Enkephalin: A potential modulator of noradrenaline release in rat brain

Taube, H. D.; Borowski, Evelyn; Endo, Takahiko; Starke, Klaus

doi:10.1016/0014-2999(76)90343-5

Cited by 139 publications

(26 citation statements)

References 8 publications

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“…The inhibitory effects of met enkephalin on both muscle contraction and transmitter release were antagonized by nalor phine, hence it is probable that these effects are mediated by opiate receptors. Tabbe et al (17) have recently shown that in rat brain slices, met-enkephalin diminished the overflow of [3H]-NE evoked by electrical stimulation or by high potassium and the effect was an tagonized by naloxone. Our results are essentially similar to these observations .…”

Section: Discussionmentioning

confidence: 98%

Effect of Enkephalin and Substance P on Sympathetic Nerve Transmission in Mouse Vas Deferens

Segawa

Murakami

Ogawa

et al. 1978

Japanese Journal of Pharmacology

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Abstract-Effect of methionine-, leucine-enkephalin (met-,leu-enkephalin) and substance P on the transmission in mouse vas deferens was studied. Both met and leu-enkephalin inhibited electrically induced contraction of vas deferens at 10-8-10-7 M, met-enkephalin being 1.4 times more active than leu-enkephalin.Nalorphine (10-6 M) antagonized these effects. Substance P (10-9-10-7 M) had no effect on the contraction.Metand leu-enkephalin (10-7-10-5 M) decreased the high potassium induced [3H]-nor epinephrine release from vas deferens, while substance P (10-5 M) significantly increased it. Nalorphine (10-5 M) reversed the inhibitory effect of met-enkephalin.These results indicate that these peptides modify the transmission of sympathetic nerve in mouse vas deferens.A variety of evidence now indicates that a certain endogenous polypeptide in the central nervous system is involved in the regulation of sensory nerve transmission. Two peptides, methionine and leucine-enkephalin (met and leu-enkephalin) which have been suggested to be endogenous ligands for opiate receptors (1), are localized in synaptosomal fractions (2) and are thought to modulate the activity of the ascending pain pathway in the spinal cord and the brain. Substance P, undecapeptide isolated from bovine hypothalamus (3), is also localized in synaptosomal fractions (4, 5). Since substance P exerts a potent de polarizing action on the motoneurons and is localized for the greater part in the dorsal area of the dorsal horn, the role of an excitatory transmitter of primary afferent neurons was suggested (6).Interestingly, these endogenous polypeptides modulate a stimulus-induced contraction of mouse vas deferens. Thus, both enkephalins depresse the contraction (1) while substance P enhances it (7, 8). In all probability, the depression and the enhancement in contraction reflect a decrease and an increase of transmitter release from sympathetic nerves in the pre paration, respectively. Henderson et al. (9) and Hughes et al. (10) demonstrated that morphine inhibits the transmitter release from mouse vas deferens. Henderson and North (11) and Henderson (12) indirectly suggested that normorphine and met-enkephalin depress the transmitter release from the vas deferens.In planning the present experiments we attempted to confirm the findings that these peptides modulate the contraction of vas deferens and second, to demonstrate the influence

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Section: Discussionmentioning

confidence: 98%

Effect of Enkephalin and Substance P on Sympathetic Nerve Transmission in Mouse Vas Deferens

Segawa

Murakami

Ogawa

et al. 1978

Japanese Journal of Pharmacology

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“…Furthermore, FARSANG and KUNOS (1979) demonstrated that the specific opiate antagonist, naloxone, prevented hypertension in spontaneously hypertensive rats. TAUBE et al (1976) suggested that an activation of opioid peptides might be involved in a presynaptic inhibition of central noradrenergic transmission.…”

Section: Discussionmentioning

confidence: 99%

Pharmacological evidence that central .ALPHA.2-adrenoceptors are involved in cardiovascular responses to intravenously injected enkephalins in anesthetized dogs.

et al. 1984

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In anesthetized dogs, intravenous injections of 30 µg/kg of leucine-and methionine-enkephalin (L-and M-enk respectively) produced a significant reduction of mean blood pressure (MBP) and heart rate (HR). The peak decreases in MBP and HR occurred within 1 min after injection and recoveries to pre-injection levels within 3 min. The depressor responses to both L-enk and M-enk were abolished by intracisternal pretreatment with yohimbine (0.5 mg/kg) but not with prazosin (0.1 mg/kg). Pretreatment with either drug did not alter the bradycardia. All cardiovascular effects of both L-enk and M-enk were prevented by intravenous pretreatment with naloxone (2 mg/kg). These results suggest that central cr2-adrenoceptors may participate in the central actions of enkephalins on blood pressure regulation. HR responses to enkephalins may be elicited by a different mechanism.

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“…In addition to the effects observed for opiate agonists in peripheral tissues, morphine-like drugs and [Met5]-enkephalin have been shown to reduce the electrically and potassium-evoked [3H]-noradrenaline overflow from slices of different regions of the rat brain: occipital cortex, hypothalamus and cerebellar cortex (Montel et al, 1974a, b;1975a, b;Taube, Borowski, Endo & Starke, 1976;Taube, Starke & Borowski, 1977;Arbilla & Langer, 1978). Naloxone blocked the inhibition of 3H-transmitter overflow obtained in the presence of morphine or [Met5]-enkephalin, but did not antagonize the inhibitory effect of the a-agonist, tramazoline (Taube et al, 1977).…”

Section: Methodsmentioning

confidence: 99%

Pharmacological Differentiation of Presynaptic Inhibitory Α‐adrenoceptors and Opiate Receptors in the Cat Nictitating Membrane

Dubocovich

Langer

1980

British J Pharmacology

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3 The synthetic opiate pentapeptides: BW 180 C (Tyr-D-Ala-Gly-Phe-E>-Leu), and BW834 C (Tyr-DAla-Gly-pClPhe-DLeu), which are resistant to enzymatic degradation were more potent than the enkephalins in reducing the stimulation-evoked transmitter overflow from the cat nictitating membrane. On the other hand, the tetrapeptide BW832 C, which lacks the D-leucine terminal of BW180 C was less potent than the enkephalins in inhibiting neurotransmission. 4 In the presence of phenoxybenzamine 1 gIM, 3H-transmitter overflow was increased 8 fold and the inhibition of neurotransmission by methionine-enkephalin was not affected. Exposure to phenoxybenzamine 10 gM increased [3H]-noradrenaline overflow 15 fold and antagonized the effects of methionine enkephalin on transmitter release. 5 In the cat nictitating membrane the inhibitory presynaptic opiate receptors are different from the presynaptic a-autoreceptors which regulate the release of noradrenaline elicited by nerve depolarization through a negative feed-back mechanism.

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Enkephalin: A potential modulator of noradrenaline release in rat brain

Cited by 139 publications

References 8 publications

Effect of Enkephalin and Substance P on Sympathetic Nerve Transmission in Mouse Vas Deferens

Effect of Enkephalin and Substance P on Sympathetic Nerve Transmission in Mouse Vas Deferens

Pharmacological evidence that central .ALPHA.2-adrenoceptors are involved in cardiovascular responses to intravenously injected enkephalins in anesthetized dogs.

Pharmacological Differentiation of Presynaptic Inhibitory Α‐adrenoceptors and Opiate Receptors in the Cat Nictitating Membrane

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