Loss of accommodation in sympathetic neurons from spontaneously hypertensive rats.

Yarowsky, Paul; Weinreich, D

doi:10.1161/01.hyp.7.2.268

Cited by 25 publications

(30 citation statements)

References 27 publications

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“…Calcium-dependent SFA has been reported in peripheral sympathetic neurons [23], NTS neurons [6,17], locus coeruleus neurons [16], hippocampal pyramidal neurons [20] or hippocampal nonpyramidal neurons [4]. In the case of cNTS neurons, the role of Ca 2+ -activated K + channels in the elicitation of SFA was speculated [3,17,19] but not hitherto verified.…”

Section: Discussionmentioning

confidence: 96%

Involvement of Apamin-Sensitive SK Channels in Spike Frequency Adaptation of Neurons in Nucleus tractus solitarii of the Rat

Yen¹,

Chan

1999

J Biomed Sci

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We delineated the role of Ca(2+)-activated K(+) channels in the phenomenon of spike frequency adaptation (SFA) exhibited by neurons in the caudal region of nucleus tractus solitarius (cNTS) using intracellular recording coupled with the current-clamp technique in rat brain slices. Intracellular injection of a constant depolarizing current evoked a train of action potentials whose discharge frequency declined rapidly to a lower steady-state level of irregular discharges. This manifested phenomenon of SFA was found to be related to extracellular Ca(2+). Low Ca(2+) (0.25 mM) or Cd(2+) (0.5 mM) in the perfusing medium resulted in a significant increase in the adaptation time constant (tau(adap)) and an appreciable reduction in the percentage adaptation of spike frequency (F(adap)). In addition, the evoked discharges were converted from an irregular to a regular pattern, accompanied by a profound increase in mean firing rate. Intriguingly, similar alterations in tau(adap), F(adap), discharge pattern and discharge rate were elicited by apamin (1 microM), a selective blocker for small-conductance Ca(2+)-activated K(+) (SK) channels. On the other hand, charybdotoxin (0.1 microM), a selective blocker for large-conductance Ca(2+)-activated K(+) channels, was ineffective. Our results suggest that SK channels of cNTS neurons may subserve the generation of both SFA and irregular discharge patterns displayed by action potentials evoked with a prolonged depolarizing current.

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Section: Discussionmentioning

confidence: 96%

Involvement of Apamin-Sensitive SK Channels in Spike Frequency Adaptation of Neurons in Nucleus tractus solitarii of the Rat

Yen¹,

Chan

1999

J Biomed Sci

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“…SHR with established hypertension have already been shown to have abnormal Ca 2+ conductance. 21 Interestingly, principal ganglionic neurons were found to have higher ami no acid uptake and protein synthesis in young SHR up to at least 30 days of age.…”

Section: Discussionmentioning

confidence: 97%

Responsiveness of noradrenergic neurons in rat experimental hypertension.

Debinski

Küchel

1989

Hypertension

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We investigated possible abnormalities of cholinergic-noradrenergic neurotransmission in superior cervical ganglia in vitro in spontaneously hypertensive, Dahl salt-sensitive and deoxycorticosterone-salt-hypertensive rats by measuring the de novo synthesis of catecholamines from their labeled precursor tritiated tyrosine in response to cholinergic stimulation. Labeled tyrosine was incorporated into dopamine and its main neuronal metabolite dihydroxyphenylacetic acid as well as into norepinephrine. Dihydroxyphenylacetic acid and norepinephrine, but not dopamine, generation was linear with time under basal and stimulated conditions. However, norepinephrine incorporation remained similar before and after cholinergic stimulation of ganglionic neurons. Only young, prehypertensive spontaneously hypertensive rats showed altered responses when compared with their controls. Although endogenous dihydroxyphenylacetic acid content and baseline tyrosine incorporation into dihydroxyphenylacetic acid were lower in 4-week-old spontaneously hypertensive rats than in age-matched Wistar-Kyoto rats, cholinergic stimulation increased labeled dopamine and dihydroxyphenylacetic acid generation significantly more in juvenile spontaneously hypertensive rats. Such a hyperresponsiveness was not observed in either young Dahl rats or in any of the other models when they became hypertensive. These results probably reflect a genuine hyperreactivity of postganglionic noradrenergic neurons to acetyicholine or then* increased catecholamine-synthesizing ability after centrally evoked enhanced sympathetic outflow known to occur during the early development of hypertension in spontaneously hypertensive rats. (Hypertension 1989;13:712-715)

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“…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.…”

mentioning

confidence: 99%

“…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.…”

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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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Loss of accommodation in sympathetic neurons from spontaneously hypertensive rats.

Cited by 25 publications

References 27 publications

Involvement of Apamin-Sensitive SK Channels in Spike Frequency Adaptation of Neurons in Nucleus tractus solitarii of the Rat

Involvement of Apamin-Sensitive SK Channels in Spike Frequency Adaptation of Neurons in Nucleus tractus solitarii of the Rat

Responsiveness of noradrenergic neurons in rat experimental hypertension.

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

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