scholarly journals Somatostatin Depresses Long-Term Potentiation and Ca2+ Signaling in Mouse Dentate Gyrus

2002 ◽  
Vol 88 (6) ◽  
pp. 3078-3086 ◽  
Author(s):  
Michael V. Baratta ◽  
Tyra Lamp ◽  
Melanie K. Tallent
Keyword(s):  
Dentate Gyrus ◽  
High Frequency ◽  
Granule Cells ◽  
Molecular Layer ◽  
Long Term Potentiation ◽  
Perforant Path ◽  
Functional Consequence ◽  
Term Potentiation ◽  
Synaptic Responses

The selective loss of somatostatin (SST)-containing interneurons from the hilus of the dentate gyrus is a hallmark of epileptic hippocampus. The functional consequence of this loss, including its contribution to postseizure hyperexcitability, remains unclear. We address this issue by characterizing the actions of SST in mouse dentate gyrus using electrophysiological techniques. Although the majority of dentate SST receptors are located in the outer molecular layer adjacent to lateral perforant path (LPP) synapses, we found no consistent action of SST on standard synaptic responses generated at these synapses. However, when SST was present during application of high-frequency trains that normally generate long-term potentiation (LTP), the induction of LTP was impaired. SST did not alter the maintenance of LTP when applied after its induction. To examine the mechanism by which SST inhibits LTP, we recorded from dentate granule cells and examined the actions of this neuropeptide on synaptic transmission and postsynaptic currents. Unlike findings in the CA1 hippocampus, we observed no postsynaptic actions on K+ currents. Instead, SST inhibited Ca2+/Ba2+ spikes evoked by depolarization. This inhibition was dependent on N-type Ca2+currents. Blocking these currents also blocked LTP, suggesting a mechanism through which SST may inhibit LTP. Our results indicate that SST reduction of dendritic Ca2+ through N-type Ca2+ channels may contribute to modulation of synaptic plasticity at LPP synapses. Therefore the loss of SST function postseizure could result in abnormal synaptic potentiation that contributes to epileptogenesis.

scholarly journals Dendritic spikes in hippocampal granule cells are necessary for long-term potentiation at the perforant path synapse

2018 ◽  
Author(s):  
Sooyun Kim ◽  
Yoonsub Kim ◽  
Suk-Ho Lee ◽  
Won-Kyung Ho
Keyword(s):  
Granule Cells ◽  
Memory Function ◽  
Brain Slices ◽  
Long Term Potentiation ◽  
Perforant Path ◽  
Term Potentiation ◽  
Dendritic Spikes ◽  
Voltage Attenuation ◽  
Synaptic Responses

AbstractLong-term potentiation (LTP) of synaptic responses is essential for hippocampal memory function. Perforant-path (PP) synapses on hippocampal granule cells (GCs) contribute to the formation of associative memories, which are considered the cellular correlates of memory engrams. However, the mechanisms of LTP at these synapses are not well understood. Due to sparse firing activity and the voltage attenuation in their dendrites, it remains unclear how associative LTP at distal synapses occurs. Here we show that NMDA receptor-dependent LTP can be induced at PP-GC synapses without backpropagating action potentials (bAPs) in acute rat brain slices. Dendritic recordings reveal substantial attenuation of bAPs as well as local dendritic Na + ‐spike generation during PP-GC input. Inhibition of Na+ ‐spikes impairs LTP suggesting that LTP at PP-GC synapse requires local Na + ‐spikes. Thus, dendritic spikes are essential for LTP induction at PP-GC synapse and may constitute a key cellular mechanism for memory formation in the dentate gyrus.

scholarly journals Dendritic spikes in hippocampal granule cells are necessary for long-term potentiation at the perforant path synapse

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Sooyun Kim ◽  
Yoonsub Kim ◽  
Suk-Ho Lee ◽  
Won-Kyung Ho
Keyword(s):  
Granule Cells ◽  
Memory Function ◽  
Brain Slices ◽  
Long Term Potentiation ◽  
Perforant Path ◽  
Term Potentiation ◽  
Dendritic Spikes ◽  
Voltage Attenuation ◽  
Synaptic Responses

Long-term potentiation (LTP) of synaptic responses is essential for hippocampal memory function. Perforant-path (PP) synapses on hippocampal granule cells (GCs) contribute to the formation of associative memories, which are considered the cellular correlates of memory engrams. However, the mechanisms of LTP at these synapses are not well understood. Due to sparse firing activity and the voltage attenuation in their dendrites, it remains unclear how associative LTP at distal synapses occurs. Here, we show that NMDA receptor-dependent LTP can be induced at PP-GC synapses without backpropagating action potentials (bAPs) in acute rat brain slices. Dendritic recordings reveal substantial attenuation of bAPs as well as local dendritic Na+ spike generation during PP-GC input. Inhibition of dendritic Na+ spikes impairs LTP induction at PP-GC synapse. These data suggest that dendritic spikes may constitute a key cellular mechanism for memory formation in the dentate gyrus.

scholarly journals Somatostatin-positive interneurons in the dentate gyrus of mice provide local- and long-range septal synaptic inhibition

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Mei Yuan ◽  
Thomas Meyer ◽  
Christoph Benkowitz ◽  
Shakuntala Savanthrapadian ◽  
Laura Ansel-Bollepalli ◽  
...  
Keyword(s):  
Dentate Gyrus ◽  
Spatial Information ◽  
Molecular Layer ◽  
Activity Patterns ◽  
Long Term Potentiation ◽  
Medial Septum ◽  
Perforant Path ◽  
Term Potentiation ◽  
Memory Acquisition

Somatostatin-expressing-interneurons (SOMIs) in the dentate gyrus (DG) control formation of granule cell (GC) assemblies during memory acquisition. Hilar-perforant-path-associated interneurons (HIPP cells) have been considered to be synonymous for DG-SOMIs. Deviating from this assumption, we show two functionally contrasting DG-SOMI-types. The classical feedback-inhibitory HIPPs distribute axon fibers in the molecular layer. They are engaged by converging GC-inputs and provide dendritic inhibition to the DG circuitry. In contrast, SOMIs with axon in the hilus, termed hilar interneurons (HILs), provide perisomatic inhibition onto GABAergic cells in the DG and project to the medial septum. Repetitive activation of glutamatergic inputs onto HIPP cells induces long-lasting-depression (LTD) of synaptic transmission but long-term-potentiation (LTP) of synaptic signals in HIL cells. Thus, LTD in HIPPs may assist flow of spatial information from the entorhinal cortex to the DG, whereas LTP in HILs may facilitate the temporal coordination of GCs with activity patterns governed by the medial septum.

In Vivo Recordings of Long-Term Potentiation and Long-Term Depression in the Dentate Gyrus of the Neonatal Rat

2004 ◽  
Vol 91 (2) ◽  
pp. 613-622 ◽  
Author(s):  
Michael P. O'Boyle ◽  
Viet Do ◽  
Brian E. Derrick ◽  
Brenda J. Claiborne
Keyword(s):  
Dentate Gyrus ◽  
Granule Cells ◽  
Long Term Potentiation ◽  
Neonatal Rat ◽  
Perforant Path ◽  
Long Term Depression ◽  
Term Potentiation ◽  
Old Rats

Previous in vitro studies demonstrated that long-term potentiation (LTP) could be elicited at medial perforant path (MPP) synapses onto hippocampal granule cells in slices from 7-day-old rats. In contrast, in vivo studies suggested that LTP at perforant path synapses could not be induced until at least days 9 or 10 and then in only a small percentage of animals. Because several characteristics of the oldest granule cells are adult-like on day 7, we re-examined the possibility of eliciting LTP in 7-day-old rats in vivo. We also recorded from 8- and 9-day-old rats to further elucidate the occurrence and magnitude of LTP in neonates. With halothane anesthesia, all animals in each age group exhibited synaptic plasticity of the excitatory postsynaptic potential following high-frequency stimulation of the MPP. In 7-day-old rats, LTP was elicited in 40% of the animals and had an average magnitude of 143%. Long-term depression (LTD) alone (magnitude of 84%) was induced in 40% of the animals, while short-term potentiation (STP) alone (magnitude of 123%) was induced in 10%. STP followed by LTD was elicited in the remaining 10%. Data were similar for all ages combined. In addition, the N-methyl-d-aspartate (NMDA) antagonist ( R,S)-3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid (CPP) blocked the occurrence of LTP at each age and doubled the percentage of animals expressing LTD alone for all ages combined. These results demonstrate that tetanic stimulation can elicit LTP or LTD at MPP synapses in 7-day-old rats, supporting our premise that at least a portion of the dentate gyrus is functional at this early age.

scholarly journals Neuroligin-3 Regulates Excitatory Synaptic Transmission and EPSP-Spike Coupling in the Dentate Gyrus In Vivo

2021 ◽  
Author(s):  
Julia Muellerleile ◽  
Matej Vnencak ◽  
Angelo Ippolito ◽  
Dilja Krueger-Burg ◽  
Tassilo Jungenitz ◽  
...  
Keyword(s):  
Synaptic Transmission ◽  
Dentate Gyrus ◽  
Long Term Potentiation ◽  
Autism Spectrum ◽  
Perforant Path ◽  
Adhesion Protein ◽  
Neuronal Excitation ◽  
Term Potentiation

Abstract Neuroligin-3 (Nlgn3), a neuronal adhesion protein implicated in autism spectrum disorder (ASD), is expressed at excitatory and inhibitory postsynapses and hence may regulate neuronal excitation/inhibition balance. To test this hypothesis, we recorded field excitatory postsynaptic potentials (fEPSPs) in the dentate gyrus of Nlgn3 knockout (KO) and wild-type mice. Synaptic transmission evoked by perforant path stimulation was reduced in KO mice, but coupling of the fEPSP to the population spike was increased, suggesting a compensatory change in granule cell excitability. These findings closely resemble those in neuroligin-1 (Nlgn1) KO mice and could be partially explained by the reduction in Nlgn1 levels we observed in hippocampal synaptosomes from Nlgn3 KO mice. However, unlike Nlgn1, Nlgn3 is not necessary for long-term potentiation. We conclude that while Nlgn1 and Nlgn3 have distinct functions, both are required for intact synaptic transmission in the mouse dentate gyrus. Our results indicate that interactions between neuroligins may play an important role in regulating synaptic transmission and that ASD-related neuroligin mutations may also affect the synaptic availability of other neuroligins.

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