Glycine receptor activation regulates short-term plasticity in CA1 area of hippocampal slices of rats

2006 ◽  
Vol 344 (3) ◽  
pp. 721-726 ◽  
Author(s):  
Long-Hua Zhang ◽  
Lin Xu ◽  
Tian-Le Xu
2010 ◽  
Vol 104 (4) ◽  
pp. 2203-2213 ◽  
Author(s):  
Debika Chatterjea ◽  
Edaeni Hamid ◽  
John P. Leonard ◽  
Simon Alford

N-methyl-d-aspartate (NMDA) receptor-mediated currents are enhanced by phosphorylation. We have investigated effects of phosphorylation-dependent short-term plasticity of NMDA receptor-mediated excitatory postsynaptic currents (EPSCs) on the induction of long-term depression (LTD). We confirmed in whole cell clamped CA1 pyramidal neurons that LTD is induced by pairing stimulus protocols. However, after serine-threonine phosphorylation was modified by postsynaptic introduction of a protein phosphatase-1 (PP1) inhibitor, the same pairing protocol evoked long-term potentiation (LTP). We determined effects of modification of phosphatase activity on evoked NMDA EPSCs during LTD induction protocols. During LTD induction, using a protocol pairing depolarization to –40 mV and 0.5 Hz stimulation, NMDA receptor-mediated EPSCs undergo a short-term enhancement at the start of the protocol. In neurons in which PP1 activity was inhibited, this short-term enhancement was markedly amplified. We then investigated the effect of this enhancement on Ca2+ entry during the start of the LTD induction protocol. Enhancement of NMDA receptor-mediated responses was accompanied by an amplification of induction protocol-evoked Ca2+ transients. Furthermore, this amplification required synaptic activation during the protocol, consistent with an enhancement of Ca2+ entry mediated by NMDA receptor activation. The sign of NMDA receptor-mediated long-term plasticity, whether potentiation or depression depends on the amplitude of the synaptic Ca2+ transient during induction. We conclude that short-term phosphorylation-dependent plasticity of the NMDA receptor-mediated EPSCs contributes significantly to the effect of phosphatase inhibition on the subsequent induction of LTD or LTP.


Author(s):  
Nahid Roohi ◽  
◽  
Mahboubeh Ahmadi ◽  
Yaghoun Fathollahi ◽  
Amir Shojaei ◽  
...  

There are many differences among dorsal and ventral hippocampal neural circuits that affect the synaptic plasticity. In this study we compared the occurrence of short-term plasticity in the field excitatory post synaptic potentials (fEPSP) in dorsal and ventral hippocampal CA1 area following kindled seizures. Animals (male C57 B6/J mice, 12 weeks of age) were kindled by intraperitoneal injections of pentylenetetrazole (PTZ) and fEPSPs were recorded from dorsal and ventral hippocampal slices. Short-term plasticity was evaluated by measuring fEPSP-slope and fEPSP-area following paired-pulse stimulation delivered at three inter-pulse intervals (20, 80 and 160 ms). Obtained results showed that in control slices fEPSP-slope was greater in ventral- compared to dorsal hippocampus, but there was no difference in fEPSP-area among two regions. In hippocampal slices of kindled animals, fEPSP-slope was similar in dorsal and ventral regions, but fEPSP-area was greater in ventral- compared to dorsal hippocampus. In addition, fEPSP-area was greater in kindled compared to control group only in ventral hippocampus. PTZ kindled slices showed impaired short-term facilitation and the paired-pulse index was reduced only at dorsal hippocampal slices. Kindling had no significant effect on paired-pulse ratio in ventral hippocampal slices. Our findings indicated that the seizure occurrence affected the neural activity of hippocampus in a regional dependent manner. Although kindling increased fEPSP-area in ventral hippocampus, kindling-induced changes in short-term synaptic plasticity was significant only in dorsal hippocampal slices compared to control group. The difference in the responses of hippocampal dorsal and ventral poles has to be considered in the future researches.


2021 ◽  
Author(s):  
NC Rodrigues ◽  
A Silva-Cruz ◽  
A Caulino-Rocha ◽  
A Bento-Oliveira ◽  
JA Ribeiro ◽  
...  

AbstractLong-term potentiation (LTP) is a highly studied phenomenon yet the essential vs. modulatory transduction and GABAergic pathways involved in LTP elicited by theta-burst stimulation (TBS) in the CA1 area of the hippocampus are still unclear, due to the use of different TBS intensities and patterns or of different rodent/cellular models. We now characterized the essential transduction and GABAergic pathways in mild TBS-induced LTP in the CA1 area of the rat hippocampus. LTP induced by TBS (5×4) (5 bursts of 4 pulses delivered at 100Hz) lasted for up to 3h and was increasingly greater from weaning to adulthood. Stronger TBS patterns - TBS (15×4) or three TBS (15×4) separated by 6 min induced nearly maximal LTP not being the best choice to study the value of LTP-enhancing drugs. LTP induced by TBS (5×4) was fully dependent on NMDA receptor and CaMKII activity but independent on PKA or PKC activity. In addition, it was partially dependent on GABAB receptor activation and was potentiated by GABAA receptor blockade and less by GAT-1 transporter blockade. AMPA GluA1 phosphorylation on Ser831 (CaMKII target) but not GluA1 Ser845 (PKA target) was essential for LTP expression. The phosphorylation of the Kv4.2 channel was observed at Ser438 (targeted by CaMKII) but not at Thr602 or Thr607 (ERK/MAPK pathway). This suggests that cellular kinases like PKA, PKC or kinases of the ERK/MAPK family although important modulators of TBS (5×4)-induced LTP are not essential for its expression in the CA1 area of the hippocampus.


2020 ◽  
Author(s):  
Sachin Makani ◽  
Stefano Lutzu ◽  
Pablo J. Lituma ◽  
David L. Hunt ◽  
Pablo E. Castillo

ABSTRACTIn the hippocampus, the excitatory synapse between dentate granule cell axons – or mossy fibers (MF) – and CA3 pyramidal cells (MF-CA3) expresses robust forms of short-term plasticity, such as frequency facilitation and post-tetanic potentiation (PTP). These forms of plasticity are due to increases in neurotransmitter release, and can be engaged when dentate granule cells fire in bursts (e.g. during exploratory behaviors) and bring CA3 pyramidal neurons above threshold. While frequency facilitation at this synapse is limited by endogenous activation of presynaptic metabotropic glutamate receptors, whether MF-PTP can be regulated in an activity-dependent manner is unknown. Here, using physiologically relevant patterns of mossy fiber stimulation in acute mouse hippocampal slices, we found that disrupting postsynaptic Ca2+ dynamics increases MF-PTP, strongly suggesting a form of Ca2+-dependent retrograde suppression of this form of plasticity. PTP suppression requires a few seconds of MF bursting activity and Ca2+ release from internal stores. Our findings raise the possibility that the powerful MF-CA3 synapse can negatively regulate its own strength not only during PTP-inducing activity typical of normal exploratory behaviors, but also during epileptic activity.SIGNIFICANCE STATEMENTThe powerful mossy fiber-CA3 synapse exhibits strong forms of plasticity that are engaged during location-specific exploration, when dentate granule cells fire in bursts. While this synapse is well-known for its presynaptically-expressed LTP and LTD, much less is known about the robust changes that occur on a shorter time scale. How such short-term plasticity is regulated, in particular, remains poorly understood. Unexpectedly, an in vivo-like pattern of presynaptic activity induced robust post-tetanic potentiation (PTP) only when the postsynaptic cell was loaded with a high concentration of Ca2+ buffer, indicating a form of Ca2+–dependent retrograde suppression of PTP. Such suppression may have profound implications for how environmental cues are encoded into neural assemblies, and for limiting network hyperexcitability during seizures.


Author(s):  
Mohammad Z. Awad ◽  
Ryan J. Vaden ◽  
Zachary T. Irwin ◽  
Christopher L. Gonzalez ◽  
Sarah Black ◽  
...  

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Nishant Singh ◽  
Thomas Bartol ◽  
Herbert Levine ◽  
Terrence Sejnowski ◽  
Suhita Nadkarni

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