Transmission in superior cervical ganglion of the dog after cholinergic suppression

Ss, Chen

doi:10.1152/ajplegacy.1971.221.1.209

Cited by 18 publications

(9 citation statements)

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“…Similar effects have been observed following preganglionic sympathetic nerve stimulation of the nictitating membrane of the cat (Alkadhi & Mclsaac, 1973) and dog (Chen, 1969(Chen, , 1971.…”

Section: Discussionsupporting

confidence: 74%

THE EFFECTS OF ANTICHOLINESTERASES ON SYNAPTIC TRANSMISSION THROUGH NICOTINIC AND MUSCARINIC RECEPTORS IN RAT SYMPATHETIC GANGLIA in vivo

Drew¹,

Leach

1974

British J Pharmacology

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1Stimulation of the entire spinal sympathetic outflow at supramaximal voltage and 25-100 Hz, in the chlorisondamine-treated, pithed, adrenalectomized rat produced a delayed pressor response (late pressor response; LPR). 2 The LPR was abolished by phenoxybenzamine, bretylium or a small dose of atropine (25-50 Mg/kg), suggesting the involvement of ganglionic muscarinic receptors. 3 In the presence of atropine at a dose level ( 15 Mg/kg) which did not influence the LPR, the anticholinesterases physostigmine, neostigmine and Ro 02-0683 but not BW 284C5 1 markedly enhanced and prolonged the LPR, whereas all of them reduced the pressor responses to AHR-602. 4 After blockade of the ganglionic muscarinic receptors with a large dose of atropine (250 Mig/kg) the four anticholinesterases did not influence responses to DMPP or noradrenaline and only slightly enhanced responses to preganglionic nerve stimulation at 6 Hz in the absence of chlorisondamine. 5 It is concluded that inhibition of butyrylcholinesterase accounts for the enhancement and prolongation of the LPR by anticholinesterases.

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“…Similar effects have been observed following preganglionic sympathetic nerve stimulation of the nictitating membrane of the cat (Alkadhi & Mclsaac, 1973) and dog (Chen, 1969(Chen, , 1971.…”

Section: Discussionsupporting

confidence: 74%

THE EFFECTS OF ANTICHOLINESTERASES ON SYNAPTIC TRANSMISSION THROUGH NICOTINIC AND MUSCARINIC RECEPTORS IN RAT SYMPATHETIC GANGLIA in vivo

Drew¹,

Leach

1974

British J Pharmacology

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“…The present results show that the late response of the superior cervical ganglion of dogs can be inhibited by close-arterial injection of catecholamines and CaCl2 to the ganglion and can be potentiated by injection of CdC12. These observations confirm that the late response represents late discharges in ganglion cells (Chen, 1971(Chen, , 1972.…”

Section: Discussionsupporting

confidence: 73%

“…The three catecholamines were also found to produce similar inhibitory effects on ganglionic activity induced by preganglionic stimulation at a low rate (4 Hz or less). As reported previously, the ganglionic response to such stimulation can be largely prevented by hexamethonium and presumably is mediated via the classical nicotinic pathway; the noncholinergic process is scarcely involved (Chen, 1971). Nevertheless, the magnitude of inhibition of such ganglionic activity is comparable to that of the late response (Table 1 A).…”

Section: Inhibition Of the Late Response By Catecholaminesmentioning

confidence: 61%

“…In the sympathetic ganglion of the bullfrog, dog and cat preganglionic stimulation at a high stimulus frequency may elicit a late response, which lasts several minutes. It probably is generated by a non-cholinergic synaptic mechanism because it is not blocked by atropine and nicotinic ganglion-blockers Chen, 1969Chen, , 1971Chen, , 1972Alkadhi & McIssac, 1973), and can neither be mimicked by acetylcholine nor potentiated by anticholinesterase (Koketsu, Nishi & Noda, 1968;Chen, 1969). Furthermore, depletion of acetylcholine stores by hemicholinum-3, which reduces the early response, does not affect the late response and subsequent administration of choline chloride restores the early response but has no effect on the late response (Chen, 1971).…”

Section: Introductionmentioning

confidence: 99%

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Effects of divalent cations and of catecholamines on the late response of the superior cervical ganglion.

Chen¹

1975

The Journal of Physiology

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The characteristics of the late response of the superior cervical ganglion of dogs were studied by close‐arterial injection of catecholamines and divalent cations to the ganglion. 2. Dopamine, noradrenaline and adrenaline inhibit the late response as well as ganglionic activity induced by other means. The effect of dopamine is brief but that of adrenaline is prolonged. 3. Cd2+, Co2+, Ni2+, Zn2+, Hg2+ and Fe2+ markedly potentiate the late response, whereas Mn2+, Ca2+ and Mg2+ inhibit it. 4. may potentiate ganglionic activity triggered by other ganglionic stimulants. The Cd‐augmented activity may be blocked by a ganglion‐blocker which is specific to the stimulant. 5. CdCl2 may exhibit a direct ganglion‐stimulating action on a ganglion which shows prominent late responses and has been conditioned by tetanic preganglionic stimulation. 6. CdCl2 and MnCl2 may inhibit ganglionic transmission by suppressing acetylcholine release from presynaptic nerve terminals. 7. It is concluded that the late response represents the late discharges of ganglion cells, which are very sensitive to inhibition by CaCl2 and MnCl2 and may be potentiated by CdCl2.

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“…Additionally, potentiated transmitter release would activate more muscarinic and noncholinergic receptors on ganglion cells, which would produce enlarged slow synaptic potentials and afterdischarges. 12 " 14 Changes in sympathetic activity could also arise from an alteration in a variety of membrane properties that control firing fre-…”

mentioning

confidence: 99%

Loss of accommodation in sympathetic neurons from spontaneously hypertensive rats.

Yarowsky

Weinreich²

1985

Hypertension

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SUMMARY Synaptic transmission and membrane properties of sympathetic neurons in superior cervical ganglia of spontaneously hypertensive rats (SHR), normotensive Wistar-Kyoto rats (VVKY), and Sprague-Dawley rats (SD) were investigated in vitro by extracellular and intracellular recording. The sympathetic neurons of SHR showed an atypical loss of spike accommodation. The spike discharge was insensitive to the sodium channel blocker tetrodotoxin, but it was reversibly blocked by a variety of calcium antagonists. The loss of accommodation in the neurons of SHR was not due to a loss of M-current, a potassium current involved in controlling spike frequency adaptation in sympathetic neurons. Superfusion of ganglia of SHR with muscarine (10 ^M), which suppresses M-current and leads to a loss of accommodation, potentiated the repetitive discharge. In the presence of muscarine the current-voltage curves in neurons of SHR and SD were shifted to similar extents. Resting membrane potentials of neurons of SHR and WKY were consistently depolarized as compared with neurons of SD. Synaptic efficacy through the ganglia of SHR, assessed by extracellular recordings of presynaptic and postsynaptic compound action potentials at 0.25 Hz stimulation, was elevated when compared with the ganglia of WKY, but was similar to that of the ganglia of SD. These results indicate that strain differences should be considered when attempting to attribute changes in sympathetic neuron membrane properties to hypertension. The sympathetic neurons of SHR appear to have lost their accommodative properties and might possess an exaggerated calcium conductance. This calcium conductance may explain the augmented calcium-dependent release of norepinephrine during sympathetic nerve stimulation in the SHR. (Hypertension 7: 268-276, 1985) KEY WORDS • membrane properties normotensive strains repetitive firing * calcium conductance E XAGGERATED activity in the sympathetic nervous system in the Okamoto-Aoki strain of spontaneously hypertensive rats (SHR) has been implicated in both the development and the maintenance of hypertension in this model. "2 Numerous studies with the SHR have shown that both central and peripheral neurogenic mechanisms are contributory factors, although they may not account for all the elevation in peripheral vascular resistance.2 There is an increased basal sympathetic tone in visceral and nonvisceral sympathetic nerves, and an elevated sympa-

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Transmission in superior cervical ganglion of the dog after cholinergic suppression

Cited by 18 publications

References 0 publications

THE EFFECTS OF ANTICHOLINESTERASES ON SYNAPTIC TRANSMISSION THROUGH NICOTINIC AND MUSCARINIC RECEPTORS IN RAT SYMPATHETIC GANGLIA in vivo

THE EFFECTS OF ANTICHOLINESTERASES ON SYNAPTIC TRANSMISSION THROUGH NICOTINIC AND MUSCARINIC RECEPTORS IN RAT SYMPATHETIC GANGLIA in vivo

Effects of divalent cations and of catecholamines on the late response of the superior cervical ganglion.

Loss of accommodation in sympathetic neurons from spontaneously hypertensive rats.

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