Cell subpopulations of nicotine-sensitive subfornical organ neurons in rat

Ono, Kentaro; Miyahara, Nobutaka; Inenaga, Kiyotoshi

doi:10.1016/j.neulet.2008.06.078

Cited by 8 publications

(4 citation statements)

References 14 publications

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“…Similar to the central NKB effects, central injection of nicotine induces the pressor response and vasopressin release [7,8], probably by nicotinic receptors in the subfornical organ [9,10]; however, it also induces a very small (but statistically significant) amount of water intake [11,12]. As we observed nicotinic excitation of angiotensin IIinsensitive subfornical organ neurons [11,13], the nucleus may be heterogeneously composed of different functionally related cell subpopulations. If so, NKB may also cause distinct neuronal effects on cell subpopulations in the subfornical organ.…”

Section: Introductionsupporting

confidence: 57%

Neuronal effects of neurokinin B on the rat subfornical organ

Ono¹,

Asami

Miyahara³

et al. 2011

NeuroReport

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The subfornical organ is an essential central nucleus for angiotensin II-induced body fluid regulation. Similar to angiotensin II, centrally injected neurokinin B (NKB) may induce cardiovascular responses by the subfornical organ; however, it does not induce water intake. To clarify this inconsistency, we investigated the neuronal effects of NKB on subfornical organ neurons in slice preparations along with its behavioral effects in vivo. In electrophysiological extracellular recordings, NKB excited angiotensin II-insensitive and inhibited angiotensin II-sensitive neurons. Centrally injected NKB inhibited peripherally injected angiotensin II-induced water intake. These results suggest that NKB-mediated neuronal effects on the subfornical organ are likely to be involved in antidipsogenic responses in addition to the previously reported cardiovascular responses.

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Section: Introductionsupporting

confidence: 57%

Neuronal effects of neurokinin B on the rat subfornical organ

Ono¹,

Asami

Miyahara³

et al. 2011

NeuroReport

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“…Intracerebroventricular injection of ANG II and nicotine have both been shown to elevate expression of c-Fos (a marker of neuronal activation) in the subfornical organ and acutely promote water drinking behavior (106,115). Patch-clamp recording of cells dissociated from this region revealed a subpopulation of neurons that have an excitatory response to both ANG II and nicotine (107). Future studies could clarify whether selective excitation of these neurons is associated with a sympathetic response such as elevated systemic BP and how nicotine and the RAS may modulate this response.…”

Section: Nicotine and The Ras In The Nervous Systemmentioning

confidence: 99%

Nicotine and the renin-angiotensin system

Oakes

Fuchs

Gardner

et al. 2018

American Journal of Physiology-Regulatory, Integrative and Comp

275

268

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Cigarette smoking is the single most important risk factor for the development of cardiovascular and pulmonary diseases (CVPD). Although cigarette smoking has been in constant decline since the 1950's, the introduction of e-cigarettes or electronic nicotine delivery systems 10 years ago has attracted former smokers as well as a new generation of consumers. Nicotine is a highly addictive substance, and it is currently unclear whether e-cigarettes are "safer" than regular cigarettes or whether they have the potential to reverse the health benefits, notably on the cardiopulmonary system, acquired with the decline of tobacco smoking. Of great concern, nicotine inhalation devices are becoming popular among young adults and youths, emphasizing the need for awareness and further study of the potential cardiopulmonary risks of nicotine and associated products. This review focuses on the interaction between nicotine and the renin-angiotensin system (RAS), one of the most important regulatory systems on autonomic, cardiovascular and pulmonary functions in both health and disease. The literature presented in this review strongly suggests that nicotine alters the homeostasis of the RAS by up-regulating the detrimental angiotensin converting enzyme (ACE)/Angiotensin (Ang)-II/Ang-II type 1 receptor (ATR) axis and down-regulating the compensatory ACE2/Ang-(1-7)/Mas receptor axis, contributing to the development of CVPD.

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“…The SFO plays an important role in body fluid homeostasis, particularly drinking, cardiovascular regulation, and vasopressin release. 94 Neurons in the SFO organ are activated by central application of nicotine and plasmatic angiotensin II. 81 Most of the fibers originating from these neurons reach the paraventricular and supraoptic hypothalamic nuclei and thus regulate the release of vasopressin.…”

Section: Circumventricular Organsmentioning

confidence: 99%

Nonlesions, Unusual Cell Types, and Postmortem Artifacts in the Central Nervous System of Domestic Animals

Wohlsein¹,

Deschl

Baumgärtner³

2012

Vet Pathol

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In the central nervous system (CNS) of domestic animals, numerous specialized normal structures, unusual cell types, findings of uncertain or no significance, artifacts, and various postmortem alterations can be observed. They may cause confusion for inexperienced pathologists and those not specialized in neuropathology, leading to misinterpretations and wrong diagnoses. Alternatively, changes may mask underlying neuropathological processes. ''Specialized structures'' comprising the hippocampus and the circumventricular organs, including the vascular organ of the lamina terminalis, subfornical organ, subcommissural organ, pineal gland, median eminence/neurohypophyseal complex, choroid plexus, and area postrema, are displayed. Unusual cell types, including cerebellar external germinal cells, CNS progenitor cells, and Kolmer cells, are presented. In addition, some newly recognized cell types as of yet incompletely understood significance and functionality, such as synantocytes and aldynoglia, are introduced and described. Unusual reactive astrocytes in cats, central chromatolysis, neuronal vacuolation, spheroids, spongiosis, satellitosis, melanosis, neuromelanin, lipofuscin, polyglucosan bodies, and psammoma bodies may represent incidental findings of uncertain or no significance and should not be confused with significant microscopic changes. Auto-and heterolysis as well as handling and histotechnological processing may cause postmortem morphological changes of the CNS, including vacuolization, cerebellar conglutination, dark neurons, Buscaino bodies, freezing, and shrinkage artifacts, all of which have to be differentiated from genuine lesions. Postmortem invasion of microorganisms should not be confused with intravital infections. Awareness of these different changes and their recognition are a prerequisite for identifying genuine lesions and may help to formulate a professional morphological and etiological diagnosis.

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Cell subpopulations of nicotine-sensitive subfornical organ neurons in rat

Cited by 8 publications

References 14 publications

Neuronal effects of neurokinin B on the rat subfornical organ

Neuronal effects of neurokinin B on the rat subfornical organ

Nicotine and the renin-angiotensin system

Nonlesions, Unusual Cell Types, and Postmortem Artifacts in the Central Nervous System of Domestic Animals

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