The secretory response of hypothalamic β-endorphin neurons to acute and chronic nicotine treatments and following nicotine withdrawal
Abstract
In the present study, we determined the effect of acute and chronic nicotine treatments on the secretion of immunoreactive beta-endorphin (IR-beta-EP) and cell viability of cultured hypothalamic neurons. Also, we determined the secretory response of IR-beta-EP following withdrawal from a long-term nicotine treatment. Fetal hypothalamic cells were dissociated and maintained in cultures for 9 days and were treated with various doses of nicotine (1, 6, 12 and 18 microM) for 6 h (acute treatment) or treated with nicotine at 12 h intervals for 96 h (chronic treatment). Determination of IR-beta-EP concentrations in the media revealed that 6-18 microM doses of nicotine increased IR-beta-EP secretion from these cultures for a period of 24 h; after this period, the cultured cells did not respond to these doses of nicotine. The desensitization of beta-EP neurons 24 h after treatment with nicotine did not appear to be related to the loss of viable cells. Determination of withdrawal response after 72 h of constant nicotine (6 microM) treatments revealed that the hypothalamic neurons secrete elevated amounts of IR-beta-EP for a period of 72 h after nicotine withdrawal. These results suggest that: 1) acute treatment with nicotine stimulates hypothalamic IR-beta-EP release; 2) chronic nicotine treatment desensitizes beta-EP-secreting neurons and, 3) beta-EP neurons in primary culture show withdrawal response to nicotine.
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Bungarotoxin-insensitive nAChR subtypes, including the α4β2-containing subtype, have been extensively implicated in the behavioral effects of nicotine, including dependence-related effects such as nicotine self-administration and neurotransmitter release (dopamine).
“Of the various types of nAChRs that exist in the central nervous system (CNS), members of the so-called bungarotoxin-insensitive subtypes, which are composed of alpha and beta subunits and includes the ubiquitous α4β2-containing subtype, have been extensively implicated in the behavioral effects of nicotine, including its dependence-related effects such as nicotine self-administration and neurotra”
From Tobacco addiction (2008) · cites this paper as [26]
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References 32 · Cited by 55
- Authors
- Boyadjieva, N. I., & Sarkar, D. K.
- Affiliations
- Washington State University (US)
- Corresponding author
- Sarkar, Dipak K.
- ORCID
- Sarkar, Dipak K.
- Venue
- Life Sciences
- Publisher
- Elsevier BV
- Published
- 1997-07
- Volume
- 61
- Issue
- 6
- Pages
- A59-A66
- ISSN
- 0024-3205 (ISSN-L)
- OpenAlex
- W2049561873
- Cited by
- 55
- References
- 32
- Citations by year
- 2019: 1 · 2017: 1 · 2016: 1 · 2015: 2 · 2014: 1 · 2013: 1 · 2012: 5
- FWCI
- 0.66
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Life Sciences (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute on Alcohol Abuse and Alcoholism (AA-08757)
- National Institute of Neurological Disorders and Stroke (NS05130)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
- Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
- Keywords
- beta-endorphin, hypothalamic neurons, nicotine, nicotine withdrawal, neurosecretion, cell viability, chronic nicotine treatment
- MeSH terms
- Animals, beta-Endorphin, Cell Survival, Cells, Cultured, Female, Hypothalamus, Neurons, Nicotine, Pregnancy, Rats, Sprague-Dawley, Rats
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