TY - JOUR
T1 - Co-induction of long-term potentiation and long-term depression at a central synapse in the leech
AU - Burrell, Brian D.
AU - Li, Qin
N1 - Funding Information:
The authors thank Dr. Brenda Moss for helpful comments in the preparation of this manuscript. Supported by grants from the National Science Foundation (IBN-0432683, BDB) and by a subproject of the National Institutes of Health Grant (P20 RR015567, BDB), which is designated as a Center of Biomedical Research Excellence (COBRE).
PY - 2008/7
Y1 - 2008/7
N2 - 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 Ca2+ 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.
AB - 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 Ca2+ 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.
KW - Invertebrate
KW - Long-term depression
KW - Long-term potentiation
KW - Metabotropic glutamate receptor
KW - Neuroplasticity
KW - Protein kinase C
KW - Voltage-dependent Ca channel
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U2 - 10.1016/j.nlm.2007.11.004
DO - 10.1016/j.nlm.2007.11.004
M3 - Article
C2 - 18182311
AN - SCOPUS:44649180127
SN - 1074-7427
VL - 90
SP - 275
EP - 279
JO - Neurobiology of Learning and Memory
JF - Neurobiology of Learning and Memory
IS - 1
ER -