Evidence for the presence of nicotinic receptors on rat subfornical organ neurons

Ono, Katsushige; Honda, Eiko; Toyono, Takashi; Kataoka, Shinji; Nakamura, Taiji; Inenaga, Kiyotoshi

doi:10.1016/s1566-0702(03)00150-4

Cited by 9 publications

(4 citation statements)

References 10 publications

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“…Nicotine levels in the plasma during cigarette smoking increase up to approximately 0.5 µM (18). We have recently reported that neurons in the subfornical organ, which lack the blood–brain barrier, are excited by 1 µ m nicotine (15). In the present study, significant responses by nicotine injection in gingival blood flow were obtained at 15 µg/20 µl.…”

Section: Discussionmentioning

confidence: 99%

“…Subcutaneous nicotine injection increases expression of c‐fos in the hypothalamus, suggesting that peripheral nicotine administration stimulates the central nervous system (14). Recently, we reported that some of the neurons in the subfornical organ, which has efferent connections to the hypothalamus, were activated by nicotine (15). However, it is unclear whether central nicotinic stimulation changes gingival blood flow and gingival vascular conductance.…”

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confidence: 99%

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Central nicotinic stimulation reduces vascular conductance in the gingiva in anesthetized rats

Nakamura

Ono²,

Honda³

et al. 2004

J of Periodontal Research

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Central nicotinic stimulation reduces vascular conductance in the gingiva in anesthetized rats

Nakamura

Ono²,

Honda³

et al. 2004

J of Periodontal Research

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“…Fluorescent immunohistochemistry was performed as reported previously (18). Three adult Wistar rats (6 -8 wk old) were used for the immunohistochemistry.…”

Section: Methodsmentioning

confidence: 99%

Activation of subfornical organ neurons in rats through pre- and postsynaptic α-adrenoceptors

Honda

Ono²,

Kataoka³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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(NA) and its analogs on subfornical organ (SFO) neurons in rat slice preparations were investigated by using whole cell patch-clamp recording. In the current-clamp mode, the application of NA at 10 -100 M produced membrane depolarization (63%, 17 responsive neurons/27 neurons tested) and hyperpolarization (22%, 6/27 neurons). In the voltage-clamp mode, NA application at 1-100 M produced inward currents (69%, 42/61 neurons) and outward currents (23%, 14/61 neurons). These currents remained in the presence of TTX or both glutamate and GABA receptor antagonists. In most of the neurons (25/31 neurons) showing inward currents in the presence of NA, the membrane conductance was not changed by voltage ramps or hyperpolarizing pulse stimulation. Similar responses were obtained by the application of the ␣ 1-agonist phenylephrine. The phenylephrineinduced inward currents were inhibited by the ␣1-antagonist prazosin. The ␣ 2-agonist clonidine decreased the frequency of spontaneous GABAergic inhibitory postsynaptic currents (4/10 neurons). In addition, RT-PCR assay and immunohistochemical staining showed the existence of ␣ 1-adrenoceptors in the SFO. The results suggest that SFO neurons in rats are activated postsynaptically through ␣ 1-adrenoceptors and that the activation is enhanced by suppressing GABAergic inhibitory synaptic inputs through presynaptic ␣ 2-adrenoceptors. patch clamp; slice preparation; noradrenaline THE SUBFORNICAL ORGAN (SFO), which juts ventrally from the hippocampal commissura into the third cerebral ventricle, is a circumventricular organ. The SFO receives various neural inputs from brain regions, whereas it lacks a blood-brain barrier and has an abundant vascular supply (for a review, see Ref. 14). From these properties, the SFO has been thought to possess various sensors for neurotransmitters and blood-and cerebrospinal fluid-borne substances, and subsequently to control body fluid balance and the cardiovascular system (for reviews, see Refs. 8 and 15). In fact, angiotensinergic, cholinergic, and hypertonic activation of SFO neurons elicits water intake (23) and vascular responses, and increases vasopressin release from the posterior pituitary (11,12). Noradrenaline (NA), which is released from catecholaminergic fibers and the adrenal medulla, may be one of such bioactive substances affecting SFO neurons. The catecholaminergic neurons in the A1 and A2 areas of the medulla project directly to various brain regions, including the SFO (3, 10). The NA level in the region of the SFO is increased by hemorrhage, whereas it is decreased by an elevation in arterial pressure (26). The peripheral baroreceptor information may be transmitted from the nucleus of the solitary tract to the SFO through ␣-adrenoceptors (16, 25). Further, microinjection of NA into the SFO increases water intake (17). Thus NA at the level of the SFO may play an important role in the regulation of cardiovascular function and body fluid homeostasis. However, little is known about whether the SFO neurons themselves are directly affec...

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“…Interestingly, the central injection of NKB or specific NK 3 agonists increases blood pressure and vasopressin release, but does not induce drinking behavior [4][5][6]. 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.…”

Section: Introductionmentioning

confidence: 94%

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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Evidence for the presence of nicotinic receptors on rat subfornical organ neurons

Cited by 9 publications

References 10 publications

Central nicotinic stimulation reduces vascular conductance in the gingiva in anesthetized rats

Central nicotinic stimulation reduces vascular conductance in the gingiva in anesthetized rats

Activation of subfornical organ neurons in rats through pre- and postsynaptic α-adrenoceptors

Neuronal effects of neurokinin B on the rat subfornical organ

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