Neurotransmission through sympathetic ganglia of spontaneously hypertensive rats.

Magee, Jeffrey C.; Schofield, Geoffrey G.

doi:10.1161/01.hyp.20.3.367

Cited by 25 publications

(16 citation statements)

References 32 publications

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“…Each bar represents the mean±SEM; ( p<0.05, n=9). Insets are representative experiments indicating occlusion due to saturation and suggesting in vivo expression of gLTP in these ganglia (Alkadhi et al 2001b;Gerges et al 2002;Alkadhi et al 2005b); and (4) a shift of input-output (I/O) curves of synaptic transmission of ganglia from hypertensive rats to the left side of those from normotensive rats (Magee and Schofield 1992;Alkadhi et al 2005b), indicating expression of gLTP (Johnston and Wu 1995). The present experiments provide molecular evidence in support of the in vivo expression of gLTP in ganglia from stressed animals.…”

Section: Discussionmentioning

confidence: 99%

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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Section: Discussionmentioning

confidence: 99%

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

2008

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“…This is again in contrast to what we and others have seen in the ouabain-dependent rats 7 or spontaneously hypertensive animals. 8,10,[32][33][34] Bath application of Ang II enhanced the efficiency of ganglionic transmission in both groups of animals, but the enhancement was more pronounced in the (mRen2)27 rats. The concentration of Ang II was in line with that used in other in vitro studies 20 and, although above that circulating in plasma, we do not know the peptide concentration at the level of the sympathetic ganglion.…”

Section: Discussionmentioning

confidence: 99%

“…Other studies show alterations in ganglionic function in spontaneously hypertensive rats (SHRs). 8,9 For example, postsynaptic spike frequency adaptation is curtailed in SHRs. 9 Presynaptically, there is enhanced release of acetylcholine.…”

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confidence: 99%

Alterations in Sympathetic Ganglionic Transmission in Response to Angiotensin II in (mRen2)27 Transgenic Rats

et al. 2004

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Abstract-Hypertension in (mRen2)27 transgenic rats is partly dependent on activation of the sympathetic nervous system, but the role of ganglionic transmission is unknown. We assessed indices of synaptic plasticity (post-tetanic short-term potentiation [PTP] and long-term potentiation [LTP]) and sympathetic ganglionic transmission without tetany in superior cervical ganglia (SCG) of Hannover Sprague-Dawley rats (HnSD) versus (mRen2)27 rats. Key Words: angiotensin II Ⅲ rats, transgenic Ⅲ autonomic nervous system Ⅲ hypertension Ⅲ arterial Ⅲ receptors I n the mammalian autonomic ganglia, post-tetanic potentiation (PTP) and long-term potentiation (LTP) of synaptic transmission are examples of activity-dependent forms of synaptic plasticity. A few seconds of repetitive presynaptic stimulation producing profound changes in the efficacy of chemical synaptic transmission that can last for seconds or minutes is designated PTP, whereas increased synaptic strength persisting for hours or days is termed LTP. Activitydependent LTP is dependent on activation of serotonin 5-HT 3 receptors in rat superior cervical ganglia (SCG) 1 and is independent of activation of either cholinergic or adrenergic receptors 2,3 in rats. In addition to activity-dependent mechanisms, enduring changes in the synaptic strength also occur through activity-independent mechanisms. For example, specific antigen challenges of isolated sympathetic ganglia activates resident mast cells to release substances that initiate long-lasting increases in synaptic efficacy. 4 Also, application of exogenous catecholamines induces LTP of cholinergic 5 or peptidergic synaptic transmission in sympathetic ganglia. 6 Although the role of ganglionic LTP in the physiology of autonomic ganglia is not understood, recent reports show a positive relationship between ganglionic LTP and blood pressure in ouabain-dependent hypertension that favors the possibility that ganglionic LTP contributes to increased sympathetic nerve activity (SNA) in hypertension or vice versa. 7 Captopril reversed both hypertension and ganglionic abnormalities, suggesting a role for angiotensin (Ang) II in an ouabain-dependent model of hypertension. Other studies show alterations in ganglionic function in spontaneously hypertensive rats (SHRs). 8,9 For example, postsynaptic spike frequency adaptation is curtailed in SHRs. 9 Presynaptically, there is enhanced release of acetylcholine. 10 Collectively, these changes in ganglionic function may contribute to increased SNA in the development and maintenance of hypertension observed in human and experimental hypertension. 11,[12][13][14][15][16][17][18][19] However, less well understood is how enhanced SNA contributes to elevated blood pressure or alters ganglionic synaptic plasticity. In the ouabain-dependent rat, SHRs, and renin-transgenic rat, Ang II acting centrally to increase sympathetic nervous system (SNS) outflow appears to be a common feature; but increased peripheral levels of Ang II, or local increases in the peptide, cannot be excluded. In fact,

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“…A strong indication of the expression of gLTP in sympathetic ganglia of SHR is the reported modification of ganglionic transmission (75,78). Increased ACh release (75) and a shortening of spike frequency adaptation in SHR ganglia (78) indicate both preand post-synaptic changes.…”

Section: Stress-induced Component Of Hypertension In Spontaneously Hymentioning

confidence: 99%

“…Exaggerated sympathetic nerve activity contributes to the development and maintenance of hypertension in humans (68)(69)(70)(71), SHR, and borderline hypertensive rats (51,(72)(73)(74)(75)(76)(77). The contribution of psychosocial stress to the elevated blood pressure in the SHR is suggested by the finding that socially isolated SHRs exhibit lower mean arterial blood pressure than those kept in groups (66).…”

Section: Stress-induced Component Of Hypertension In Spontaneously Hymentioning

confidence: 99%

Role of Long-Term Potentiation of Sympathetic Ganglia (gLTP) in Hypertension

Alkadhi

Alzoubi

2007

Clinical and Experimental Hypertension

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Ganglionic long-term potentiation (gLTP) is an activity-dependent sustained increase in the synaptic efficacy of the nicotinic pathway that has been demonstrated in autonomic ganglia. Sustained enhancement in ganglionic transmission as in chronic mental stress may affect the activity of autonomic functions, including blood pressure and heart rate. An increase in sympathetic activity associated with psychosocial stress and stress-prone conditions such as obesity and aging could result in in vivo expression of gLTP leading to hypertension of a neural origin. Recent reports indicated that the prevention of the expression of gLTP in animal models of hypertension prevented or reduced high blood pressure. Although stress-induced hypertension normalizes within a few days of stress relief, prolonged mild-moderate hypertension may contribute to atherosclerotic cardiovascular diseases. The relation between hypertension and enhanced ganglionic transmission as a result of in vivo expression of gLTP is discussed in this review.

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Neurotransmission through sympathetic ganglia of spontaneously hypertensive rats.

Cited by 25 publications

References 32 publications

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

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

Alterations in Sympathetic Ganglionic Transmission in Response to Angiotensin II in (mRen2)27 Transgenic Rats

Role of Long-Term Potentiation of Sympathetic Ganglia (gLTP) in Hypertension

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