ArticleNeurobiology of learning and memory2008
Co-induction of long-term potentiation and long-term depression at a central synapse in the leech.
Article in Neurobiology of learning and memory, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
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- Is plasticity of synapses the mechanism of long-term memory storage?NPJ science of learning · 2019Review
- A computational framework for understanding decision making through integration of basic learning rules.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Differentially expressed genes in Hirudo medicinalis ganglia after acetyl-L-carnitine treatment.PloS one · 2013Article
- SCRAPPER regulates the thresholds of long-term potentiation/depression, the bidirectional synaptic plasticity in hippocampal CA3-CA1 synapses.Neural plasticity · 2012Article
- Seasonal variation of long-term potentiation at a central synapse in the medicinal leech.The Journal of experimental biology · 2011Article
- The theoretical model of theta burst form of repetitive transcranial magnetic stimulation.Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology · 2011Article
- Associative, bidirectional changes in neural signaling utilizing NMDA receptor- and endocannabinoid-dependent mechanisms.Learning & memory (Cold Spring Harbor, N.Y.) · 2011Article
- Properties of cannabinoid-dependent long-term depression in the leech.Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2010Article
- Two forms of long-term depression in a polysynaptic pathway in the leech CNS: one NMDA receptor-dependent and the other cannabinoid-dependent.Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2009Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Most studies of long-term potentiation (LTP) have focused on potentiation induced by the activation of postsynaptic NMDA receptors (NMDARs). However, it is now apparent that NMDAR-dependent signaling processes are not the only form of LTP operating in the brain [Malenka, R. C., & Bear, M. F. (2004). LTP and LTD: An embarrassment of riches. Neuron, 44, 5-21]. Previously, we have observed that LTP in leech central synapses made by the touch mechanosensory neurons onto the S interneuron was NMDAR-independent [Burrell, B. D., & Sahley, C. L. (2004). Multiple forms of long-term potentiation and long-term depression converge on a single interneuron in the leech CNS. Journal of Neuroscience, 24, 4011-4019]. Here we examine the cellular mechanisms mediating T-to-S (T-->S) LTP and find that its induction requires activation of metabotropic glutamate receptors (mGluRs), voltage-dependent Ca(2+) channels (VDCCs) and protein kinase C (PKC). Surprisingly, whenever LTP was pharmacologically inhibited, long-term depression (LTD) was observed at the tetanized synapse, indicating that LTP and LTD were activated at the same time in the same synaptic pathway. This co-induction of LTP and LTD likely plays an important role in activity-dependent regulation of synaptic transmission.
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