Role of presynaptic and postsynaptic IP3‐dependent intracellular calcium release in long‐term potentiation in sympathetic ganglion of the rat

Abstract

In the rat superior cervical ganglion, a form of long term potentiation (LTP) can be elicited by a brief high frequency stimuli applied to the preganglionic nerve. Cumulative evidence shows that a transient increase in cytoplasmic Ca²+ concentration is essential for the generation of the ganglionic LTP. Calcium influx and calcium release from intracellular calcium stores contribute to LTP. However, the differential role of presynaptic and postsynaptic calcium signaling has not been established. Herein, by using heparin, a membrane-impermeant inositol trisphosphate receptor (IP3R) blocker, we explored the contribution of presynaptic and postsynaptic IP3-sensitive calcium stores to the ganglionic LTP. The LTP was produced by a conditioning train of 40 Hz for 3 s. We analyzed the effects of heparin on the posttetanic potentiation: PTP magnitude and PTP time constant, and on two parameters that describe the LTP: LTP decay time (elapsed time required by the potentiated response to fall to 20% above the basal value) and LTP extent (the integral of the potentiated response). Heparin (100 and 200 μg/ml) was loaded in the preganglionic, the postganglionic, or in both nerves. We found that in all tested conditions heparin significantly decreased LTP but practically did not affect PTP. The preganglionic and postganglionic inhibitory effects of heparin were not additive. De-N-sulfated heparin, an ineffective IP3R blocker, had no effect on LTP, but abolished the heparin blocking effect. Data suggest that presynaptic and postsynaptic IP3-dependent intracellular calcium release equally contribute to ganglionic LTP, supporting our proposal of a trans-synaptic mechanism for LTP.

A recurrent SHANK1 mutation implicated in autism spectrum disorder causes autistic-like core behaviors in mice via downregulation of mGluR1-IP3R1-calcium signaling

“…IP3R1 is an intracellular calcium channel that mediates intracellular calcium release from ER calcium storage by binding with and being activated by IP3 generated through mGluR1 [ 38 ]. Since mGluR1 and IP3R1 levels were diminished in R882H-KI mice, we speculated that the amount of calcium released from the ER might have been lessened, affecting the concentration of neuronal cytosolic calcium [ 39 ]. To test this hypothesis, we measured the calcium transients in the hippocampus stimulated by DHPG, a specific group I metabotropic receptor agonist.…”

Ganglionic Long-Term Potentiation in Prehypertensive and Hypertensive Stages of Spontaneously Hypertensive Rats Depends on GABA Modulation

“…The underlying mechanisms are not completely understood. gLTP is a Ca 2+ -dependent phenomenon resulting from the participation of several intracellular signaling pathways [5, 7–12] and may play a role in the modulation of peripheral autonomic nervous system activity, including the regulation of blood vessel tone. The sustained presence of gLTP in vivo would reinforce neural outflow to blood vessels, resulting in an increase of peripheral resistance that elevates blood pressure [13].…”

Effect of Dopaminergic D1 Receptors on Plasticity Is Dependent of Serotoninergic 5-HT1A Receptors in L5-Pyramidal Neurons of the Prefrontal Cortex

“…These effects were due to the activation of NMDARs and their blockade with D-L-AP5 prevent the induction of plasticity in L5PyNs [ 17 , 36 ]. In order to sort L5PyNs displaying LTP or LTD, we retained an enhancement or a depression of IntgT higher or lower than 20% of the control IntgT before the HFS protocol as already described elsewhere [ 40 , 41 ]. L5PyNs exhibiting an IntgT change ranging between ± 20% of the control conductance before the HFS protocol were classified as “no plasticity”.…”