrne, J. Neurophysiol. 64, 978 (1990); E. T. Walters, J. H. Byrne, T. J. Carew, E. R. Kandel, ibid. 50, 1543 (1983)]. For procedural details, see (3).
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note
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3.27 = 0.72; P = 0.55) tests.
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note
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2.12 = 4.99; P = 0.027). Significant STF was expressed in all groups: controls, +154.8 ± 15.5%; synaptic-emetine, +92.9 ± 29.5%; somatic-emetine, +109.7 ± 33.6%; P < 0.02 in all cases.
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The magnitude of coincident LTF in the controls as well as in the somatic-emetine (Fig. 3A) and somatic-emetine (4 to 6 hours) (Fig. 3B) groups is quite comparable [see also (3)]. However, the absolute magnitude of LTF in these groups is less than that observed in our initial experiments (Fig.1). We do not know the source of this variability, but it underscores the importance of having each experimental group compared with its own set of controls (run simultaneously), which was the case in all our experiments.
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STF: -16.0 ± 2.8%, NS (somatic-emetine); -15.5 ± 2.4%, NS (synaptic-emetine). LTF: -15.8 ± 10.4%, NS (somatic-emetine); -4.0 ± 12.2%, NS (synaptic emetine), paired t tests.
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It is possible that our results reflect a capture-like mechanism [see (8)]. For example, if the 25-min 5HT pulse to the somatic compartment induced LTF at SN-INT synapses in the pleural ganglion, the synaptic pulse in the pedal ganglion could be viewed as inducing capture at the remote synapse. If true, this would extend the notion of capture in two ways: (i) in this case, protein synthesis is required immediately at the site of capture, and (ii) there is a tight temporal constraint (15 min) imposed on the induction-capture process occurring at two anatomically remote sites.
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A. Barzilai, T. E. Kennedy, J. D. Sweatt, E. R. Kandel, Neuron 2, 1577 (1989).
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note
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2.11 = 4.24; P = 0.043).
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The synaptic compartment (pedal ganglion) contains both the presynaptic SN terminals and postsynaptic MN neurites and somata. Thus the translation-dependent synaptic signal required for LTF induction (Fig. 3A) could be presynaptic, postsynaptic, or both. Distinguishing between pre- and postsynaptic contributions is experimentally feasible in this system [L.-E. Trudeau and V. F. Castellucci, J. Neurosci. 5, 1275 (1995); D. L. Glanzman, J. Neurobiol. 25, 666 (1994)]. Thus we are currently examining the effects of blocking translation in individual SNs and MNs.
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The synaptic compartment (pedal ganglion) contains both the presynaptic SN terminals and postsynaptic MN neurites and somata. Thus the translation-dependent synaptic signal required for LTF induction (Fig. 3A) could be presynaptic, postsynaptic, or both. Distinguishing between pre- and postsynaptic contributions is experimentally feasible in this system [L.-E. Trudeau and V. F. Castellucci, J. Neurosci. 5, 1275 (1995); D. L. Glanzman, J. Neurobiol. 25, 666 (1994)]. Thus we are currently examining the effects of blocking translation in individual SNs and MNs.
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The length of the connective is 2 to 3 mm, and the estimated rate of fast transport in Aplysia neurons is about 1.5 mm/hour [J. D. Gunstream, G. A. Castro, E. T. Walters, J. Neurosci. 15, 439 (1995); R. T. Ambron, R. Schmied, C. C. Huang, M. Smedman, ibid. 12, 2813 (1992)]. Thus communication between synapse and soma requires 40 min to >1 hour by this mechanism.
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The length of the connective is 2 to 3 mm, and the estimated rate of fast transport in Aplysia neurons is about 1.5 mm/hour [J. D. Gunstream, G. A. Castro, E. T. Walters, J. Neurosci. 15, 439 (1995); R. T. Ambron, R. Schmied, C. C. Huang, M. Smedman, ibid. 12, 2813 (1992)]. Thus communication between synapse and soma requires 40 min to >1 hour by this mechanism.
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In CA1 cells of the hippocampus, the soma is not essential for induction of long-term synaptic plasticity (12) [U. Frey, M. Krug, R. Brodemann, K. Reymann, H. Matthies, Neurosci. Lett. 97, 135 (1989)]; however, this does not indicate that the soma is unable to participate in the induction process, especially under conditions of subthreshold activation at remote synaptic sites.
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Supported by National Institutes of Health grant F32-MH12004 to C.M.S. and National Institute of Mental Health grant RO1MH-14-1083 to T.J.C. We thank E. Kandel, S. McKay, and M. Sutton for helpful comments on a previous draft of this paper.
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