Flattening plasma corticosterone levels increases the prevalence of serotonergic dorsal raphe neurons inhibitory responses to nicotine in adrenalectomised rats
Highlights • Adrenalectomised and chronic corticosterone rats had flat corticosterone plasma levels. • In corticosterone treated rats, nicotine inhibited the firing of 5-HT dorsal raphe neurons. • In corticosterone treated rats nicotine and 5-HT increase IKIR. • Nicotine seems to induced 5-HT releas...
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Published in | Brain research bulletin Vol. 98; pp. 10 - 22 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
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Elsevier Inc
01.09.2013
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Abstract | Highlights • Adrenalectomised and chronic corticosterone rats had flat corticosterone plasma levels. • In corticosterone treated rats, nicotine inhibited the firing of 5-HT dorsal raphe neurons. • In corticosterone treated rats nicotine and 5-HT increase IKIR. • Nicotine seems to induced 5-HT release in the dorsal raphe nucleus. • Nicotine effects are mediated by α4β2 nicotinic receptors. |
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AbstractList | Major depression is characterized by a diminished activity of the brain serotonergic system as well as by the flattening of plasma cortisol levels. Nicotine improves mood in patients with major depression and in experimentally depressed animals by increasing brain serotonin (5-HT), noradrenaline and dopamine levels. The present study was directed to determine if flattening plasma glucocorticoid levels changes nicotine's stimulatory effects upon 5-HT DRN neurons. The experiments were performed in brain slices obtained from rats previously (14 days) adrenalectomised and implanted subcutaneously with one pellet containing 75mg of corticosterone (Adx+CSR rats). Whole cell voltage and current clamp techniques were used to study the activity of immunocitochemically identified 5-HT DRN neurons. Administration of nicotine (1μM) in sham-operated animals produced stimulatory effects in all 5-HT DRN neurons studied. In Adx+CSR rats however, nicotine inhibited 75% of 5-HT DRN neurons and increased the potassium-dependent inward rectifying current. The inhibitory effect of nicotine upon 5-HT DRN neurons was dependent on serotonin release inside the DRN, since it was converted into a stimulatory response by the selective antagonist of 5-HT1A receptors N-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-N-(2-pyridyl)cyclohexanecarboxamide (WAY100635, 25nM). Adx+CSR rats also presented an increased function of 5-HT1A autoreceptors, since, in these rats, serotonin (1-10μM) produced a higher increase in the potassium dependent inward rectifying current in comparison with sham-operated animals. Serotonin release inside DRN was mediated by α4β2 nicotinic acetylcholine receptors since the selective antagonist of these receptors dihydro-β-erytroidine hydrobromide (DHβE, 100nM) blocked the inhibitory effects of nicotine 5-HT DRN neurons. These data indicate that, in the experimental model of adrenalectomised rats implanted with corticosterone pellets, nicotine increases the function of 5-HT1A receptors of 5-HT DRN neurons. •Adrenalectomised and chronic corticosterone rats had flat corticosterone plasma levels.•In corticosterone treated rats, nicotine inhibited the firing of 5-HT dorsal raphe neurons.•In corticosterone treated rats nicotine and 5-HT increase IKIR.•Nicotine seems to induced 5-HT release in the dorsal raphe nucleus.•Nicotine effects are mediated by α4β2 nicotinic receptors. Major depression is characterized by a diminished activity of the brain serotonergic system as well as by the flattening of plasma cortisol levels. Nicotine improves mood in patients with major depression and in experimentally depressed animals by increasing brain serotonin (5-HT), noradrenaline and dopamine levels. The present study was directed to determine if flattening plasma glucocorticoid levels changes nicotine's stimulatory effects upon 5-HT DRN neurons. The experiments were performed in brain slices obtained from rats previously (14 days) adrenalectomised and implanted subcutaneously with one pellet containing 75mg of corticosterone (Adx+CSR rats). Whole cell voltage and current clamp techniques were used to study the activity of immunocitochemically identified 5-HT DRN neurons. Administration of nicotine (1μM) in sham-operated animals produced stimulatory effects in all 5-HT DRN neurons studied. In Adx+CSR rats however, nicotine inhibited 75% of 5-HT DRN neurons and increased the potassium-dependent inward rectifying current. The inhibitory effect of nicotine upon 5-HT DRN neurons was dependent on serotonin release inside the DRN, since it was converted into a stimulatory response by the selective antagonist of 5-HT1A receptors N-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-N-(2-pyridyl)cyclohexanecarboxamide (WAY100635, 25nM). Adx+CSR rats also presented an increased function of 5-HT1A autoreceptors, since, in these rats, serotonin (1–10μM) produced a higher increase in the potassium dependent inward rectifying current in comparison with sham-operated animals. Serotonin release inside DRN was mediated by α4β2 nicotinic acetylcholine receptors since the selective antagonist of these receptors dihydro-β-erytroidine hydrobromide (DHβE, 100nM) blocked the inhibitory effects of nicotine 5-HT DRN neurons. These data indicate that, in the experimental model of adrenalectomised rats implanted with corticosterone pellets, nicotine increases the function of 5-HT1A receptors of 5-HT DRN neurons. Highlights • Adrenalectomised and chronic corticosterone rats had flat corticosterone plasma levels. • In corticosterone treated rats, nicotine inhibited the firing of 5-HT dorsal raphe neurons. • In corticosterone treated rats nicotine and 5-HT increase IKIR. • Nicotine seems to induced 5-HT release in the dorsal raphe nucleus. • Nicotine effects are mediated by α4β2 nicotinic receptors. |
Author | Garduño, Julieta Drucker-Colin, René Hernández, Salvador Mihailescu, Stefan Frías-Domínguez, Carmen |
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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23872451$$D View this record in MEDLINE/PubMed |
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CitedBy_id | crossref_primary_10_1152_jn_00223_2014 crossref_primary_10_1515_revneuro_2018_0014 |
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Keywords | nAChRs DRN Serotonin Adx + CSR rats Corticosterone Dorsal raphe nucleus adrenalectomised and corticosterone-treated rats nicotinic acetylcholine receptors 5-HT1A receptor Nicotine Adx+CSR rats |
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Snippet | Highlights • Adrenalectomised and chronic corticosterone rats had flat corticosterone plasma levels. • In corticosterone treated rats, nicotine inhibited the... •Adrenalectomised and chronic corticosterone rats had flat corticosterone plasma levels.•In corticosterone treated rats, nicotine inhibited the firing of 5-HT... Major depression is characterized by a diminished activity of the brain serotonergic system as well as by the flattening of plasma cortisol levels. Nicotine... |
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SubjectTerms | 5-HT1A receptor Aconitine - analogs & derivatives Aconitine - pharmacology Action Potentials - drug effects Adrenalectomy Animals Corticosterone Corticosterone - blood Dihydro-beta-Erythroidine - pharmacology Dorsal raphe nucleus Dose-Response Relationship, Drug Male Neural Inhibition - drug effects Neurology Nicotine Nicotine - pharmacology Nicotinic Agonists - pharmacology Nicotinic Antagonists - pharmacology Piperazines - pharmacology Pyridines - pharmacology Raphe Nuclei - cytology Raphe Nuclei - drug effects Rats Rats, Wistar Serotonergic Neurons - drug effects Serotonin Serotonin - metabolism Serotonin - pharmacology Serotonin Antagonists - pharmacology |
Title | Flattening plasma corticosterone levels increases the prevalence of serotonergic dorsal raphe neurons inhibitory responses to nicotine in adrenalectomised rats |
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