Basic Mechanisms of Prostaglandin Action on Autonomic Neurotransmission

Hedqvist, Per

doi:10.1146/annurev.pa.17.040177.001355

Cited by 328 publications

(104 citation statements)

References 36 publications

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“…However, the response to FMRFamide is most likely due to direct actions on the LFS neurons since FMRFamide exerts modulatory effects on LFS neurons in both high divalent saline and in TTX, conditions in which input from interneurons would be greatly reduced. Nevertheless, because FMRFamide causes an increase in production of arachidonic acid in the sensory neurons (Piomelli et al, 1987), and because arachidonic acid is known to act as an intercellular messenger in other systems (Hedqvist, 1977), it is possible that the effects of presynaptic release of arachidonic acid might contribute to the modulation of LFS neurons that we have described.…”

Section: Discussionmentioning

confidence: 91%

FMRFamide produces biphasic modulation of the LFS motor neurons in the neural circuit of the siphon withdrawal reflex of Aplysia by activating Na+ and K+ currents

Belkin

Abrams

1993

J. Neurosci.

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The molluscan neuropeptide FMRFamide has an inhibitory effect on transmitter release from the presynaptic sensory neurons in the neural circuit for the siphon withdrawal reflex. We have explored whether FMRFamide also acts postsynaptically in motor neurons in this circuit, focusing on the LFS motor neurons. FMRFamide typically produces a biphasic response in LFS neurons: a fast excitatory response followed by a prolonged inhibitory response. We have analyzed these postsynaptic actions and compared them with the mechanism of FMRFamide's inhibition of the presynaptic sensory neurons. The transient excitatory effect of FMRFamide, which desensitizes rapidly, is due to activation of a TTX- insensitive, Na(+)-dependent inward current. The late hyperpolarizing phase of the FMRFamide response results from activation of at least two K+ currents. One component of the hyperpolarizing response is active at rest and at more hyperpolarized membrane potentials, and is blocked by 5 mM 4-aminopyridine, suggesting that it differs from the previously described FMRFamide-modulated K+ currents in the presynaptic sensory neurons. In addition, FMRFamide increases a 4-aminopyridine-insensitive K+ current. Presynaptically, FMRFamide increases K+ conductance, acting via release of arachidonic acid. In the LFS motor neurons, application of arachidonic acid mimicked the prolonged, hyperpolarizing phase of the FMRFamide response; 4-bromophenacyl bromide, an inhibitor of phospholipase A2, selectively blocked this component of the FMRFamide response. Thus, FMRFamide may act in parallel pre- and post- synaptically to inhibit the output of the siphon withdrawal reflex circuit, producing this inhibitory effect via the same second messenger in the sensory neurons and motor neurons, though a number of the K+ currents modulated in these two types of neurons are different.

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Section: Discussionmentioning

confidence: 91%

FMRFamide produces biphasic modulation of the LFS motor neurons in the neural circuit of the siphon withdrawal reflex of Aplysia by activating Na+ and K+ currents

Belkin

Abrams

1993

J. Neurosci.

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“…Therefore, PGs may be used for modulating or fundamentally maintaining neural activity, rather than as synaptic transmitters. In AVP secretion and other phenomena, PGs are known to interact with AVP-releasing factors such as catecholamines (39,40) and ANG II (7,8). Consequently, it could be speculated that PGs might exert their effects by modulating the activities of catecholaminergic and angiotensinergic neurons in the AV3V.…”

Section: Figure 4 Effects Of Meclofenamate (Mcl) Infusion Into the Acmentioning

confidence: 99%

Possible participation of prostaglandins generated in the anteroventral third ventricular region in the hypovolemia-induced vasopressin secretion of conscious rats

Yamaguchi

Hama²,

Watanabe

1998

European Journal of Endocrinology

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Objective: The aim of this study was to investigate the roles of prostaglandins (PGs) in the anteroventral third ventricular region (AV3V), a cerebral site for cardiovascular homeostasis, in hypovolemiainduced vasopressin (AVP) secretion. Methods: We infused meclofenamate (78.3 nmol in 1 ml), a PG synthesis inhibitor, or PGE 2 (7.1 nmol in 0.5 ml) into the AV3V of conscious rats, examining their effects on plasma AVP and other variables in the presence or absence of hemorrhages. The hemorrhages (about 14% of blood volume) were conducted successively by taking femoral arterial blood over a 30-s period at 10-min intervals.Results: The first hemorrhage increased plasma AVP in blood samples obtained 10 min later, without affecting plasma angiotensin II (ANG II), arterial pressure and heart rate. The second hemorrhage after 10 min raised plasma AVP further and, remarkably, augmented plasma ANG II, and reduced arterial pressure. The AVP responses to both the first and second hemorrhages were attenuated by meclofenamate infusion into the AV3V performed 35 min before the first hemorrhage. The meclofenamate infusion did not alter the response of ANG II, while that of arterial pressure was potentiated and heart rate was decreased after the second hemorrhage. These effects of meclofenamate on plasma AVP and the cardiovascular parameters were not found when the drug was infused into the nucleus accumbens, the region slightly distant from the AV3V, or the lateral cerebral ventricle. In the normovolemic state, meclofenamate administered into the three brain regions did not affect any of the variables monitored. In contrast, application of PGE 2 into the AV3V enhanced plasma AVP, heart rate and arterial pressure after 5 and 15 min. Histological examination indicated that infusion sites of meclofenamate in the AV3V were close to those of PGE 2 in several cases and included areas such as the organum vasculosum of the lamina terminalis, periventricular hypothalamic nucleus, and the median and medial preoptic nuclei. Conclusion: These results suggest that PGs synthesized in and/or near the AV3V may be involved in the regulation of AVP release and cardiovascular function in the hypovolemic state.

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“…Sympathetic nerve stimulation is also known to increase the production of prostaglandins, which are released together with noradrenaline (Hedqvist, 1977). We therefore examined the effect of blocking prostaglandin formation on hepatic phosphorylase activation in response to splanchnic nerve stimulation.…”

Section: Resultsmentioning

confidence: 99%

Further studies on the mechanism of phosphorylase activation in rabbit liver in response to splanchnic nerve stimulation

Shimazu

Usami

1982

The Journal of Physiology

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SUMMARY1. The mechanism of activation of liver phosphorylase after splanchnic nerve stimulation has been investigated in rabbits and compared with the effects of intraportal injections of noradrenaline.2. The increase in the activity of liver phosphorylase-a, the active form of this key glycogenolytic enzyme, in response to injections of noradrenaline was blocked by ,f-adrenergic antagonists, but not by a-adrenergic antagonists, suggesting that the effect of noradrenaline is mediated mainly through f-adrenoceptors in vivo. In contrast, the increase in phosphorylase activity in response to stimulation of the peripheral end of the splanchnic nerve was resistant to both a-and f-adrenoceptor blockade.3. When diltiazem and verapamil, selective Ca2+ antagonists that restrict calcium influx across the cell membrane, were infused intraportally, the phosphorylase response to splanchnic nerve stimulation was virtually abolished, while the response to noradrenaline was unaltered.4. Infusion of the prostaglandin-synthesis inhibitor indomethacin at a dose of 3-4 ,sg/min was found to block the activation of liver phosphorylase in response to stimulation of the splanchnic innervation. 5. These results suggest that the mechanism whereby stimulation ofthe sympathetic innervation to the liver leads to activation of phosphorylase is not mediated by either a-or 8f-adrenoceptors, but appears to depend upon prostaglandin formation and influx of Ca2+ ions into the hepatocytes.

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Basic Mechanisms of Prostaglandin Action on Autonomic Neurotransmission

Cited by 328 publications

References 36 publications

FMRFamide produces biphasic modulation of the LFS motor neurons in the neural circuit of the siphon withdrawal reflex of Aplysia by activating Na+ and K+ currents

FMRFamide produces biphasic modulation of the LFS motor neurons in the neural circuit of the siphon withdrawal reflex of Aplysia by activating Na+ and K+ currents

Possible participation of prostaglandins generated in the anteroventral third ventricular region in the hypovolemia-induced vasopressin secretion of conscious rats

Further studies on the mechanism of phosphorylase activation in rabbit liver in response to splanchnic nerve stimulation

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