Differential contribution of extracellular and intracellular calcium sources to basal transmission and long‐term potentiation in the sympathetic ganglion of the rat

Abstract

Calcium involved in basal ganglionic transmission and long-term potentiation (LTP) can arise either by influx from the extracellular medium or release from intracellular stores. No attempts have yet been made to concurrently explore the contributions of extracellular and intracellular Ca2+ to basal ganglionic transmission or LTP. Here, we investigate this subject using the superior cervical ganglion of the rat. To explore the extracellular Ca2+ contribution, we evaluated basal transmission and LTP at different extracellular Ca2+ concentrations. To assess intracellular Ca2+ release, we explored the contribution of the calcium-induced calcium release process by overactivation or blockade of ryanodine-sensitive Ca2+ receptor channel with caffeine, and also by blocking either IP3R with Xestospongin C or the sarco(endo)plasmic reticulum Ca2+-ATPase pump with thapsigargin. Extracellular Ca2+ affected ganglionic basal transmission and LTP to different extents. While 25% of the physiological Ca2+ concentration supported 80% of basal transmission, 50% of normal Ca2+ was required to achieve 80% of LTP. Notably, disruption of intracellular Ca2+ release by all the drugs tested apparently did not affect basal ganglionic transmission but impaired LTP. We conclude that basal transmission requires only a small level of Ca2+ entry, while LTP expression not only requires more Ca2+ entry but is also dependent on Ca2+ release from intracellular stores.

Co-Induction of LTP and LTD and Its Regulation by Protein Kinases and Phosphatases

“…In addition to NMDARs, other sources of Ca 2ϩ may also contribute to the increase in postsynaptic Ca 2ϩ seen in this pairing-induced potentiation, such as voltage-gated Ca 2ϩ channels (VGCCs) and release of Ca 2ϩ from internal stores, the latter potentially mediated by either IP 3 or ryanodine receptors (Balschun et al 1999;Kapur et al 1998;Vargas et al 2007). To test whether LTP requires VGCC activation, nimodipine (10 M) was superfused during administration of the pairing protocol.…”

Prenatal Ethanol Exposure Misregulates Genes Involved in Iron Homeostasis Promoting a Maladaptation of Iron Dependent Hippocampal Synaptic Transmission and Plasticity

“…We can speculate that the elevated postsynaptic expression of TfR in PAE animals masks the presynaptic effect because it regulates the iron concentration in the synaptic cleft. However, deferiprone incubation slightly decreased AMPAR synaptic transmission in control as well in PAE animals denoting that the mechanism involving basal synaptic transmission is a complex process, therefore we cannot discard that other mechanisms are affecting by Iron, such as presynaptic and postsynaptic events (Vargas et al, 2007; Fioravante and Regehr, 2011; Ramaswami et al, 2016) and the complex regulation by astrocytes (Navarrete and Araque, 2011; Panatier et al, 2011). Additional studies are necessary to determine which is the putative mechanism.…”

Involvement of ryanodine receptors in tetanic sciatic stimulation‐induced long‐term potentiation of spinal dorsal horn and persistent pain in rats

“…Raymond and Redman (2006) reported that the induction of short‐lasting LTP required activation of RyRs, which selectively increased Ca 2+ in hippocampal synaptic spines. Furthermore, a study showed that LTP expression not only requires more Ca 2+ entry but is also dependent on Ca 2+ release from intracellular stores in the superior cervical ganglion (Vargas et al, 2007). Similarly, the ryanodine‐sensitive intracellular calcium store was involved in the induction of spinal synaptic LTP (Drdla et al, 2009).…”