Accumulation of Enkephalin, Proenkephalin mRNA, and Neuropeptide Y in Immunologically Denervated Rat Adrenal Glands: Evidence for Divergent Peptide Regulation
| Autor: | Åke Dagerlind, Sanna McKinzie, Rammohan V. Rao, P. Hammond, Stephen Brimijoin |
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| Rok vydání: | 2002 |
| Předmět: |
Atropine
Male endocrine system medicine.medical_specialty Epinephrine Enkephalin Molecular Sequence Data Neuropeptide Biochemistry Cholinergic Antagonists Rats Sprague-Dawley Norepinephrine Cellular and Molecular Neuroscience Internal medicine Adrenal Glands medicine Animals Neuropeptide Y RNA Messenger Protein Precursors DNA Primers Base Sequence Chemistry Enkephalins Neuropeptide Y receptor Chlorisondamine Rats Proenkephalin medicine.anatomical_structure Endocrinology Chromaffin cell Acetylcholinesterase Catecholamine Adrenal medulla medicine.drug |
| Zdroj: | Journal of Neurochemistry. 64:1281-1287 |
| ISSN: | 0022-3042 |
| DOI: | 10.1046/j.1471-4159.1995.64031281.x |
| Popis: | To investigate transsynaptic effects on peptides of adrenal chromaffin cells in the rat, presynaptic sympathetic terminals were destroyed by intravenous injection of monoclonal antibodies to acetylcholinesterase. At several times thereafter, neuropeptide Y (NPY)-like immunoreactivity (NPY-IR) and methionine-enkephalin-like immunoreactivity (Met-Enk-IR) were measured by radioimmunoassay. Within 2 days of antibody injection, adrenal Met-Enk-IR increased five- to 10-fold and NPY-IR increased 50%. These effects were accompanied by large increases in proenkephalin A mRNA assayed by polymerase chain reaction. The peptide responses could reflect either an acute activation, as presynaptic terminals degenerated, or a chronic synaptic inactivation after terminal degeneration. To test the possibilities, muscarinic and nicotinic receptors were inhibited by repeated injection of atropine (1 mg/kg) and chlorisondamine (5 mg/kg). Measurements of urinary free catecholamine excretion showed that this treatment prevented the paroxysmal release of norepinephrine and reduced the release of epinephrine that normally followed injection of acetylcholinesterase antibodies. When the drugs were given alone for 2 or 4 days, adrenal Met-Enk-IR increased modestly and NPY-IR remained steady or declined. When given together with acetylcholinesterase antibodies, the cholinergic antagonists blocked the increase of NPY-IR but not Met-Enk-IR. Adding naloxone (1 mg/kg) to the treatment regimen enhanced the blockade of epinephrine excretion and largely prevented the antibody-induced increase in Met-EnK-IR. These findings indicate that adrenal NPY and enkephalin are not regulated identically. Adrenal NPY behaves as though controlled by transsynaptic cholinergic input. On the other hand, adrenal enkephalin may be regulated by additional or different mechanisms, possibly involving peptidergic transmission or synaptic inactivation. |
| Databáze: | OpenAIRE |
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