Heterosynaptic expression of depolarization-induced suppression of inhibition (DSI) in rat hippocampal cultures

Ohno‐Shosaku, Takako; Sawada, Satsuki; Kano, Masanobu

doi:10.1016/s0168-0102(99)00110-8

Cited by 15 publications

(9 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The data indicate that the endocannabinoids released from a pyramidal cell can influence the synaptic input to nearby neurons in the hippocampus. Significant spread of DSI to nondepolarized neurons was also reported in cultured hippocampal neurons (396).…”

Section: Spread Of Ecb-stdmentioning

confidence: 63%

Endocannabinoid-Mediated Control of Synaptic Transmission

Kano¹,

Ohno‐Shosaku²,

Hashimotodani³

et al. 2009

Physiological Reviews

Self Cite

1,314

1,431

View full text Add to dashboard Cite

The discovery of cannabinoid receptors and subsequent identification of their endogenous ligands (endocannabinoids) in early 1990s have greatly accelerated research on cannabinoid actions in the brain. Then, the discovery in 2001 that endocannabinoids mediate retrograde synaptic signaling has opened up a new era for cannabinoid research and also established a new concept how diffusible messengers modulate synaptic efficacy and neural activity. The last 7 years have witnessed remarkable advances in our understanding of the endocannabinoid system. It is now well accepted that endocannabinoids are released from postsynaptic neurons, activate presynaptic cannabinoid CB1 receptors, and cause transient and long-lasting reduction of neurotransmitter release. In this review, we aim to integrate our current understanding of functions of the endocannabinoid system, especially focusing on the control of synaptic transmission in the brain. We summarize recent electrophysiological studies carried out on synapses of various brain regions and discuss how synaptic transmission is regulated by endocannabinoid signaling. Then we refer to recent anatomical studies on subcellular distribution of the molecules involved in endocannabinoid signaling and discuss how these signaling molecules are arranged around synapses. In addition, we make a brief overview of studies on cannabinoid receptors and their intracellular signaling, biochemical studies on endocannabinoid metabolism, and behavioral studies on the roles of the endocannabinoid system in various aspects of neural functions.

show abstract

Section: Spread Of Ecb-stdmentioning

confidence: 63%

Endocannabinoid-Mediated Control of Synaptic Transmission

Kano¹,

Ohno‐Shosaku²,

Hashimotodani³

et al. 2009

Physiological Reviews

Self Cite

1,314

1,431

View full text Add to dashboard Cite

show abstract

“…Other evidence for changes in efficacy of GABAergic synapses have been reported, including Hebbian LTP (Lamsa et al, 2005), as well as depression, as in the case of depolarization-induced suppression of inhibition (DSI) (Ohno-Shosaku et al, 1998;Ohno-Shosaku et al, 2000). However, DSI is much shorter lasting and involves changes in postsynaptic Ca 2ϩ concentration.…”

Section: Discussionmentioning

confidence: 99%

“…Our study demonstrates that the change is not likely to take place at the GABAergic somata, axon, or the postsynaptic receptor because no change in mIPSCs has been detected, but rather in the linkage between the axonal action potential and the release mechanism, and involves activation of the GABA B receptor. Whether a retrograde messenger other then NO is responsible for this long-lasting change in efficacy of the GABAergic synapse is not known as yet, but several candidates for such an action exists (Ohno-Shosaku et al, 2000;Ohno-Shosaku et al, 2002;Yanovsky et al, 2003). In any case, the retrograde effect is likely to involve a GABA B receptor.…”

Section: Discussionmentioning

confidence: 99%

Simultaneous NMDA-Dependent Long-Term Potentiation of EPSCs and Long-Term Depression of IPSCs in Cultured Rat Hippocampal Neurons

Ivenshitz

Segal²

2006

J. Neurosci.

View full text Add to dashboard Cite

A fundamental issue in understanding activity-dependent long-term plasticity of neuronal networks is the interplay between excitatory and inhibitory synaptic drives in the network. Using dual whole-cell recordings in cultured hippocampal neurons, we examined synaptic changes occurring as a result of a transient activation of NMDA receptors in the network. This enhanced transient activation led to a long-lasting increase in synchrony of spontaneous activity of neurons in the network. Simultaneous long-term potentiation of excitatory synaptic strength and a pronounced long-term depression of inhibitory synaptic currents (LTDi) were produced, which were independent of changes in postsynaptic potential and Ca 2ϩ concentrations. Surprisingly, miniature inhibitory synaptic currents were not changed by the conditioning, whereas both frequency and amplitudes of miniature EPSCs were enhanced. LTDi was mediated by activation of a presynaptic GABA B receptor, because it was blocked by saclofen and CGP55845 [(2S)-3-{[(15)-1-(3,4-dichlorophenyl)ethyl]amino-2-hydroxypropyl)(phenylmethyl)phosphinic acid].The cAMP antagonist Rp-adenosine 3Ј,5Ј-cyclic monophosphothioate abolished all measured effects of NMDA-dependent conditioning, whereas a nitric oxide synthase inhibitor was ineffective. Finally, network-induced plasticity was not occluded by a previous spike-timing-induced plasticity, indicating that the two types of plasticity may not share the same mechanism. These results demonstrate that network plasticity involves opposite affects on inhibitory and excitatory neurotransmission.

show abstract

“…Indeed, some experimental results are consistent with this idea. DSI induced on one pyramidal cell spreads to other nondepolarized cells within 20 m of the depolarized cell (90,131). In hippocampal slices, LTP induced at synaptic inputs on a single CA1 pyramidal neuron spreads to synapses formed by the same set of afferent fibers on the neighboring neurons (132,133) or to adjacent synapses made by different inputs onto the same postsynaptic cell (134).…”

Section: Retrograde Signaling During Synaptogenesismentioning

confidence: 99%

Retrograde signaling at central synapses

Tao

Poo

2001

Proc. Natl. Acad. Sci. U.S.A.

124

View full text Add to dashboard Cite

Transcellular retrograde signaling from the postsynaptic target cell to the presynaptic neuron plays critical roles in the formation, maturation, and plasticity of synaptic connections. We here review recent progress in our understanding of the retrograde signaling at developing central synapses. Three forms of potential retrograde signals-membrane-permeant factors, membrane-bound factors, and secreted factors-have been implicated at both developing and mature synapses. Although many of these signals may be active constitutively, retrograde factors produced in association with activity-dependent synaptic plasticity, e.g., long-term potentiation and long-term depression, are of particular interest, because they may induce modification of neuronal excitability and synaptic transmission, functions directly related to the processing and storage of information in the nervous system. N eural information coded by the action potential is transmitted through a chemical synapse in the anterograde direction by release of neurotransmitters, neuropeptides, and other protein factors from the presynaptic terminal. These molecules produce immediate changes in the membrane potential as well as long-term structural and metabolic changes in the postsynaptic cell. Over the past several decades, it has become increasingly clear that information exchange at the synapse is bidirectional: the postsynaptic cell also provides a variety of retrograde signals to the presynaptic neuron. This reciprocal interaction is crucial for the differentiation and maintenance of the presynaptic cell as well as the formation and maturation of the synapse. The general notion of retrograde signaling involves postsynaptic production of a signal, either constitutively or triggered by synaptic activity, that acts on the presynaptic neuron through the following mechanisms. First, the retrograde signal can be carried by a membrane-permeant molecule that diffuses across the plasma membranes from the postsynaptic cell directly into the presynaptic nerve terminal. Second, membraneimpermeant but soluble factors can be packaged and secreted via exocytotic vesicles by the postsynaptic cell and exert the retrograde action by binding and activation of receptors on the presynaptic membrane. Third, direct signaling through the synaptic cleft may be accomplished through mediation of physically coupled pre-and postsynaptic membrane-bound proteins, including transmembrane proteins as well as those secreted and immobilized in the extracellular matrix within the synaptic cleft. This review will summarize recent progress in the study of retrograde regulation at central synapses, with a focus on the role of retrograde interaction in the formation and activitydependent plasticity of synapses. Some aspects of this subject have been more extensively reviewed elsewhere (1). An excellent review of signaling at developing neuromuscular junctions (NMJs) has also appeared recently (2). Retrograde Signaling During SynaptogenesisOur present understanding of the process of synaptogenesis...

show abstract

Heterosynaptic expression of depolarization-induced suppression of inhibition (DSI) in rat hippocampal cultures

Cited by 15 publications

References 16 publications

Endocannabinoid-Mediated Control of Synaptic Transmission

Endocannabinoid-Mediated Control of Synaptic Transmission

Simultaneous NMDA-Dependent Long-Term Potentiation of EPSCs and Long-Term Depression of IPSCs in Cultured Rat Hippocampal Neurons

Retrograde signaling at central synapses

Contact Info

Product

Resources

About