Nitric oxide mediates long-term potentiation in rat superior cervical ganglion

Alkadhi, Karim A.; Altememi, Ghazi F

doi:10.1016/s0006-8993(97)00028-0

Cited by 20 publications

(20 citation statements)

References 11 publications

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“…We have shown previously that NO synthase inhibitors reversibly blocked the expression of LTP, indicating requirement of NO for maintenance, but not induction, of LTP (Alkadhi and Altememi, 1997;Altememi and Alkadhi, 1999). Figure 3 represents two new series of experiments to confirm previous results.…”

Section: Inhibition Of Nitric Oxide Synthasesupporting

confidence: 81%

“…Compliant with these findings is the recent demonstration that NO is required only for the maintenance and not for initiation of ganglionic LTP (Alkadhi and Altememi, 1997;Altememi and Alkadhi, 1999). Therefore, a second similar messenger may be required for the process of induction of LTP.…”

mentioning

confidence: 68%

“…However, previously, we have shown that inhibitors of NO synthase reversibly blocked tetanus-induced ganglionic LTP, indicating the involvement of NO in maintenance, but not induction, of LTP (Alkadhi and Altememi, 1997;Altememi and Alkadhi, 1999). If CO is involved in the induction of ganglionic LTP by permeating from the extracellular space, then the presence of Hb will prevent induction.…”

Section: Effect Of Oxyhemoglobinmentioning

confidence: 82%

“…Because we have shown previously that NO is not required for induction of ganglionic LTP (Alkadhi and Altememi, 1997;Altememi and Alkadhi, 1999), the alternative would have to be an agent that also has a strong affinity for and is readily taken up by Hb. Therefore, we investigated the role of CO in the induction of ganglionic LTP.…”

Section: Resultsmentioning

confidence: 99%

“…This has been demonstrated in vivo (Alonso-deFlorida et al, 1991;, as well as in vitro (Brown and McAfee, 1982;Briggs et al, 1985Minota et al, 1991;Alkadhi et al, 1996;Alkadhi and Altememi, 1997;Altememi and Alkadhi, 1999). This LTP is independent of the activation of either cholinergic or adrenergic receptors and may be attributable to an increase in acetylcholine release as measured by biochemical assay (Briggs et al, 1985).…”

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confidence: 75%

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Retrograde Carbon Monoxide Is Required for Induction of Long-Term Potentiation in Rat Superior Cervical Ganglion

et al. 2001

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Carbon monoxide (CO), produced in the body by the enzyme heme oxygenase (HO), has been suggested as a retrograde synaptic messenger with a prominent role in the long-term potentiation (LTP) of certain areas of the brain. LTP of sympathetic ganglia is 5-HT 3 receptor-dependent and has been shown to require nitric oxide for the maintenance, but not for the induction, phase. We investigated the possibility of CO being required for the induction of ganglionic LTP. Pretreatment of rat isolated superior cervical ganglia with oxyhemoglobin (25-100 M) completely blocked LTP. In the same ganglia, prolonged washout of oxyhemoglobin did not uncover any potentiation of the compound action potential. Oxyhemoglobin had no significant effect on the maintenance phase in ganglia with established LTP. Pretreatment of ganglia with the HO inhibitor zinc protoporphyrin-IX (ZnPP) (10 M) completely and irreversibly prevented the expression of tetanus-evoked LTP. However, in the same ganglia, after superfusion of CO in the presence of ZnPP, tetanic stimulation readily evoked LTP. No effect was seen on the maintenance phase when ZnPP was superfused on ganglia with established LTP. Pretreatment of ganglia with the 5-HT 3 receptor antagonist ondansetron (0.4 M) alone completely and irreversibly blocked LTP. However, in the presence of CO, ondansetron did not block LTP. These results suggest that activation of 5-HT 3 receptors may be involved in the production of CO. The results also suggest that CO, probably originating outside the presynaptic nerve terminal, is involved in the induction of LTP.

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Section: Inhibition Of Nitric Oxide Synthasesupporting

confidence: 81%

mentioning

confidence: 68%

Section: Effect Of Oxyhemoglobinmentioning

confidence: 82%

Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 75%

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Retrograde Carbon Monoxide Is Required for Induction of Long-Term Potentiation in Rat Superior Cervical Ganglion

et al. 2001

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Hypothyroidism impairs long‐term potentiation in sympathetic ganglia: Electrophysiologic and molecular studies

Alzoubi

Bedawi

Aleisa

et al. 2004

J of Neuroscience Research

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Electrophysiologic and molecular techniques were used to study the effect of adult-onset hypothyroidism on synaptic plasticity in the superior cervical sympathetic ganglion. Ganglia excised from adult thyroidectomized and sham-operated rats were subjected to a brief high-frequency stimulation of the preganglionic nerve to express long-term potentiation (gLTP). Western blotting was carried out to determine the protein levels of key signaling molecules that may be involved in the expression of gLTP. Input/output relationship in ganglia from hypothyroid rats indicated a normal basal synaptic transmission, whereas activity-dependent types of synaptic plasticity, posttetanic potentiation (PTP) and gLTP, were impaired. Immunoblot analysis showed that both calcium/calmodulin kinase II (CaMKII) and phosphorylated CaMKII (P-CaMKII) levels were reduced markedly in hypothyroid rat ganglia compared to those from euthyroid controls. Additionally, protein levels of nitric oxide synthase-1, heme oxygenase-2, calmodulin, protein kinase C (PKC), and calcineurin were also reduced in hypothyroid rat ganglia. The results indicate that abnormally low basal levels of signaling molecules may be responsible for hypothyroidism-induced impairment of gLTP in superior cervical ganglia. In addition, the results indicate that synaptic plasticity in sympathetic ganglia may involve a molecular sequence of events similar to that proposed for LTP in the hippocampus.

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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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Nitric oxide mediates long-term potentiation in rat superior cervical ganglion

Cited by 20 publications

References 11 publications

Retrograde Carbon Monoxide Is Required for Induction of Long-Term Potentiation in Rat Superior Cervical Ganglion

Retrograde Carbon Monoxide Is Required for Induction of Long-Term Potentiation in Rat Superior Cervical Ganglion

Hypothyroidism impairs long‐term potentiation in sympathetic ganglia: Electrophysiologic and molecular studies

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

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