Plasticity of synaptic transmission in autonomic ganglia

Alkadhi, Karim A.; Alzoubi, Karem H.; Aleisa, Abdulaziz M.

doi:10.1016/j.pneurobio.2005.02.002

Cited by 58 publications

(38 citation statements)

References 245 publications

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“…Consistent with this hypothesis, we detected robust expression of PCP4 in cardiac ganglia and a complete abrogation of lethality with vagal antagonism. Interestingly, CaMKII-dependent signaling has been implicated in synaptic plasticity in autonomic ganglia and the regulation of autonomic tone (25). Lineage-restricted gene targeting will be required to formally distinguish PC-autonomous from autonomically mediated effects of PCP4 on cardiac rhythmicity.…”

Section: Discussionmentioning

confidence: 99%

PCP4 regulates Purkinje cell excitability and cardiac rhythmicity

Kim¹,

Shekhar²,

Jia³

et al. 2014

J. Clin. Invest.

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Section: Discussionmentioning

confidence: 99%

PCP4 regulates Purkinje cell excitability and cardiac rhythmicity

Kim¹,

Shekhar²,

Jia³

et al. 2014

J. Clin. Invest.

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“…We determined the levels of two calcium-activated isoforms of PKC, both of which seemed to have normal levels in ganglia from stress rats. As in vivo-induced gLTP in ganglia from stressed rats have been expressed for weeks (4-6 weeks, Alkadhi et al 2005a), the levels of PKC, whose role is limited to the brief induction phase of gLTP (Alkadhi et al 2005b), may have reverted back to normal. The specificity of the various antibodies used in this study has been established in several published reports from this laboratory (e.g., Gerges et al 2004;Alzoubi et al 2006).…”

Section: Discussionmentioning

confidence: 99%

“…Calmodulin and CaMKII According to our putative cascade of events leading to gLTP expression (Alkadhi et al 2005a), presynaptic activity-induced elevated intracellular calcium binds to calmodulin, forming calcium/calmodulin (Ca/cam) complex, which activates CaMKII, forming P-CaMKII (Wang and Kelly 1995). Therefore, if gLTP had been already expressed in ganglia, then there would be an increase in the protein levels or activities of these molecules.…”

Section: Signaling Molecules Protein Levelsmentioning

confidence: 99%

“…Protein Kinase C According to our putative molecular cascade of events leading to the expression of gLTP, HFSinduced calcium influx activates PKC, which, in turn, activates hemeoxygenase-2 (HO-2) to produce the CO necessary for the brief induction phase of gLTP (Alkadhi et al 2005a). Immunoblot analysis revealed increases in the protein levels of PKCγ (157 ± 15%) and PKCβ (182 ± 20%) in stimulated ganglia compared to control ganglia (Fig.…”

Section: Signaling Molecules Protein Levelsmentioning

confidence: 99%

“…Expression of gLTP is independent of activation of cholinergic, adrenergic (Briggs et al 1985), or adenosine (Hogan et al 1998) receptors and does not involve changes in the acetylcholine (ACh) content of the ganglion (Briggs et al 1985) or in the sensitivity of nicotinic ACh receptors ). Uniquely different from other forms of synaptic LTP, both the induction and maintenance of gLTP require activation of 5-HT 3 receptors (Alkadhi et al 1996; see Alkadhi et al 2005a for review) by serotonin, likely released upon high frequency stimulation (HFS) from serotonincontaining small intensely florescent (SIF) cells within the superior cervical ganglion (SCG; Hadjiconstantinou et al 1982).…”

Section: Introductionmentioning

confidence: 99%

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Expression of gLTP in Sympathetic Ganglia from Stress-hypertensive Rats: Molecular Evidence

2008

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We previously reported behavioral and electrophysiological evidence indicating that superior cervical ganglia (SCG) from rats that developed hypertension as a result of chronic psychosocial stress expressed ganglionic long-term potentiation (gLTP) in vivo. In the present study, we present additional supportive evidence by measuring changes in protein levels of essential signaling molecules in ganglia from chronically stressed rats. We compared protein levels of essential, LTP-related signaling molecules in ganglia isolated from chronic stress-hypertensive rats, known to have expressed gLTP, with those of the same molecules in normal ganglia 1h after eliciting gLTP by high frequency stimulation (HFS) in vitro. Immunoblot analysis showed a significant increase in the levels of phosphorylated CaMKII, total CaMKII, nitric oxide synthase (NOS-1), and calmodulin in SCG from both chronically stressed rats and from normal rat ganglia in which gLTP was expressed by HFS in vitro. Additionally, there was a parallel reduction in calcineurin protein levels in ganglia from both groups. The present results confirm that ganglia from stressed rats have expressed gLTP in vivo and that synaptic plasticity in sympathetic ganglia may involve a molecular cascade largely similar to that of LTP in the hippocampal CA1 region.

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

Vargas

Cifuentes

Morales

2007

Developmental Neurobiology

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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.

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Plasticity of synaptic transmission in autonomic ganglia

Cited by 58 publications

References 245 publications

PCP4 regulates Purkinje cell excitability and cardiac rhythmicity

PCP4 regulates Purkinje cell excitability and cardiac rhythmicity

Expression of gLTP in Sympathetic Ganglia from Stress-hypertensive Rats: Molecular Evidence

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

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