Long-lasting rebound potentiation of GABAA receptor-mediated inhibitory synaptic currents in cerebellar purkinje cells

Kano, Masanobu; Rexhausen, U.; Dreessen, J.; Konnerth, Arthur

doi:10.1016/0921-8696(92)90775-v

Cited by 4 publications

(8 citation statements)

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“…A number of studies in various brain regions have found that Ca 2+ enters the postsynaptic cell through NMDARs or voltage‐gated Ca 2+ channels (Kano, 1994; Glaum & Brooks, 1996; Grunze et al 1996; McLean et al 1996; Caillard et al 1999 a , b ; Lu et al 2000; Ouardouz et al 2000; Nugent et al 2007). For example, early in postnatal development, hippocampal GABAergic synapses can exhibit bi‐directional plasticity.…”

Section: Gabaa Synapses In Developing Brainmentioning

confidence: 99%

“…In neonates, at this and many synapses, GABA A receptor‐mediated currents are depolarizing, because the expression of specific Cl − transporters promotes high levels of intracellular Cl − (Cherubini et al 1991; Akerman & Cline, 2007). The activation of these receptors therefore can provide the initial membrane depolarization required to open NMDAR channels resulting in LTD (Kano, 1994; McLean et al 1996; Caillard et al 1999 b ), or to open voltage‐gated calcium channels resulting in LTP at these synapses (McLean et al 1996). This form of LTP at hippocampal synapses is restricted to the first postnatal week, a period when the GABAergic synapses are reaching maturity.…”

Section: Gabaa Synapses In Developing Brainmentioning

confidence: 99%

“…At other GABA A synapses, plasticity is dependent on intracellular sources of Ca 2+ such as InsP 3 -sensitive stores, or Ca 2+ -induced Ca 2+ release stores (Hashimoto et al 1996;Komatsu, 1996). Several of these examples of GABA A synapse LTP result from postsynaptic increases in GABA A receptor number or sensitivity to GABA (Kano, 1994;Ouardouz et al 2000;Maffei et al 2006), although the cellular mechanisms that underlie these changes remain poorly understood. Aizenman et al (1998) studied the cerebellar Purkinje cell-deep cerebellar nuclei synapse and first proposed a novel model to explain how LTP and LTD can be triggered solely by the activity of inhibitory synapses.…”

Section: Gaba a Synapses In Developing Brainmentioning

confidence: 99%

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LTP of GABAergic synapses in the ventral tegmental area and beyond

Nugent

Kauer

2008

The Journal of Physiology

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One of the mechanisms by which the experience-dependent reorganization of neural circuitry can occur is through changes in synaptic strength. Almost every excitatory synapse in the mammalian brain exhibits LTP (long-term potentiation) or LTD (long-term depression), two cellular mechanisms of synaptic plasticity. However, LTP and LTD have been reported much more rarely at fast inhibitory GABA A receptor synapses. Our recent study suggests that in vivo morphine initiates a long-lasting alteration of GABAergic synapses in the ventral tegmental area (VTA) by blocking the mechanisms required for LTP of GABAergic synapses. Here we put this work into the context of other examples of synaptic plasticity at GABAergic synapses.

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Section: Gabaa Synapses In Developing Brainmentioning

confidence: 99%

Section: Gabaa Synapses In Developing Brainmentioning

confidence: 99%

Section: Gaba a Synapses In Developing Brainmentioning

confidence: 99%

See 1 more Smart Citation

LTP of GABAergic synapses in the ventral tegmental area and beyond

Nugent

Kauer

2008

The Journal of Physiology

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“…Since they are modi®able, they contribute towards memory dynamics in the same way that excitatory connections do. The existence of use-dependent plasticity in inhibitory systems has recently received some empirical support (Kano 1994). We view the modi®able intralayer inhibitory connections in our model as a mechanism for generating an eective representation within the multilayer hierarchy.…”

Section: Discussionmentioning

confidence: 98%

“…A key feature of cortical inhibition is that it is quite long-lasting compared with excitatory input, which may enhance its ability to create competitive interactions among sets of cortical pyramidal cells. Our model also incorporates recent evidence that inhibitory synapses are modi®able (Kano 1994) and thus may contribute to memory storage.…”

Section: Biological Constraints On the Computational Modelmentioning

confidence: 96%

Cortical memory dynamics

Kairiss

Miranker

1998

Biological Cybernetics

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Biological memories have a number of unique features, including (1) hierarchical, reciprocally interacting layers, (2) lateral inhibitory interactions within layers, and (3) Hebbian synaptic modifications. We incorporate these key features into a mathematical and computational model in which we derive and study Hebbian learning dynamics and recall dynamics. Introducing the construct of a feasible memory (a memory that formally responds correctly to a specified collection of noisy cues that are known in advance), we study stability and convergence of the two kinds of dynamics by both analytical and computational methods. A conservation law for memory feasibility under Hebbian dynamics is derived. An infomax net is one where the synaptic weights resolve the most uncertainty about a neural input based on knowledge of the output. The infomax notion is described and is used to grade memories and memory performance. We characterize the recall dynamics of the most favorable solutions from an infomax perspective. This characterization includes the dynamical behavior when the net is presented with external stimuli (noisy cues) and a description of the accuracy of recall. The observed richness of dynamical behavior, such as its initial state sensitivity, provides some hints for possible biological parallels to this model.

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CB1 cannabinoid receptor-mediated plasticity of GABAergic synapses in the mouse insular cortex

Toyoda

2020

Sci Rep

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The insular cortex plays pivotal roles in taste learning. As cellular mechanisms of taste learning, long-term potentiation (LTP) at glutamatergic synapses is well studied. However, little is known about long-term changes of synaptic efficacy at GABAergic synapses in the insular cortex. Here, we examined the synaptic mechanisms of long-term plasticity at GABAergic synapses in layer V pyramidal neurons of the mouse insular cortex. In response to a prolonged high-frequency stimulation (HFS), GABAergic synapses displayed endocannabinod (eCB)-mediated long-term depression (LTD GABA ). When cannabinoid 1 receptors (CB1Rs) were blocked by a CB1R antagonist, the same stimuli caused LTP at GABAergic synapses (LTP GABA ) which was mediated by production of nitric oxide (NO) via activation of NMDA receptors. Intriguingly, NO signaling was necessary for the induction of LTD GABA . In the presence of leptin which blocks CB1 signaling, the prolonged HFS caused LTP GABA which was mediated by NO signaling. These results indicate that long-term plasticity at GABAergic synapses in the insular cortex can be modulated by combined effects of eCB and NO signaling. These forms of GABAergic synaptic plasticity in the insular cortex may be crucial synaptic mechanisms in taste learning.The insular cortex plays critical roles in sensory and cognitive functions, such as pain perception, taste memory and interoceptive awareness 1-3 . The insular cortex can be generally divided into the gustatory and visceral insular cortex 4 . The gustatory insular cortex is associated with taste learning such as conditioned taste aversion (CTA) 5-9 . However, synaptic mechanisms underlying taste learning remains largely unknown.Long-term potentiation (LTP) and long-term depression (LTD) of synaptic transmission are considered to be key synaptic mechanisms involved in learning and memory 10 . In the insular cortex, long-term plasticity at glutamatergic synapses has been well investigated [11][12][13][14] , and this form of synaptic plasticity is considered to be closely correlated with the taste learning 7,11,13,15,16 . In contrast, much less is known about long-term changes of synaptic efficacy at GABAergic synapses in the insular cortex. Because cortical interneurons dynamically control the excitability of pyramidal neurons 17 , plasticity of inhibitory synaptic transmission may exert major influences on insular excitability and function.Long-term changes in synaptic efficacy can be caused by various synaptic mechanisms including presynaptic release properties and changes in subunit composition of postsynaptic receptors. As one of the potential mechanisms, retrograde messengers that are released from postsynaptic neurons play important roles in synaptic plasticity. The endocannabinoids (eCBs) and nitric oxide (NO) are well-known retrograde messengers. Thus far, the roles of eCBs and NO in plasticity at GABAergic synapses have been widely studied in the central nervous system (CNS) 18 . eCBs are synthesized postsynaptically in neurons following activation o...

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Long-lasting rebound potentiation of GABAA receptor-mediated inhibitory synaptic currents in cerebellar purkinje cells

Cited by 4 publications

References 0 publications

LTP of GABAergic synapses in the ventral tegmental area and beyond

LTP of GABAergic synapses in the ventral tegmental area and beyond

Cortical memory dynamics

CB1 cannabinoid receptor-mediated plasticity of GABAergic synapses in the mouse insular cortex

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