Calcium stores and synaptic plasticity
Section snippets
INTRODUCTION
The ability to modify synaptic connections is a fundamental property of the CNS. During development, synapses are strengthened and weakened and during life changes occur as a result of incoming information. Thus processes such as learning, memory and addiction involve changes in synaptic transmission. At the cellular level, long-term potentiation (LTP) and long-term depression (LTD) of synaptic transmission have received much attention as models of learning and memory (for example, see [1]).
HIPPOCAMPAL NMDA RECEPTOR-DEPENDENT PLASTICITY
At the CA3-CA1 synapses in the hippocampus, AMPA receptors mediate the vast majority of basal transmission whereas NMDA receptors are largely silent during basal periods due to a block by Mg2+ ions at negative membrane potentials [8]. NMDA receptor activation, however, is a critical trigger for the induction of both LTP and LTD in the hippocampus and other brain regions 2., 3.. For example, at the CA3-CA1 synapse in the hippocampus, blockade of NMDA receptors prevents the induction of LTP [9]
CEREBELLAR LTD
The role of calcium release from the ER is clearer in the case of LTD in the cerebellum than in LTP and LTD in the hippocampus. Purkinje cells (PCs) in the cerebellar cortex receive inputs from the inferior olive via climbing fibres (CFs) and from granule cells in the cerebellum via parallel fibres (PFs; reviewed in [30]). Repeated associative activation of the two inputs onto a single Purkinje cell results in LTD of the PF input. Cerebellar LTD is thought to be critical for various types of
SHORT-TERM PLASTICITY AT PRESYNAPTIC TERMINALS
The plasticity described above, both in the hippocampus and cerebellum, involves calcium release from the ER in the postsynaptic neurone. However, ER and the associated ryanodine receptors are also present in presynaptic axon terminals [43]. Basal action potential-stimulated release of transmitter is known to be elicited by calcium entry through voltage gated calcium channels, but the role of CICR in the presynaptic terminal is unclear. Emptage et al. [44] recently investigated whether calcium
OTHER FORMS OF SYNAPTIC PLASTICITY
In addition to the main forms of plasticity discussed above, release of calcium from intracellular stores may also be involved in other forms of plasticity in the CNS. High frequency stimulation of afferent fibres to CA3 pyramidal cells elicits an LTD of inhibitory GABAA receptor-mediated responses [47]. Such LTD is prevented by inhibitors of CICR, but not by inhibitors of IP3-mediated calcium release, and the calcium stores involved may be located both pre and postsynaptically [47]. LTP of GABA
CONCLUSION
Rises in intracellular calcium levels is a common property of multiple forms of synaptic plasticity. In some cases calcium entry through NMDA receptors is the initial trigger for plasticity changes which may then also include CICR from ER. Activation of mglu receptors can also contribute to plasticity induction by stimulating calcium release from the ER via production of IP3. Several forms of plasticity are known to be inhibited by blocking calcium release from intracellular stores but until
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Orai1 Channels Are Essential for Amplification of Glutamate-Evoked Ca<sup>2+</sup> Signals in Dendritic Spines to Regulate Working and Associative Memory
2020, Cell ReportsCitation Excerpt :On the basis of the findings presented here, we conclude that stimulation of synaptic GluRs on dendritic spines triggers [Ca2+]i rises that are critically dependent on the opening of Orai1 channels (Figure S6). In line with previous proposals (Fitzjohn and Collingridge, 2002; Rose and Konnerth, 2001), opening of NMDARs by AMPAR-mediated depolarization of the postsynaptic membrane potential provides an initial trigger for Ca2+ entry. As shown by the measurements of Glu-uncaging-evoked decreases in [Ca2+]ER (Figure 3), this in turn evokes rapid depletion of ER Ca2+ stores to stimulate Orai1 channel activation, presumably through the ER Ca2+ sensors, STIM1 and/or STIM2.
Calcium-Permeable AMPA Receptors Promote Endocannabinoid Signaling at Parvalbumin Interneuron Synapses in the Nucleus Accumbens Core
2020, Cell ReportsCitation Excerpt :Additionally, prior application of AM251 significantly reduced the magnitude of DSE, indicating that synapses onto PV(+)-INs undergo CB1R-dependent short-term plasticity facilitated by intracellular Ca2+ signaling (Figures 5D and 5E; 86.14% ± 3.78%, n = 7, p = 0.007). Increased intracellular Ca2+ signaling contributes to the induction of signaling events required for the expression of LTD (Winder and Sweatt, 2001; Grueter et al., 2010; Fitzjohn and Collingridge, 2002). Given that eCBs regulate glutamatergic transmission onto PV(+)-INs in a CP-AMPAR-dependent manner, we hypothesized that CB1R activity underlies the expression of LFS-induced LTD at glutamatergic synapses onto PV(+)-INs.
Priming of GABAergic Long-term Potentiation by Muscarinic Receptors
2020, NeuroscienceCalcium channelopathies and Alzheimer's disease: Insight into therapeutic success and failures
2014, European Journal of PharmacologyCitation Excerpt :The activation of these channels is amplified by the phenomenon of calcium-induced calcium release (CICR), a regenerative mechanism by which calcium enhances its own release from inositol triphosphate and ryanodine receptors (Finch et al., 1991; Friel and Tsien, 1992). Long term synaptic plasticity, the cellular correlate of learning and memory (Martin et al., 2000; Whitlock et al., 2006), is also modulated by ER calcium signaling (Bardo et al., 2006; Fitzjohn and Collingridge, 2002; Park et al., 2008). The link between ryanodine receptor-evoked calcium signaling and memory encoding has been demonstrated in many studies, and show that altered ryanodine receptor function (type 2 and type 3 ryanodine receptors in particular) disrupts synaptic transmission, long term plasticity, and memory performance (Adasme et al., 2011; Baker et al., 2013; Balschun et al., 1999; Fujii et al., 2000; Futatsugi et al., 1999; Oules et al., 2012; Peng et al., 2012).