Growth cones of cultured sympathetic neurons contain adrenergic vesicles.

Landis, Story C.

doi:10.1083/jcb.78.1.r8

Cited by 43 publications

(12 citation statements)

References 22 publications

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“…However, despite using a wide range of concentrations, dobutamine had no effect on neurite outgrowth. Since sympathetic neurons display features that suggest that they continue to synthesize NE in vitro (Landis, 1978), we postulated that cultured neurons may be releasing NE in quantities sufficient to maximally activate β1ARs, such that additional ligand is ineffective. To test this hypothesis, we used the tyrosine hydroxylase inhibitor AMPT to prevent catecholamine biosynthesis.…”

Section: Discussionmentioning

confidence: 99%

β-Adrenoceptor Blockers Increase Cardiac Sympathetic Innervation by Inhibiting Autoreceptor Suppression of Axon Growth

Clarke¹,

Bhattacherjee²,

Tague³

et al. 2010

J. Neurosci.

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␤-Adrenoceptor antagonists are used widely to reduce cardiovascular sympathetic tone, but withdrawal is accompanied by sympathetic hyperactivity. Receptor supersensitivity accounts for some but not all aspects of this withdrawal syndrome. Therefore, we investigated effects of ␤-blockers on sympathetic innervation. Rats received infusions of adrenergic receptor blockers or saline for 1 week. The nonselective ␤-blocker propranolol and the ␤ 1 -antagonist metoprolol both increased myocardial sympathetic axon density. At 2 d after propranolol discontinuation, ␤-receptor sensitivity and responsiveness to isoproterenol were similar to controls. However, tyramineinduced mobilization of norepinephrine stores produced elevated ventricular contractility consistent with enhanced sympathetic neuroeffector properties. In addition, rats undergoing discontinuation showed exaggerated increases in mean arterial pressure in response to air puff or noise startle. In sympathetic neuronal cell cultures, both propranolol and metoprolol increased axon outgrowth but the ␤ 2 -blocker ICI 118551 did not. Norepinephrine synthesis suppression by ␣-methyl-p-tyrosine also increased sprouting and concurrent dobutamine administration reduced it, confirming that locally synthesized norepinephrine inhibits outgrowth via ␤ 1 -adrenoceptors. Immunohistochemistry revealed ␤ 1 -adrenoceptor protein on sympathetic axon terminations. In rats with coronary artery ligation, propranolol reversed heart failure-induced ventricular myocardial sympathetic axon depletion, but did not affect infarct-associated sympathetic hyperinnervation. We conclude that sympathetic neurons possess ␤ 1 -autoreceptors that negatively regulate axon outgrowth. Chronic ␤-adrenoceptor blockade disrupts this feedback system, leading to ventricular sympathetic axon proliferation and increased neuroeffector gain, which are likely to contribute to ␤-blocker withdrawal syndrome.

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Section: Discussionmentioning

confidence: 99%

β-Adrenoceptor Blockers Increase Cardiac Sympathetic Innervation by Inhibiting Autoreceptor Suppression of Axon Growth

Clarke¹,

Bhattacherjee²,

Tague³

et al. 2010

J. Neurosci.

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“…The increase in the number of these growth cones could underlie an increase in the arborization of sympathetic fibers. Alternatively, since morphologically similar structures have been described as growth cones in the initial stages of becoming synapses (Landis, 1978;Burry, 1991;Okada et al, 1994), the increase in SV2-containing growth cones could reflect an increase synaptic contacts as myocytes mature.…”

Section: Changes In Synaptic Vesicle Protein Expression At Growth Conmentioning

confidence: 99%

Nerve growth factor collaborates with myocyte-derived factors to promote development of presynaptic sites in cultured sympathetic neurons

et al. 2000

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Nerve growth factor (NGF) acutely modulates synaptic transmission between sympathetic neurons and their cardiac myocyte targets. NGF also has developmental effects in establishing the level of synaptic transmission between sympathetic neurons and myocytes in culture, although little is known about the mechanisms by which NGF influences this synaptic connectivity. Here we report that NGF acts in conjunction with factors produced by cardiac myocytes to promote neuronal contact with the target and the extension of synaptic vesicle-containing growth cones. In conjunction with previously published results showing that NGF has long-term effects on synaptic transmission between sympathetic neurons and myocytes, this work suggests that NGF acts to promote sympathetic neurotransmission by increasing the number of sympathetic fibers establishing target contact. Further, we found that developmental changes in cardiac myocytes led to an increase in the density of synaptic vesicle-containing variocosities along sympathetic fibers, a process regulated by NGF. Thus, as myocytes mature they produce factors that promote the formation of sympathetic presynaptic structures. These results argue that multiple target interactions regulate the extent of synapse formation between sympathetic neurons and cardiac cells and suggest that NGF promotes presynaptic development by increasing neuronal contact with myocyte-derived cell surface or matrix-associated factors.

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“…Alternatively since the s.d.p.s were recorded during periods of fibre ingrowth and branching, it might be that the transmitter responsible for the occurrence of s.d.p.s is released from growth cones rather than from true synaptic structures. There is evidence that sympathetic growth cones contain noradrenaline (Landis, 1978); it has also been reported that cholinergic growth cones are able to support neuromuscular tranmission in Xenopus embryos (Kullberg, Lentz & Cohen, 1977). The lack of sensitivity of s.d.p.s to changes in the external concentrations of divalent cations may reflect differences between the release processes of growth cones and mature synapses.…”

Section: Changes In the Pattern Of Adrenergic Nerves During Developmentmentioning

confidence: 99%

Development of sympathetic innervation to proximal and distal arteries of the rat mesentery.

Hill¹,

Hirst²,

Helden³

1983

The Journal of Physiology

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SUMMARY1. The changes which occur during the post-natal development of sympathetic innervation to proximal and distal arteries of the rat mesentery have been examined using intracellular recording and histochemical techniques.2. In the youngest animals examined, single perivascular stimuli initiated slow depolarizing potentials which were not calcium-dependent.3. After day 4, single stimuli failed to initiate membrane potential changes in a proportion of preparations. This stage coincided with the period of extensive ramification of sympathetic nerve fibres over the surface of the arterioles.4. From day 9 onwards, membrane potential changes were again initiated by single stimuli in the distal arteries. These responses were distinct from those recorded from the younger animals and in many ways resembled excitatory junction potentials recorded from the arteries of mature animals.5. There was a gradient in the development of the innervation to the arteries of the rat mesentery, with that to the distal vessels maturing earlier than that to the more proximal vessels.

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Growth cones of cultured sympathetic neurons contain adrenergic vesicles.

Cited by 43 publications

References 22 publications

β-Adrenoceptor Blockers Increase Cardiac Sympathetic Innervation by Inhibiting Autoreceptor Suppression of Axon Growth

β-Adrenoceptor Blockers Increase Cardiac Sympathetic Innervation by Inhibiting Autoreceptor Suppression of Axon Growth

Nerve growth factor collaborates with myocyte-derived factors to promote development of presynaptic sites in cultured sympathetic neurons

Development of sympathetic innervation to proximal and distal arteries of the rat mesentery.

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