Synaptic transmission is required for initiation of long-term potentiation

Dunwiddie, Thomas V.; Madison, Daniel V.; Lynch, Gary

doi:10.1016/0006-8993(78)90293-7

Cited by 115 publications

(22 citation statements)

References 9 publications

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“…2) is necessary for adaptive presynaptic silencing. This result is surprising because multiple persistent forms of hippocampal synaptic plasticity depend on calcium (Dunwiddie et al, 1978; Wigström et al, 1979; Lynch et al, 1983; Williams and Johnston, 1989; Wickens and Abraham, 1991; Mulkey and Malenka, 1992; Xie et al, 1992; Tzounopoulos et al, 1998; Patenaude et al, 2003; Izumi et al, 2008; Kellogg et al, 2009). Other adaptive forms of plasticity, including synaptic scaling and plasticity of intrinsic excitability, require changes in intracellular calcium (Thiagarajan et al, 2002; Cudmore and Turrigiano, 2004; Frank et al, 2006; Ibata et al, 2008; Wu et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

Calcium-Independent Inhibitory G-Protein Signaling Induces Persistent Presynaptic Muting of Hippocampal Synapses

Crawford¹,

Chang²,

Hyrc³

et al. 2011

J. Neurosci.

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Adaptive forms of synaptic plasticity that reduce excitatory synaptic transmission in response to prolonged increases in neuronal activity may prevent runaway positive feedback in neuronal circuits. In hippocampal neurons, for example, glutamatergic presynaptic terminals are selectively silenced, creating “mute” synapses, after periods of increased neuronal activity or sustained depolarization. Previous work suggests that cAMP-dependent and proteasome-dependent mechanisms participate in silencing induction by depolarization, but upstream activators are unknown. We, therefore, tested the role of calcium and G-protein signaling in silencing induction in cultured hippocampal neurons. We found that silencing induction by depolarization was not dependent on rises in intracellular calcium, from either extracellular or intracellular sources. Silencing was, however, pertussis toxin sensitive, which suggests that inhibitory G-proteins are recruited. Surprisingly, blocking four common inhibitory G-protein-coupled receptors (GPCRs) (adenosine A1 receptors, GABAB receptors, metabotropic glutamate receptors, and CB1 cannabinoid receptors) and one ionotropic receptor with metabotropic properties (kainate receptors) failed to prevent depolarization-induced silencing. Activating a subset of these GPCRs (A1 and GABAB ) with agonist application induced silencing, however, which supports the hypothesis that G-protein activation is a critical step in silencing. Overall, our results suggest that depolarization activates silencing through an atypical GPCR or through receptor-independent G-protein activation. GPCR agonist-induced silencing exhibited dependence on the ubiquitin-proteasome system, as was shown previously for depolarization-induced silencing, implicating the degradation of vital synaptic proteins in silencing by GPCR activation. These data suggest that presynaptic muting in hippocampal neurons uses a G-protein-dependent but calcium-independent mechanism to depress presynaptic vesicle release.

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Section: Discussionmentioning

confidence: 99%

Calcium-Independent Inhibitory G-Protein Signaling Induces Persistent Presynaptic Muting of Hippocampal Synapses

Crawford¹,

Chang²,

Hyrc³

et al. 2011

J. Neurosci.

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“…Slices were allowed to recover from cutting for 2 h. A bipolar stimulation electrode (Fredrick Haer, Bowdowinham, ME, USA) was positioned in the stratum radiatum of the CA1 region. A metal recording electrode (platinum/tungsten core, impedance: 0.5 MX; Thomas Recording, Germany) was paced in the apical dendrites of the CA1 region (Dunwiddie et al, 1978;Frey et al, 1988). Test-pulse stimuli, at low frequency (0.025 Hz) and 0.2-ms duration, were applied and evoked fEPSPs were recorded with a sample rate of 10,000 Hz.…”

Section: In Vitro Electrophysiologymentioning

confidence: 99%

Hippocampal function is compromised in an animal model of multiple sclerosis

et al. 2015

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“…APB has been shown to depress synaptic transmission but not block the action of exogenous glutamate and various glutamate analogs in other areas of the brain, such as the pyriform cortex (24,25), the lateral perforant pathway (26), and the spinal cord (27). While there was no clear evidence for a precise mechanism or site of action, the results in these previous studies as well as the present one are consistent with a presynaptic effect of APB.…”

Section: Discussionmentioning

confidence: 99%