Nicotine, the Thyroid and Hashimoto's: The Research

Autoimmune thyroiditis appears less often in smokers and more often after quitting, and nicotine also affects thyroid hormone levels. This page collects the published research on nicotine and the thyroid, including Hashimoto's thyroiditis, each paper summarised in plain language with its PubMed record.

This collection is research only: papers found on PubMed, each described as its own abstract reports it. Cell and animal results are labelled as such, and harms are listed beside benefits. It is not medical advice.

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The Papers (26)

Newest first. Study types on this page — Human observational study: 1 · Review: 2 · Animal study: 20 · Cell study: 3. Each summary is written from the paper’s own abstract; follow the PubMed link for the full record.

Nicotine increases hepatocyte transthyretin turnover: A possible mechanism for the protective effect of smoking on preeclampsia?

Cell study, 2025. Researchers tested how nicotine affects transthyretin, a blood protein that carries thyroid hormone, in liver cells grown in the lab. Nicotine raised the amount of transthyretin the cells made, and it increased how much transthyretin and soluble endoglin the cells took in. Soluble endoglin is a substance the failing placenta releases in preeclampsia, where it damages blood vessels. The authors suggest that nicotine might protect against preeclampsia by helping clear soluble endoglin from the blood, but this result comes only from cells in a dish, and they say more research is needed.

Young M, McLeod DSA, Richard K (2025). Nicotine increases hepatocyte transthyretin turnover: A possible mechanism for the protective effect of smoking on preeclampsia?. Mol Cell Endocrinol. — PubMed PMID: 39725350 · doi:10.1016/j.mce.2024.112446

Prenatal Nicotine or Cannabis Exposure and Offspring Neurobehavioral Outcomes

Human observational study, 2022. Researchers looked at 1,197 pregnant people and their children who were already part of two thyroid-treatment trials. They tested the mothers' urine early in pregnancy for cotinine, a breakdown product of nicotine, and for a cannabis breakdown product, then compared the children's development. 99 mothers (8.3%) tested positive for cotinine. At 60 months of age, median IQ was 90 in nicotine-exposed children and 95 in unexposed children, a difference the study did not count as meaningful once other factors were taken into account. The authors found no link between prenatal nicotine exposure and child IQ, and they say more studies are needed that look at when and how much exposure happened.

Smid MC, Metz TD, McMillin GA et al. (2022). Prenatal Nicotine or Cannabis Exposure and Offspring Neurobehavioral Outcomes. Obstet Gynecol. — PubMed PMID: 34856574 · doi:10.1097/AOG.0000000000004632

Molecular insights into the benefits of nicotine on memory and cognition (Review)

Review, 2021. This review looks at research on how nicotine affects memory and thinking in the brain. It notes that nicotine's health risks are well known, but reports evidence that nicotine can improve memory and thinking problems in Alzheimer's disease, and movement and memory problems in Parkinson's disease. It also reports benefits for memory loss caused by sleep deprivation, chronic stress and an underactive thyroid, acting through several brain signalling pathways and the alpha-7 nicotinic receptor. The authors say more research is needed on how short-term and long-term nicotine use affects memory.

Alhowail A (2021). Molecular insights into the benefits of nicotine on memory and cognition (Review). Mol Med Rep. — PubMed PMID: 33786606 · doi:10.3892/mmr.2021.12037

Early life nicotine exposure alters mRNA and microRNA expressions related to thyroid function and lipid metabolism in liver and BAT of adult wistar rats

Animal study, 2021. This rat study looked at what happens in adulthood when newborn rats are exposed to nicotine through their mother's milk. Nursing mother rats got either salt water or nicotine (6 mg/kg) from a small pump placed under the skin, and their male and female offspring were studied at 180 days old. Compared with controls, the nicotine-exposed offspring showed changes in the liver and brown fat in genes and microRNAs (small molecules that switch genes down) linked to thyroid hormone activity and fat handling. These included lower Dio1 and higher SCD1 and miR-224 in the liver of both sexes, and more changes in females, so the effect differed by sex. These results come from rats only.

Peixoto TC, Gaspar de Moura E, Quitete FT et al. (2021). Early life nicotine exposure alters mRNA and microRNA expressions related to thyroid function and lipid metabolism in liver and BAT of adult wistar rats. Mol Cell Endocrinol. — PubMed PMID: 33359828 · doi:10.1016/j.mce.2020.111141

Thyroid redox imbalance in adult Wistar rats that were exposed to nicotine during breastfeeding

Animal study, 2020. This study used rats only. Nursing mother rats received nicotine (6 mg/kg/day) or salt water through a small implanted pump from day 2 to day 16 after birth, and their offspring's thyroid glands were then examined at 180 days old. As adults, male offspring exposed to nicotine had lower levels of the thyroid hormones T3 and T4 and of TSH, the hormone that stimulates the thyroid. Female offspring had higher T3 and T4. The thyroid's antioxidant enzymes were weakened in both sexes, but only the females showed oxidative stress damage in the gland, so the authors conclude that nicotine exposure during breastfeeding upset thyroid balance in different ways in males and females.

Miranda RA, de Moura EG, Soares PN et al. (2020). Thyroid redox imbalance in adult Wistar rats that were exposed to nicotine during breastfeeding. Sci Rep. — PubMed PMID: 32973319 · doi:10.1038/s41598-020-72725-w

Comparison of Effects of Spatial and Non-Spatial Memory Acquisition on the CaMKII Pathway During Hypothyroidism and Nicotine Treatment

Animal study, 2020. This study used adult rats whose thyroid glands were surgically removed to make them hypothyroid. The rats were trained to find either a hidden platform (spatial memory) or a visible platform (non-spatial memory) in a water maze. Some received nicotine injections under the skin (1 mg/kg twice a day) for 4 weeks. In the hypothyroid rats, levels of several memory-related proteins in the hippocampus, a memory centre of the brain, were abnormal after both kinds of training, and nicotine brought these levels back to normal. The findings come from rats only.

Alkadhi KA, Alzoubi KH (2020). Comparison of Effects of Spatial and Non-Spatial Memory Acquisition on the CaMKII Pathway During Hypothyroidism and Nicotine Treatment. Mol Neurobiol. — PubMed PMID: 31900862 · doi:10.1007/s12035-019-01865-6

Pharmacological exposures may precipitate craniosynostosis through targeted stem cell depletion

Animal study, 2019. This study looked at whether certain exposures during pregnancy, including nicotine and a common type of antidepressant (an SSRI), might help cause craniosynostosis. In this birth defect, which the abstract says occurs in about 1 in 1,800 to 2,500 births, the seams of a baby's skull close too early. In mice, exposure to nicotine or the SSRI before birth raised the risk of early skull-seam fusion. It also lowered the number of a type of stem cell (Gli1+ cells) in those seams and changed the normal balance of the surrounding tissue. These results come only from mice. The authors conclude that these exposures can deplete skull stem cells, but that stem-cell loss does not explain every exposure linked to craniosynostosis.

Durham E, Howie RN, Larson N et al. (2019). Pharmacological exposures may precipitate craniosynostosis through targeted stem cell depletion. Stem Cell Res. — PubMed PMID: 31415959 · doi:10.1016/j.scr.2019.101528

Thyroid hormone signaling: Contribution to neural function, cognition, and relationship to nicotine

Review, 2015. This review looks at earlier research on how thyroid hormones support brain function, learning and memory, and how nicotine changes thyroid hormone signaling. The authors suggest that nicotine's effects on the thyroid may change learning and memory, and that this could be part of why nicotine is addictive. They note that changes in thinking are a major symptom of nicotine addiction and that current quit-smoking treatments work only modestly at best. They propose that drugs that act like thyroid hormone could be explored as new quit-smoking treatments, but this is an idea to test, not a proven result.

Leach PT, Gould TJ (2015). Thyroid hormone signaling: Contribution to neural function, cognition, and relationship to nicotine. Neurosci Biobehav Rev. — PubMed PMID: 26344666 · doi:10.1016/j.neubiorev.2015.09.001

Thyroid receptor β involvement in the effects of acute nicotine on hippocampus-dependent memory

Animal study, 2015. This mouse study looked at whether thyroid hormone signaling helps explain how a single dose of nicotine improves learning. A screen of gene-switch proteins showed that nicotine combined with learning increased the activity of thyroid receptors, but nicotine and learning did not change thyroid hormone levels. Normal mice and mice missing the thyroid receptor alpha-1 gene learned a fear-linked context better after nicotine, but mice missing the thyroid receptor beta gene did not. The authors say the beta form of the thyroid receptor appears to be involved in nicotine's short-term boost to memory that depends on the hippocampus, the brain's memory center. These results are from mice only.

Leach PT, Kenney JW, Connor DA et al. (2015). Thyroid receptor β involvement in the effects of acute nicotine on hippocampus-dependent memory. Neuropharmacology. — PubMed PMID: 25666034 · doi:10.1016/j.neuropharm.2015.01.026

Effects of maternal nicotine exposure on thyroid hormone metabolism and function in adult rat progeny

Animal study, 2015. In this rat study, nursing mother rats were given nicotine (6 mg/kg per day through an implanted pump) or saline from day 2 to day 16 after giving birth, and their offspring were examined as adults at 180 days. Offspring exposed to nicotine through nursing had signs of low thyroid function in the liver, muscle, brown fat, heart and testis, along with lower levels of the brain and pituitary hormones that drive the thyroid (TRH and TSH) and a weaker pituitary response to TRH. The authors conclude that this adult hypothyroidism was partly caused by suppression of the TRH-TSH signal, while the brain, pituitary and thyroid appeared to adapt to keep thyroid hormone activation steady in those central tissues. These results are in rats only.

Lisboa PC, de Oliveira E, Manhães AC et al. (2015). Effects of maternal nicotine exposure on thyroid hormone metabolism and function in adult rat progeny. J Endocrinol. — PubMed PMID: 25653393 · doi:10.1530/JOE-14-0473

Withdrawal From Chronic Nicotine Reduces Thyroid Hormone Levels and Levothyroxine Treatment Ameliorates Nicotine Withdrawal-Induced Deficits in Hippocampus-Dependent Learning in C57BL/6J Mice

Animal study, 2015. Researchers gave mice nicotine over a long period, then stopped it, and measured thyroid hormone levels in their blood. Withdrawal from nicotine lowered thyroid hormone levels by 9%. Giving the mice synthetic thyroid hormone (levothyroxine) improved memory in mice that had never had nicotine, and it also reduced the learning and memory problems seen during nicotine withdrawal. These results come from mice only; the authors suggest that thyroid function should be watched in people trying to quit smoking.

Leach PT, Holliday E, Kutlu MG et al. (2015). Withdrawal From Chronic Nicotine Reduces Thyroid Hormone Levels and Levothyroxine Treatment Ameliorates Nicotine Withdrawal-Induced Deficits in Hippocampus-Dependent Learning in C57BL/6J Mice. Nicotine Tob Res. — PubMed PMID: 25358661 · doi:10.1093/ntr/ntu229

Effect of maternal nicotine/thiocyanate exposure during gestational period upon pituitary, thyroid and parathyroid function/morphology of 1-month-old rat offspring

Animal study, 2014. This study in rats looked at what happens to the hormone glands of offspring when the mother is given nicotine or a related chemical, thiocyanate, from day 4 to day 20 of pregnancy. In male offspring examined at 1 month old, both nicotine and thiocyanate made the thyroid's hormone-making cells more active: the cells were about 30% taller, and the pituitary cells that signal the thyroid showed reduced activity. Nicotine in particular enlarged the parathyroid's main cells by about 45% but made them less active, while the calcitonin-producing cells in the thyroid grew larger and multiplied by 25%. The authors conclude that these effects of exposure in the womb lasted until 1 month after birth; these results come from rats only.

Abdelhafez AM, Eltony SA, Abdelhameed SY et al. (2014). Effect of maternal nicotine/thiocyanate exposure during gestational period upon pituitary, thyroid and parathyroid function/morphology of 1-month-old rat offspring. J Endocrinol Invest. — PubMed PMID: 24639120 · doi:10.1007/s40618-013-0043-8

Neonatal hypothyroidism caused by maternal nicotine exposure is reversed by higher T3 transfer by milk after nicotine withdraw

Animal study, 2011. This study was done in rats, not people. Mother rats were given nicotine through an implanted pump (6 mg/kg/day for 13 days) starting the day after birth, and the researchers looked at thyroid hormones and how iodine and the thyroid hormone T3 passed through milk to the pups. While nicotine was being given, both mothers and pups showed signs of an underactive thyroid (lower T4, higher TSH), and the pups also had lower T3. After the nicotine stopped, the pups' thyroid function had returned to normal by weaning, which the authors think was probably because the mothers' milk carried more T3, linked to higher activity of a thyroid-hormone-converting enzyme in the mammary gland.

de Oliveira E, de Moura EG, Santos-Silva AP et al. (2011). Neonatal hypothyroidism caused by maternal nicotine exposure is reversed by higher T3 transfer by milk after nicotine withdraw. Food Chem Toxicol. — PubMed PMID: 21624425 · doi:10.1016/j.fct.2011.04.040

Adult-onset hypothyroidism facilitates and enhances LTD: reversal by chronic nicotine treatment

Animal study, 2007. This study in rats looked at how an underactive thyroid (hypothyroidism, caused by removing the thyroid gland) affects long-term depression, a process in the brain's memory area (the hippocampus) in which connections between nerve cells weaken. Hypothyroid rats showed stronger long-term depression, and it was easier to trigger than in normal rats. Nicotine given twice a day for a long period (1 mg/kg) reversed these changes and also reversed the hypothyroidism-linked shifts in NMDA receptor subunits, which are proteins involved in learning. Nicotine also raised levels of BDNF, a nerve growth protein, and of nicotinic receptors in both normal and hypothyroid rats. These results come from rats only, not people.

Alzoubi KH, Aleisa AM, Alkadhi KA (2007). Adult-onset hypothyroidism facilitates and enhances LTD: reversal by chronic nicotine treatment. Neurobiol Dis. — PubMed PMID: 17331737 · doi:10.1016/j.nbd.2007.01.002

Nicotine reverses adult-onset hypothyroidism-induced impairment of learning and memory: Behavioral and electrophysiological studies

Animal study, 2006. Researchers removed the thyroid gland from adult rats to cause hypothyroidism (an underactive thyroid), then gave them nicotine injections twice a day for 4-6 weeks. In a water maze test, the hypothyroid rats did worse at learning and at short-term and long-term memory, and nicotine treatment reversed these problems. Nicotine had no effect on learning or memory in rats with normal thyroids. Recordings from the brain's memory center showed that hypothyroidism weakened the strengthening of connections between nerve cells, and nicotine restored it. These results come from rats only, not people.

Alzoubi KH, Aleisa AM, Gerges NZ et al. (2006). Nicotine reverses adult-onset hypothyroidism-induced impairment of learning and memory: Behavioral and electrophysiological studies. J Neurosci Res. — PubMed PMID: 16902999 · doi:10.1002/jnr.21014

Effect of prenatal or perinatal nicotine exposure on neonatal thyroid status and offspring growth in rats

Animal study, 2005. This study looked at whether nicotine by itself, apart from the other chemicals in cigarettes, affects the growth and thyroid hormones of offspring. Pregnant rats were given nicotine throughout pregnancy, and some of their pups kept getting nicotine for a short time after birth. Female offspring exposed to nicotine weighed more from day 35 after birth into adulthood, while males weighed more only briefly at day 35. Nicotine did not change thyroid hormone levels in 10-day-old pups, so the authors suggest that smoking's effects on thyroid status may come from chemicals in cigarettes other than nicotine; these results are in rats only.

Chen WJ, Kelly RB (2005). Effect of prenatal or perinatal nicotine exposure on neonatal thyroid status and offspring growth in rats. Life Sci. — PubMed PMID: 15642595 · doi:10.1016/j.lfs.2004.08.022

Effects of adrenoceptor blockers on the glycemic response to nicotine in thyroidectomised rats

Animal study, 2000. This study was done only in rats, and looked at why nicotine raises blood sugar. Fasted rats were given nicotine (50 micrograms per kilogram) by injection into a vein. Some had normal thyroid glands and some had their thyroid removed. In normal rats, a drug that blocks alpha-adrenergic receptors or one that blocks beta-adrenergic receptors (the receptors that respond to adrenaline) each significantly reduced the rise in blood sugar, and giving both together stopped it completely. Rats without a thyroid still had a rise in blood sugar after nicotine, but their starting and peak blood sugar levels were lower than in rats with a thyroid, which the authors say suggests both receptor types are involved in nicotine's blood-sugar effect in rats.

Ogwumike OO, Fasanmade AA (2000). Effects of adrenoceptor blockers on the glycemic response to nicotine in thyroidectomised rats. Afr J Med Med Sci. — PubMed PMID: 11379450

Effect of nicotine on type 2 deiodinase activity in cultured rat glial cells

Cell study, 1999. Researchers grew brain support cells (glial cells) from newborn rats in the lab and tested how nicotine affects type 2 deiodinase, an enzyme that turns the thyroid hormone T4 into its more active form, T3, inside the brain. Very small amounts of nicotine raised the enzyme's activity to about 2.2 to 3.5 times its normal level, and the effect peaked after 9 hours. A drug that stops nicotine from attaching to nicotinic receptors (mecamylamine) completely blocked this increase. The authors concluded that nicotine probably raises this enzyme's activity through nicotinic receptors and may affect brain function partly by changing thyroid hormone processing; these results come only from rat cells grown in a dish.

Gondou A, Toyoda N, Nishikawa M et al. (1999). Effect of nicotine on type 2 deiodinase activity in cultured rat glial cells. Endocr J. — PubMed PMID: 10426574 · doi:10.1507/endocrj.46.107

The effect of nicotine on thyroid function in rats

Animal study, 1998. Researchers wanted to know whether nicotine, rather than other parts of cigarette smoke, is behind the poorer thyroid function seen in some women who smoke. They gave large doses of nicotine by continuous infusion for 7 days to three groups of rats: rats with normal thyroids, rats with half their thyroid removed (mildly underactive), and rats with the thyroid fully removed that were given thyroid hormone. Nicotine did not change blood levels of the thyroid hormones T4 and T3, thyroid-stimulating hormone (TSH) or cholesterol in any group. It also did not change how the thyroid handled iodine, the liver and kidney enzymes that activate thyroid hormone, or a liver marker of thyroid hormone action. The authors conclude that nicotine is not responsible for the harmful effects of smoking on the thyroid, though this was shown only in rats.

Colzani R, Fang SL, Alex S et al. (1998). The effect of nicotine on thyroid function in rats. Metabolism. — PubMed PMID: 9472962 · doi:10.1016/s0026-0495(98)90212-8

Examination of antithyroid effects of smoking products in cultured thyroid follicles: only thiocyanate is a potent antithyroid agent

Cell study, 1992. Researchers grew pig thyroid follicles in the lab and tested three chemicals that come from cigarette smoking: nicotine, cotinine (the substance nicotine breaks down into) and thiocyanate. They used concentrations from 0 to 200 micromoles per litre. Nicotine and cotinine did not block the thyroid's uptake of iodide or its production of thyroid hormone. Thiocyanate, at levels like those in smokers' blood, did block both. It also made the thyroid lose iodide faster. The authors say thiocyanate could harm thyroid function, especially in people who are low in iodine. These results come from lab-grown thyroid tissue only, not from people.

Fukayama H, Nasu M, Murakami S et al. (1992). Examination of antithyroid effects of smoking products in cultured thyroid follicles: only thiocyanate is a potent antithyroid agent. Acta Endocrinol (Copenh). — PubMed PMID: 1283478 · doi:10.1530/acta.0.1270520

Involvement of D1 dopamine receptors in the nicotine-induced neuro-endocrine effects and depletion of diencephalic catecholamine stores in the male rat

Animal study, 1988. This study was done only in male rats. They were given four doses of nicotine (2 mg/kg each, 30 minutes apart) or exposed to cigarette smoke. Nicotine lowered blood levels of the hormones prolactin, LH and TSH, raised the stress hormone corticosterone, and did not change FSH, vasopressin or testosterone; cigarette smoke had smaller effects. Nicotine and smoke also depleted the chemical messengers dopamine and noradrenaline in nerve endings in hormone-control areas of the brain. A drug that blocks D1 dopamine receptors prevented this depletion and the drop in LH, while drugs that block D2 dopamine or 5-HT2 serotonin receptors did not, which suggests D1 receptors help carry some of nicotine's effects on brain hormone control.

Andersson K, Fuxe K, Eneroth P et al. (1988). Involvement of D1 dopamine receptors in the nicotine-induced neuro-endocrine effects and depletion of diencephalic catecholamine stores in the male rat. Neuroendocrinology. — PubMed PMID: 2975769 · doi:10.1159/000125007

Evaluation of the effects of cotinine and nicotine-N'-oxides on the development of tumors in rats initiated with N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide

Animal study, 1985. This study in rats tested whether three substances the body makes when it breaks down nicotine (cotinine and two forms of nicotine-N'-oxide) cause cancer or help it grow. The rats were first given a chemical known to start bladder tumors, then given the nicotine breakdown products in their drinking water for 78 weeks. None of the breakdown products caused cancer or promoted bladder tumors, and rats given the mix of the two nicotine-N'-oxide forms had fewer bladder tumors. However, rats given either trans-nicotine-N'-oxide or the mixture had significantly more tumors in the forestomach, a part of the stomach that rats have and people do not. These results come from rats only.

LaVoie EJ, Shigematsu A, Rivenson A et al. (1985). Evaluation of the effects of cotinine and nicotine-N'-oxides on the development of tumors in rats initiated with N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide. J Natl Cancer Inst. — PubMed PMID: 3865011

Thyroid hormone concentrations in rats after chronic nicotine metabolite administration

Animal study, 1984. Researchers tested whether the main breakdown products of nicotine affect the thyroid, because long-term smoking has been linked to lower thyroid hormone activity. For 78 weeks, rats were given one of three nicotine breakdown products, cotinine or one of two forms of nicotine-N'-oxide, and compared with an untreated group of 33 rats. The rats given nicotine-N'-oxide had markedly lower levels of the thyroid hormone T3 and changes in several other thyroid measures, and the rats given the pure trans form also had lower T4, while cotinine did not change T3. The authors suggest these breakdown products may affect the thyroid partly by being converted back into nicotine in the body, but this was found only in rats.

Sepkovic DW, Haley NJ, Axelrad CM et al. (1984). Thyroid hormone concentrations in rats after chronic nicotine metabolite administration. Proc Soc Exp Biol Med. — PubMed PMID: 6514716 · doi:10.3181/00379727-177-41965

Differential effects of mecamylamine on the nicotine induced changes in amine levels and turnover in hypothalamic dopamine and noradrenaline nerve terminal systems and in the secretion of adenohypophyseal hormones in the castrated female rat. Evidence for involvement of cholinergic nicotine-like receptors

Animal study, 1984. This study looked at female rats whose ovaries had been removed one month earlier, to see how nicotine affects two brain chemical messengers, dopamine and noradrenaline, in the hypothalamus, and how it affects hormones released by the pituitary gland. Nicotine lowered the stores of these messengers and sped up their turnover in several hypothalamic areas. It also sharply reduced the release of prolactin, luteinizing hormone (LH), thyroid-stimulating hormone (TSH) and growth hormone, raised corticosterone (a stress hormone) and did not change follicle-stimulating hormone (FSH). Mecamylamine, a drug that blocks nicotinic receptors, partly reversed some of these effects but not others, which the authors say suggests there may be different types of nicotinic receptors. These results come from rats only.

Anderson K, Fuxe K, Eneroth P et al. (1984). Differential effects of mecamylamine on the nicotine induced changes in amine levels and turnover in hypothalamic dopamine and noradrenaline nerve terminal systems and in the secretion of adenohypophyseal hormones in the castrated female rat. Evidence for involvement of cholinergic nicotine-like receptors. Acta Physiol Scand. — PubMed PMID: 6148837 · doi:10.1111/j.1748-1716.1984.tb07412.x

The effect of acute nicotine administration on plasma levels of the thyroid hormones and corticosterone in the rat

Animal study, 1983. Researchers gave rats a single injection of nicotine (200 micrograms per kilogram of body weight) into the abdomen and measured three hormones in their blood over 24 hours: the thyroid hormones thyroxine and triiodothyronine, and corticosterone, the rat's main stress hormone. Nicotine did not change the levels of either thyroid hormone. It did significantly raise corticosterone, which peaked 20 minutes after the injection and stayed raised for 45 minutes. These results come from rats only, not people.

Cam GR, Bassett JR (1983). The effect of acute nicotine administration on plasma levels of the thyroid hormones and corticosterone in the rat. Pharmacol Biochem Behav. — PubMed PMID: 6634906 · doi:10.1016/0091-3057(83)90135-1

Involvement of cholinergic nicotine-like receptors as modulators of amine turnover in various types of hypothalamic dopamine and noradrenaline nerve terminal systems and of prolactin, LH, FSH and TSH secretion in the castrated male rat

Animal study, 1982. This study was done only in male rats that had been castrated long before. The rats were given repeated high doses of nicotine (4 injections of 2 mg/kg under the skin), and the researchers measured how fast two brain messengers, dopamine and noradrenaline, were used up in the hypothalamus, along with blood levels of four hormones: prolactin, LH, FSH and TSH. Nicotine sped up the turnover of dopamine and noradrenaline in several hypothalamic areas and lowered blood prolactin and TSH; LH and FSH also fell when a drug blocking dopamine and noradrenaline production was given as well. Most of these effects were blocked by mecamylamine, a drug that blocks nicotinic receptors, so the authors suggest nicotine acts through these receptors to change the nerve signals that control hormone release.

Andersson K, Fuxe K, Eneroth P et al. (1982). Involvement of cholinergic nicotine-like receptors as modulators of amine turnover in various types of hypothalamic dopamine and noradrenaline nerve terminal systems and of prolactin, LH, FSH and TSH secretion in the castrated male rat. Acta Physiol Scand. — PubMed PMID: 6818838 · doi:10.1111/j.1748-1716.1982.tb10597.x

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