Co-induction of long-term potentiation and long-term depression at a central synapse in the leech

Burrell, Brian D.; Li, Qin

doi:10.1016/j.nlm.2007.11.004

Cited by 23 publications

(25 citation statements)

References 27 publications

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“…1A) consists of both a monosynaptic electrical component and a polysynaptic, glutamatergic component (Muller and Scott 1981;Li and Burrell 2008), although the identities of the interneurons that mediate the glutamatergic component are not known. Previous studies have shown that this synaptic circuit can undergo LTP and LTD as a result of tetanic stimulation and low-frequency stimulation (LFS), respectively (Burrell and Sahley 2004;Burrell and Li 2008;Li and Burrell 2009), but it was unknown whether pairing of T-and S-cell activity results in persistent changes in synaptic signaling.In this paper, both LTP and LTD were observed following pairing spike trains that mimic the physiologically relevant patterns of T-and S-cell activity during whole-body shortening. The pattern of this plasticity was similar to that observed during STDP; LTP following presynaptic-before-postsynaptic pairings and LTD following postsynaptic-before-presynaptic pairings.…”

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Associative, bidirectional changes in neural signaling utilizing NMDA receptor- and endocannabinoid-dependent mechanisms

Li¹,

Burrell²

2011

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Persistent, bidirectional changes in synaptic signaling (that is, potentiation and depression of the synapse) can be induced by the precise timing of individual pre-and postsynaptic action potentials. However, far less attention has been paid to the ability of paired trains of action potentials to elicit persistent potentiation or depression. We examined plasticity following the pairing of spike trains in the touch mechanosensory neuron (T cell) and S interneuron (S cell) in the medicinal leech. Long-term potentiation (LTP) of T to S signaling was elicited when the T-cell spike train preceded the S-cell train. An interval 0 to +1 sec between the T-and S-cell spike trains was required to elicit long-term potentiation (LTP), and this potentiation was NMDA receptor (NMDAR)-dependent. Long-term depression (LTD) was elicited when S-cell activity preceded T-cell activity and the interval between the two spike trains was 20.2 sec to 210 sec. This surprisingly broad temporal window involved two distinct cellular mechanisms; an NMDAR-mediated LTD (NMDAR-LTD) when the pairing interval was relatively brief (,21 sec) and an endocannabinoid-mediated LTD (eCB-LTD) when longer pairing intervals were used (21 to 210 sec). This eCB-LTD also required activation of a presynaptic transient receptor potential vanilloid (TRPV)-like receptor, presynaptic Ca 2+ release from intracellular stores and activation of voltage-gated Ca 2+ channels (VGCCs). These findings demonstrate that the pairing of spike trains elicits timing-dependent forms of LTP and LTD that are supported by a complex set of cellular mechanisms involving NMDARs and endocannabinoid activation of TRPV-like receptors.[Supplemental material is available for this article.]Associative forms of long-term neuroplasticity, as first proposed by Hebb (1949), depend on the temporal relationship between pre-and postsynaptic activity. Studies of spike-timing-dependent plasticity (STDP) have provided experimental confirmation of this principle, specifically that in most connections long-term potentiation (LTP) is produced when a presynaptic action potential (or spike) precedes the postsynaptic spike, whereas long-term depression (LTD) is produced when the order is reversed (see review by Caporale and Dan 2008). In addition to the temporal order being important in determining the sign of the synaptic change, temporal proximity is also critical in that the time between the pre-and postsynaptic activity must be sufficiently brief, usually ,40 msec, to support potentiation or depression.It has been noted that the time intervals between pre-and postsynaptic activity that support STDP are not as long as those observed in many associative learning experiments, in which interstimulus intervals on the scale of seconds can be used to elicit successful conditioning (Drew and Abbott 2006). Most studies of STDP involve pairing single pre-and postsynaptic spikes or brief bursts of two to three spikes; however, many neurons communicate using relatively long trains of action potentials that are tens...

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Associative, bidirectional changes in neural signaling utilizing NMDA receptor- and endocannabinoid-dependent mechanisms

Li¹,

Burrell²

2011

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“…It is not clear whether this variation is due to differences intrinsic to the different synapses, differences in the stimulation protocols used to induce LTP/LTD, or both. Our studies in other synapses used either tetanic stimulation or low frequency stimulation to induce LTP and LTD, respectively (Burrell and Sahley, 2004;Burrell and Li, 2008;Li and Burrell, 2009;Yuan and Burrell, 2010), or used more pairings of presynaptic and postsynaptic activity than utilized in the current study [5 in the present study versus 10 pairings in another recent study (Li and Burrell, 2011)]. It is possible that these other studies stimulated the synapses in a strong enough manner to overcome any seasonal influences on LTP or LTD.…”

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confidence: 98%

Seasonal variation of long-term potentiation at a central synapse in the medicinal leech

Grey

Burrell

2011

Journal of Experimental Biology

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SUMMARYLong-term potentiation (LTP) is a persistent increase in synaptic transmission that is thought to contribute to a variety of adaptive processes including learning and memory. Although learning is known to undergo circannual variations, it is not known whether LTP undergoes similar changes despite the importance of LTP in learning and memory. Here we report that synapses in the CNS of the medicinal leech demonstrate seasonal variation in the capacity to undergo LTP following paired presynaptic and postsynaptic stimulation. LTP was observed during the April-October period, but no LTP was observed during the November-March period. Application of forskolin, a technique often used to produce chemical LTP, failed to elicit potentiation during the November-March period. Implementing stimulation patterns that normally result in long term depression (LTD) also failed to elicit any change in synaptic strength during the November-March period. These experiments indicate that LTP and LTD can be influenced by circannual rhythms and also suggest a seasonal influence on learning and memory.

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“…The type of LTP and LTD depends on the synapse [15]. LTP and LTD are dependent on several molecular players including receptors, enzymes, and several signaling molecules such as hormones, neurotransmitters, peptides, and ions [16,17]. The transmitter molecules implicated in LTP and LTD induction include dopamine, glutamate, noradrenaline, serotonin, and acetylcholine [18][19][20].…”

Section: Mechanisms Of Neurometaplasticitymentioning

confidence: 99%

“…Ca 2+ channels, sodium channels, transient receptor potential vanilloid), transporters (dopamine transporter, serotonin transporter, etc.) [13,16,36]. The enzymes involved in neurometaplasticity are calmodulin-dependent kinase II (CaMKII), protein kinase A (PKA), protein kinase C (PKC), cAMP-dependent protein kinase (PKA), tyrosine kinase src (Src), mitogen activated protein kinases (MAPK), phospholipases, phosphatidylinositol-3-kinase, among others [16][17][18][19][37][38][39].…”

Section: Mechanisms Of Neurometaplasticitymentioning

confidence: 99%

“…[13,16,36]. The enzymes involved in neurometaplasticity are calmodulin-dependent kinase II (CaMKII), protein kinase A (PKA), protein kinase C (PKC), cAMP-dependent protein kinase (PKA), tyrosine kinase src (Src), mitogen activated protein kinases (MAPK), phospholipases, phosphatidylinositol-3-kinase, among others [16][17][18][19][37][38][39]. Intracellular signaling molecules involved in neurometaplastic events, mediated via induction of LTP and LTD include Ca 2+ , inositol trisphosphate, cAMP-responsive element binding protein (CREB), nuclear factor-kappa-B (NF- [39].…”

Section: Mechanisms Of Neurometaplasticitymentioning

confidence: 99%

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Neurometaplasticity: Glucoallostasis control of plasticity of the neural networks of error commission, detection, and correction modulates neuroplasticity to influence task precision

Welcome

Dane

Mastorakis

et al. 2017

AIP Conference Proceedings

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Abstract. The term "metaplasticity" is a recent one, which means plasticity of synaptic plasticity. Correspondingly, neurometaplasticity simply means plasticity of neuroplasticity, indicating that a previous plastic event determines the current plasticity of neurons. Emerging studies suggest that neurometaplasticity underlie many neural activities and neurobehavioral disorders. In our previous work, we indicated that glucoallostasis is essential for the control of plasticity of the neural network that control error commission, detection and correction. Here we review recent works, which suggest that task precision depends on the modulatory effects of neuroplasticity on the neural networks of error commission, detection, and correction. Furthermore, we discuss neurometaplasticity and its role in error commission, detection, and correction.

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Co-induction of long-term potentiation and long-term depression at a central synapse in the leech

Cited by 23 publications

References 27 publications

Associative, bidirectional changes in neural signaling utilizing NMDA receptor- and endocannabinoid-dependent mechanisms

Associative, bidirectional changes in neural signaling utilizing NMDA receptor- and endocannabinoid-dependent mechanisms

Seasonal variation of long-term potentiation at a central synapse in the medicinal leech

Neurometaplasticity: Glucoallostasis control of plasticity of the neural networks of error commission, detection, and correction modulates neuroplasticity to influence task precision

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