Selective processing of β-endorphin in regions of porcine pituitary

Smyth, Derek G.; Zakarian, S.

doi:10.1038/288613a0

Cited by 128 publications

(28 citation statements)

References 14 publications

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“…This part of the hypophysis is virtually devoid of dynorphin (Watson et al 1981), contains only small amounts, if any, of enkephalin (Rossier et al 1979) but high concentrations of peptides exhibiting /?-endorphin-like immunoreactivity (Pelletier et al 1977;Bloom et al 1977). The presence of biologically active fl-endorphin-(1-31) has been revealed by chromatographic techniques, notwithstanding that the forms of fl-endorphin which predominate are those which have undergone proteolysis or acetylation (Smyth & Zakarian, 1980;Seizinger & H6llt, 1980;Weber, Evans, Chang & Barchas, 1982).…”

Section: Discussionmentioning

confidence: 99%

The effect of naloxone on vasopressin release from rat neurohypophysis incubated in vitro.

Knepel¹,

Meyer²

1983

The Journal of Physiology

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SUMMARY1. Rat posterior pituitaries were superfused in vitro and stimulated electrically. The concentrations of vasopressin in the superfusion medium were determined by radioimmunoassay.2. When the pulses were applied in 10 sec trains with 10 see intervals, vasopressin release per pulse increased progressively over the frequency range of 3-12 pulses/sec applied within the trains. The release was blocked by addition of tetrodotoxin or by removal of calcium ions from the superfusion medium.3. The opiate antagonist naloxone 1 or 10/M was introduced into the superfusion medium before a second period of stimulation and enhanced vasopressin release from neurointermediate lobes after phasic stimulation at 9 pulses/sec within the trains, when compared to controls. However, naloxone 10 #M had not effect on vasopressin release from isolated neural lobes (intermediate lobes removed), although the addition of camel fl-endorphin 2 1M inhibited vasopressin release in a naloxonereversible manner.4. After continuous stimulation at a frequency of 13 Hz naloxone 10/M did not influence the release of vasopressin from neurointermediate lobes.5. We conclude that the evoked release of vasopressin from the neurointermediate lobe is reduced by an endogenous opiate of intermediate lobe origin, possibly ,/-endorphin. Appropriate stimulation conditions are necessary for this mechanism to function.

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Section: Discussionmentioning

confidence: 99%

The effect of naloxone on vasopressin release from rat neurohypophysis incubated in vitro.

Knepel¹,

Meyer²

1983

The Journal of Physiology

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“…There is evidence suggesting that the enzymes responsible for processing different precursors may differ slightly from each other (reviewed in 200). The corticotropin precursor is processed into different peptides in different cell types (212). This may prove to be true for other precursors also, such as the enkephalin precursor (e.g.…”

Section: Metabolism Of Peptide and Classical Transmittersmentioning

confidence: 99%

A Molecular Description of Nerve Terminal Function

Reichardt¹,

Kelly²

1983

Annu. Rev. Biochem.

226

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The nerve terminal is a specialized region of a neuron, separated from the neuronal soma by an axon that can be exceedingly long, whose function is to release neurotransmitter when stimulated by an electrical signal carried by the axon. In this review, we describe the enzymes, channels, and other proteins presently thought to be important in nerve terminal function. Recent progress in the area has been so dramatic that it is becoming possible to relate simple changes in behavior to modifications of defined proteins in particular nerve terminals.Neurotransmitters are stored in synaptic vesicles and are released by fusion of these vesicles to the plasma membrane. Vesicle fusion is triggered by Ca 2+ -influx through specific Ca 2+ channels that open in response to depolarization of the plasma membrane and is terminated by the disappearance of Ca 2+ from the vicinities of the active zones. The voltage signal that opens the Ca 2+ gates is not constant, but also subject to regulation. The key elements are the Na + and K + channels in the nerve terminal. These channels are localized to distinct regions of many neurons and different neurons have different quantities of the different channel types. The voltage sensitive Na + channel is responsible for depolarizing the membrane. This channel has recently been purified and reconstituted in artificial membranes, so many of its properties are known. K + channels are responsible for repolarizing the membrane. Several K + channels have been identified: some activated by voltage, some by intracellular Ca 2+ and others by neurotransmitters. The properties of several of these have recently been shown to be altered by cAMP-dependent protein kinases, resulting in long-term changes in neuronal activity and the efficiency of synaptic transmission. The voltage-dependent Ca 2+ channels can also be modified by cAMP-dependent protein kinases. Many of the neurotransmitters and hormones that modulate the efficiency of transmitter release apparently do so by modifying the Ca 2+ channels. Much of the recent progress in molecular studies on the K + and Ca 2+ channels has been made possible by a dramatic new technique called "patch clamping" that permits individual ion channels to be examined on the tip of a microelectrode. In many ways this technology circumvents the need for biochemical isolation and reconstitution.Maintenance of the Na + and K + concentrations in neurons requires the classical Na, + K + -ATPase that is found in all cell types. Recent experiments suggest that a novel form of this enzyme exists in neural tissues. This pump appears to be localized to anatomically and functionally distinct regions of many neurons. To restore the cytoplasmic Ca 2+ concentrations to original levels, the nerve terminal has an array of Ca 2+ removal systems including a Na + :Ca 2+ antiporter in the plasma membrane, a Ca 2+ porter in the mitochondrial inner membrane and several distinct ATP-dependent Ca 2+ uptake systems in the plasma membrane, smooth endoplasmic reticulum, and synaptic vesicles.The...

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“…The predominant form of β-endorphin in rat anterior pituitary was β-endorphin(1-31), but the principal forms in the pars intermedia were acetylated at their N-terminus and/or truncated at their C-terminus (Smyth & Zakarian 1980, Smyth 1981, Smyth et al 1981a,b, Zakarian & Smyth 1982a (Fig. 6).…”

Section: β-Endorphin In Pituitary: Tissue-specific Processingmentioning

confidence: 99%

60 YEARS OF POMC: Lipotropin and beta-endorphin: a perspective

Smyth

2016

Journal of Molecular Endocrinology

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Many important fields of research had a humble origin. In the distant past, A J P Martin's discovery that amino acids could be separated by paper chromatography and Moore and Stein's use of columns for quantitative amino acid analysis provided the first steps towards the determination of structure in complex biologically active molecules. They opened the door to reveal the essential relationship that exists between structure and function. In molecular endocrinology, for example, striking advances have been made by chemists with their expertise in the identification of structure working with biologists who contributed valuable knowledge and experience. Advantage was gained from the convergence of different background, and it is notable that the whole is greater than the sum. In the determination of structure, it may be recalled that four of the world's great pioneers (Archibald Martin, Rodney Porter, Fred Sanger and Vincent du Vigneaud) were acknowledged for their fundamental contributions when individually they were awarded the Nobel Prize. They foresaw that the identification of structure would prove of outstanding importance in the future. Indeed, study of the structures of β-endorphin and enkephalin and the different forms of opiate activity they engender has led to a transformation in our understanding of chemical transmission in the brain.

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Selective processing of β-endorphin in regions of porcine pituitary

Cited by 128 publications

References 14 publications

The effect of naloxone on vasopressin release from rat neurohypophysis incubated in vitro.

The effect of naloxone on vasopressin release from rat neurohypophysis incubated in vitro.

A Molecular Description of Nerve Terminal Function

60 YEARS OF POMC: Lipotropin and beta-endorphin: a perspective

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