Depolarization of rat isolated superior cervical ganglia mediated by β<sub>2</sub>‐adrenoceptors

Brown, David A.; Dunn, Philip M.

doi:10.1111/j.1476-5381.1983.tb11016.x

Cited by 45 publications

(36 citation statements)

References 29 publications

(36 reference statements)

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“…Thus about a 10fold higher concentration was required to elevate cyclic AMP than that which depolarized the ganglion (interrupted line in Figure 2; cf. Figure 4 in Brown & Dunn, 1983 (Brown & Dunn, 1983) did not significantly elevate cyclic AMP levels at concentrations up to 100IM (Figure 2). In a further test of salbutamol and isoprenaline, the effects of a single concentration of each agonist (1 Mm and 30 nM respectively) which had previously been found to produce an equivalent submaximal depolarization of the ganglion were compared.…”

Section: I) the Macmillan Press Ltd 1983mentioning

confidence: 84%

“…Methods Freshly-dissected superior cervical ganglia were obtained from rats anaesthetized with urethane and prepared for extracellular recording of ganglionic d.c. potentials and transmitted action potentials as described in the preceding paper (Brown & Dunn, 1983). For cyclic AMP measurements, which required larger numbers of ganglia, the ganglia were obtained rapidly from rats killed by decapitation, then cleaned of connective tissue and maintained in Krebs solution at 22°C under the same conditions as for electrical recording.…”

Section: I) the Macmillan Press Ltd 1983mentioning

confidence: 99%

“…The significance of this is unclear, since the principal effect of catecholamines previously detected in this tissue, postsynaptic hyperpolarization, depression of transmission and inhibition of Ca2+-currents, were clearly mediated by a-receptors (Suzuki & Volle, 1978;Quenzer etal., 1979;Horn & McAfee, 1979 Turner, 1980;Adams & Galvan, 1981). However, we (Dunn, 1982;Brown & Dunn, 1983) have recently detected additional ,8-mediated 'excitatory' effects of catecholamines on rat superior cervical ganglion in vitro, comprising pre-and postsynaptic depolarization and, under conditions of reduced transmitter release, facilitation of submaximal transmission. The present experiments were undertaken to see if these effects could reasonably be attributed to the increased levels of cyclic AMP.…”

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confidence: 99%

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Cyclic adenosine 3′,5′‐monophosphate and β‐effects in rat isolated superior cervical ganglia

Brown

Dunn

1983

British J Pharmacology

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Brunswick Square, London WC 1 N 1 AX 1 Isoprenaline (0.01-1 IM) increased the amount of cyclic adrenosine 3',5'-monophosphate (cyclic AMP) in rat isolated superior cervical ganglia by up to 10 times after 10 min application. Cyclic AMP levels returned to control values after 20 min washing. 2 Salbutamol, in concentrations (1-100 iM) that depolarized the ganglion and facilitated submaximal transmission, did not significantly raise ganglionic cyclic AMP levels. 3The action of isoprenaline was antagonized by butoxamine (apparent KI-0. 14 MtM) and weakly by practolol (apparent KI 9.1 jIM). 4 The effect of 0.1 plM isoprenaline was also inhibited 94% by 100 jIM of the adenylate cyclase inhibitor, 9-(tetrahydro-2-furyl)adenine (SQ 22,536

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Section: I) the Macmillan Press Ltd 1983mentioning

confidence: 84%

Section: I) the Macmillan Press Ltd 1983mentioning

confidence: 99%

mentioning

confidence: 99%

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Cyclic adenosine 3′,5′‐monophosphate and β‐effects in rat isolated superior cervical ganglia

Brown

Dunn

1983

British J Pharmacology

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“…Similarly, the high affinity of haloperidol at D2 binding sites excludes their involvement. (-)-Noradrenaline and dopamine hyperpolarize the rat SCG via E2-adrenoceptors (Brown & Caulfield, 1979; see also Brown & Dunn, 1983). However, it is unlikely that 5-HT-induced hyperpolarization of this tissue was mediated either directly or indirectly via these sites, since it was unaffected by phentolamine.…”

Section: Discussionmentioning

confidence: 95%

Pharmacological characterization of 5‐hydroxytryptamine‐induced hyperpolarization of the rat superior cervical ganglion

Ireland

Jordan

1987

British J Pharmacology

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A study has been made of the pharmacology of 5‐hydroxytryptamine (5‐HT)‐induced hyperpolarization responses recorded extracellularly from the rat isolated superior cervical ganglion (SCG). Hyperpolarization responses induced by 5‐HT (1 × 10−8‐1 × 10−4 m) in the presence of MDL 72222 (1 × 10−5 m) were not antagonized by phentolamine (1 × 10−6 m), prazosin (1 × 10−7‐3 × 10−7 m), haloperidol (1 × 10−6 m) or ketanserin (1 × 10−7‐1 × 10−6 m). However, the latter two compounds both potentiated and increased the persistence of the hyperpolarization induced by moderate to high concentrations of 5‐HT. Spiperone (1 × 10−7 m) caused similar effects. All further experiments were performed in the presence of ketanserin (1 × 10−6 m) as well as MDL 72222. 8‐Hydroxy‐2(di‐n‐propylamino)‐tetralin (8‐OH‐DPAT; 1 × 10−7‐1 × 10−4 m) and ipsapirone (3 × 10−5‐3 × 10−4 m) behaved as weak hyperpolarizing agonists on the SCG. However, at concentrations below those required to produce hyperpolarization, both compounds acted as unsurmountable antagonists of 5‐HT‐induced hyperpolarization. 5‐Carboxamidotryptamine (5‐CT; 1 × 10−9‐1 × 10−5 m) mimicked the hyperpolarizing activity of 5‐HT on the SCG. The EC50 for 5‐CT was approximately 9 fold lower than that for 5‐HT. Spiperone (1 × 10−7‐1 × 10−5 m) behaved as a reversible competitive antagonist of hyperpolarization responses induced by 5‐HT with a pKB value of 7.40 ± 0.09. Spiperone (1 × 10−7‐1 × 10−6 m) also caused concentration‐dependent rightward displacement of the 5‐CT concentration‐hyperpolarization response curve. In this case, the pKB was 7.80 ± 0.05. (±)‐Cyanopindolol (3 × 10−7‐3 × 10−6 m) caused non‐parallel rightward displacements of the 5‐HT concentration‐response curve. Against 5‐CT, (±)‐cyanopindolol (3 × 10−7‐3 × 10−6 m) caused a concentration‐independent rightward displacement of the concentration‐response curve, accompanied by a large increase in the maximum response. 5‐CT‐induced hyperpolarization recorded in the presence of (±)‐cyanopindolol (3 × 10−7 m) was not significantly antagonized by methiothepin (1 × 10−6 m) or methysergide (1 × 10−6 m). It is concluded that 5‐HT‐induced hyperpolarization of the rat SCG is mediated via a 5‐HT1‐like receptor which resembles the 5‐HT1A binding site. However, a lack of selective drugs precludes more definitive characterization of this receptor.

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“…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.…”

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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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Depolarization of rat isolated superior cervical ganglia mediated by β₂‐adrenoceptors

Cited by 45 publications

References 29 publications

Cyclic adenosine 3′,5′‐monophosphate and β‐effects in rat isolated superior cervical ganglia

Cyclic adenosine 3′,5′‐monophosphate and β‐effects in rat isolated superior cervical ganglia

Pharmacological characterization of 5‐hydroxytryptamine‐induced hyperpolarization of the rat superior cervical ganglion

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

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Depolarization of rat isolated superior cervical ganglia mediated by β2‐adrenoceptors

Cited by 45 publications

References 29 publications

Cyclic adenosine 3′,5′‐monophosphate and β‐effects in rat isolated superior cervical ganglia

Cyclic adenosine 3′,5′‐monophosphate and β‐effects in rat isolated superior cervical ganglia

Pharmacological characterization of 5‐hydroxytryptamine‐induced hyperpolarization of the rat superior cervical ganglion

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

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Depolarization of rat isolated superior cervical ganglia mediated by β₂‐adrenoceptors