Differential effects of electrical stimulation on release of 3H-noradrenaline and 14C-α-aminoisobutyrate from brain slices

Orrego, Fernando; Jankelevich, J; Ceruti, Leonor; Ferrera, E

doi:10.1038/251055a0

Cited by 44 publications

(7 citation statements)

References 18 publications

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“…Release of noradrenaline from rat brain cortical slices by electric stimuli represents a well-established model for the investigation of release modulating mechanisms [Starke, 1979), the Ca2+ dependency has been charac terized as main evidence for specific trans mitter release [Orrego et al, 1974). Our re sults confirm the need of Ca2* for the electri cally evoked release of noradrenaline and show the relation between the extracellular Ca2+-concentration and the amount of re leased transmitter.…”

Section: Discussionsupporting

confidence: 75%

Voltage-Sensitive Ca<sup>2+</sup> Channels in Rat Brain Neocortical Noradrenergic Nerve Terminals

Reimann¹,

Köllhofer²

1988

Pharmacology

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In rat cerebral cortex slices we investigated the Ca²⁺ dependency of noradrenaline release and the influence of inorganic and organic Ca²⁺ antagonists. Slices were prein-cubated with ³H-noradrenaline and then superfused with noradrenaline-free medium. Release of ³H-noradrenaline was elicited by electrical pulses. The stimulation-evoked release was dependent on the external Ca²⁺ concentration and was inhibited by Co²⁺, Co²⁺ and Mg²⁺ in a concentration-related manner. These results indicate that electrically stimulated noradrenaline release depends on the Ca²⁺ influx after opening of voltage-sensitive Ca²⁺ channels. Organic Ca²⁺ antagonists were used in concentrations which had no major influence on the basal release rate. Of the drugs tested (bepridil, diltiazem, flunarizine, nimodipine, isradipine, prenylamine, verapamil) only flunarizine and nimodipine showed a minor inhibition of the stimulation-evoked release, which was less than 20% at 1 μmol/l. With nimodipine 10 μmol/l, there was a 6 % facilitation of release. All other drugs except flunarizine and verapamil caused a slight facilitation of the stimulation-evoked release. The results provide evidence that the organic Ca²⁺ channel antagonists investigated do not or only minimally interfere with the noradrenergic nerve terminal Ca²⁺ channels in a tissue slice preparation. The release-facilitating effects of most organic Ca²⁺ antagonists cannot be interpreted by the present results.

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Section: Discussionsupporting

confidence: 75%

Voltage-Sensitive Ca<sup>2+</sup> Channels in Rat Brain Neocortical Noradrenergic Nerve Terminals

Reimann¹,

Köllhofer²

1988

Pharmacology

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“…DOPA and the transmitter DA were both released by biphasic stimulation at 2 Hz. Biphasic pulses were used to avoid leakage of DOPA due to nonspecific tissue damage (Orrego et al, 1974;Orrego, 1979). The fractional impulse-evoked release of DOPA was 20 times higher than that of DA.…”

Section: Discussionmentioning

confidence: 99%

Transmitter‐Like Release of Endogenous 3,4‐Dihydroxyphenylalanine from Rat Striatal Slices

Goshima

Kubo

Misu

1988

Journal of Neurochemistry

105

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Biphasic electrical field stimulation (0.5-5 Hz, 2 ms, 25 V, 3 min) and high K+ (10-30 mM, 5 min) released endogenous 3,4-dihydroxyphenylalanine (DOPA) from superfused rat striatal slices. Characteristics of the DOPA release were compared with those of 3,4-dihydroxyphenylethylamine (dopamine, DA). Electrical stimulation at 2 Hz evoked DOPA and DA over similar time courses. alpha-Methyl-p-tyrosine (0.2 mM) markedly reduced release of DOPA but not of DA. Maximal release (0.3 pmol) of DOPA was obtained at 2 Hz and at 15 mM K+. The impulse-evoked release of DOPA and DA was completely tetrodotoxin (0.3 microM) sensitive and Ca2+ dependent and the 15 mM K+-evoked release was also Ca2+ dependent. On L-[3,5-3H]tyrosine (1 microM) superfusion, high K+ (15 and 60 mM) released DOPA and DA together with concentration-dependent decreases in tyrosine 3-monooxygenase (EC 1.14.16.2) activity as indicated by [3H]H2O formation, followed by concentration-dependent increases after DOPA and DA release ended. These findings suggest that striatal DOPA is released by a Ca2+-dependent excitation-secretion coupling process similar to that involved in transmitter release.

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“…In some areas of the cerebral cortex, [3H]NE may be also taken up into dopaminergic nerve endings, but low concentrations (under 1 [IM) of [3H]NE used for labeling ensure a high degree of specific incorporation into adrenergic nerve endings (16,17). Electrical stimula tion does not release substances located in glial elements (18).…”

Section: Discussionmentioning

confidence: 99%

Mechanism of Pindolol-Induced Vasoconstriction in Isolated and Perfused Dog Coronary Arteries

Takata

Shimada

Kato

1993

Japanese Journal of Pharmacology

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ABSTRACT-By using rat brain cortical slices preloaded with [3H]norepinephrine, we examined whether ATP-sensitive K+ channels are involved in altered adrenergic neurotransmission during hypoxia. The tritium overflow evoked by transmural nerve stimulation (TNS) was significantly inhibited at 5 min of hypoxia and reached the maximum inhibition at 20 min. The inhibition of the TNS-evoked tritium overflow under a 20-min hypoxia was reversed by subsequent reoxygenation and was concentration-dependently antagonized by glibenclamide (0.1 and 1 pM). 86Rb+ efflux was increased after introduction of hypoxia and reached the peak value at about 20 min, which was concentration-dependently antagonized by glibenclamide (0.1-10 uM). Hypoxia decreased cortical ATP content. Linear correlations were mutually observed among the changes by hypoxia in the TNS-evoked tritium overflow, tissue ATP content and 86Rb+ efflux. The spontaneous tritium outflow was inhibited only after hypoxic periods of more than 16 min, the inhibition being reversed by reoxygenation and antagonized by 1 uM glibenclamide. These results suggest that the inhibition of rat central adrenergic neurotransmission during hypoxia may be associated with an activation of ATP-sensitive K+ channels. Keywords:Hypoxia, ATP-sensitive K+ channel, Central adrenergic neurotransmission, 86Rb+ efflux, ATP content Neuronal transmission in the brain is highly sensitive to the lack of oxygen (1). However, the effects of anoxia/ hypoxia or ischemia on adrenergic neurotransmission in the brain seem to be discrepant; the activity of nor adrenergic neurons is decreased in the rat cerebral cortex and hippocampus during in vivo hypoxia (2). In contrast, K+-evoked norepinephrine (NE) release is elevated in the cortical slices of Mongolian gerbils subjected to cerebral ischemia (3). On the other hand, depolarization-induced catecholamine release from the rat brain synaptosomes is unaffected by in vitro hypoxia (4).It is well accepted that oxygen deficiency or deprivation decreases the amount of high-energy phosphates (adeno sine 5'-triphosphate (ATP) and creatine phosphate) in the brain. A decreased ATP content is expected to open ATP-sensitive K+ (KATP) channels. Recent studies dem onstrated that KATP channels are present in the central nervous system (5) and modulate transmitter release in rat hippocampal CA3 neurons under anoxic conditions (6). On the other hand, antidiabetic sulfonylurea tol butamide, a KATP channel blocker, did not alter the anox ic response of rat hippocampal CAI neurons (7). Thus, it is likely that there are regional differences in the involve ment of KATP channels in the anoxic response. In addi tion, the localization of binding sites for sulfonylurea ([3H]glibenclamide) is heterogeneous in the rat brain and the motor neocortex is one of the five regions containing the highest concentrations of the sulfonylurea binding sites (8). We recently reported that KATP channels modu late electrically stimulated NE release from the rat motor neocortex slices under normoxic con...

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Differential effects of electrical stimulation on release of 3H-noradrenaline and 14C-α-aminoisobutyrate from brain slices

Cited by 44 publications

References 18 publications

Voltage-Sensitive Ca<sup>2+</sup> Channels in Rat Brain Neocortical Noradrenergic Nerve Terminals

Voltage-Sensitive Ca<sup>2+</sup> Channels in Rat Brain Neocortical Noradrenergic Nerve Terminals

Transmitter‐Like Release of Endogenous 3,4‐Dihydroxyphenylalanine from Rat Striatal Slices

Mechanism of Pindolol-Induced Vasoconstriction in Isolated and Perfused Dog Coronary Arteries

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