Forebrain and brainstem afferents to the arcuate nucleus in the rat: Potential pathways for the modulation of hypophyseal secretions

Gruber, Kenneth A.; McRae-Degueurce, A.; Wilkin, Lawrence D.; Mitchell, L.D.; Johnson, Alan Kim

doi:10.1016/0304-3940(87)90065-6

Cited by 54 publications

(23 citation statements)

References 4 publications

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“…Because the SFO has been implicated in mediating the pressor responses of circulating ANG II (14) and we have shown that the pressor effects of intravenous ANG II and ANG-(1-12) are attenuated when the ARCN is inhibited by muscimol, it appears that direct or indirect projections from the SFO to the ARCN may exist. Indeed, direct projections from the SFO to the ARCN have been reported based on a retrograde tracing study (16). In this context, it may be noted that direct or indirect projections from the ARCN to the SFO have also been reported (39,40).…”

Section: Discussionmentioning

confidence: 91%

The hypothalamic arcuate nucleus: a new site of cardiovascular action of angiotensin-(1–12) and angiotensin II

Arakawa

Chitravanshi

Sapru

2011

American Journal of Physiology-Heart and Circulatory Physiology

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Arakawa H, Chitravanshi VC, Sapru HN. The hypothalamic arcuate nucleus: a new site of cardiovascular action of angiotensin-(1-12) and angiotensin II. Am J Physiol Heart Circ Physiol 300: H951-H960, 2011. First published December 24, 2010 doi:10.1152/ajpheart.01144.2010.-The hypothalamic arcuate nucleus (ARCN) has been reported to play a significant role in cardiovascular regulation. It has been hypothesized that the ARCN may be one of the sites of cardiovascular actions of angiotensins (ANGs). Experiments were carried out in urethaneanesthetized, artificially ventilated, adult male Wistar rats. The ARCN was identified by microinjections of N-methyl-D-aspartic acid (NMDA; 10 mM). Microinjections (50 nl) of ANG-(1-12) (1 mM) into the ARCN elicited increases in mean arterial pressure (MAP), heart rate (HR), and greater splanchnic nerve activity (GSNA). The tachycardic responses to ANG-(1-12) were attenuated by bilateral vagotomy. The cardiovascular responses elicited by ANG-(1-12) were attenuated by microinjections of ANG II type 1 receptor (AT1R) antagonists but not ANG type 2 receptor (AT2R) antagonist. Combined inhibition of ANG-converting enzyme (ACE) and chymase in the ARCN abolished ANG-(1-12)-induced responses. Microinjections of ANG II (1 mM) into the ARCN also increased MAP and HR. Inhibition of ARCN by microinjections of muscimol (1 mM) attenuated the pressor and tachycardic responses to intravenously administered ANG-(1-12) and ANG II (300 pmol/kg each). These results indicated that 1) microinjections of ANG-(1-12) into the ARCN elicited increases in MAP, HR, and GSNA; 2) HR responses were mediated via both sympathetic and vagus nerves; 3) AT1Rs, but not AT2Rs, in the ARCN mediated ANG-(1-12)-induced responses; 4) both ACE and chymase were needed to convert ANG-(1-12) to ANG II in the ARCN; and 5) ARCN plays a role in mediating the cardiovascular responses to circulating ANGs. blood pressure; heart rate; microinjection; N-methyl-D-aspartic acid; sympathetic nerve activity THE HYPOTHALAMIC ARCUATE NUCLEUS (ARCN) may play a significant role in cardiovascular regulation (10, 38). Consistent with this notion, we (31) have recently reported that chemical stimulation of the ARCN elicited increases in mean arterial pressure (MAP), heart rate (HR), and sympathetic nerve activity (SNA). These reports have provided a basis for investigations on different neurotransmitters and neuromodulators in the ARCN that may play a role in the regulation of cardiovascular function in normal and pathological states.A new endogenous angiotensin (ANG), ANG-(1-12), has recently been identified (30,44). Intravenous administration of this peptide has been reported to elicit an immediate pressor response in the rat, and this effect was blocked by prior administration of an ANG-converting enzyme (ACE) inhibitor or an ANG II type 1 receptor (AT 1 R) antagonist (30). These data indicated that in the periphery, ANG-(1-12) exerts its actions via a rapid conversion to ANG II (30). High concentrations of ANG-(1-12) have been reported in th...

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Section: Discussionmentioning

confidence: 91%

The hypothalamic arcuate nucleus: a new site of cardiovascular action of angiotensin-(1–12) and angiotensin II

Arakawa

Chitravanshi

Sapru

2011

American Journal of Physiology-Heart and Circulatory Physiology

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“…SFO neurons send dense efferent projections to important hypothalamic autonomic control centers including the paraventricular (PVN), supraoptic (SON), arcuate, median preoptic, and lateral hypothalamic nuclei of the hypothalamus (21,28,30,33,34). SFO neurons also receive afferent inputs primarily derived from lateral hypothalamus (29, 53), median preoptic nucleus (29), lateral parabrachial nucleus (22), and nucleus tractus solitarius (52, 57).…”

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confidence: 99%

“…It is one of the sensory circumventricular organs (CVOs) and as such is distinct from the rest of the central nervous system (CNS) in its extensive vascular supply, which is derived from specialized capillaries lacking the normal blood-brain barrier (20). The SFO has also been shown to contain receptors for, and that respond to, a variety of different peripheral signals including regulatory peptides (e.g., angiotensin, amylin, ghrelin, atrial natriuretic peptide, and endothelin) (7, 32, 40, 48, 55), steroids (e.g., estradiol) (45), and ionic constituents of the extracellular environment (e.g., osmolarity, Ca 2ϩ , Na ϩ ) (3, 37, 44).SFO neurons send dense efferent projections to important hypothalamic autonomic control centers including the paraventricular (PVN), supraoptic (SON), arcuate, median preoptic, and lateral hypothalamic nuclei of the hypothalamus (21,28,30,33,34). SFO neurons also receive afferent inputs primarily derived from lateral hypothalamus (29, 53), median preoptic nucleus (29), lateral parabrachial nucleus (22), and nucleus tractus solitarius (52, 57).…”

mentioning

confidence: 99%

Microarray analysis of the transcriptome of the subfornical organ in the rat: regulation by fluid and food deprivation

Hindmarch

Fry²,

Yao³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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We have employed microarray technology using Affymetrix 230 2.0 genome chips to initially catalog the transcriptome of the subfornical organ (SFO) under control conditions and to also evaluate the changes (common and differential) in gene expression induced by the challenges of fluid and food deprivation. We have identified a total of 17,293 genes tagged as present in one of our three experimental conditions, transcripts, which were then used as the basis for further filtering and statistical analysis. In total, the expression of 46 genes was changed in the SFO following dehydration compared with control animals (22 upregulated and 24 downregulated), with the largest change being the greater than fivefold increase in brain-derived neurotrophic factor (BDNF) expression, while significant changes in the expression of the calcium-sensing (upregulated) and apelin (downregulated) receptors were also reported. In contrast, food deprivation caused greater than twofold changes in a total of 687 transcripts (222 upregulated and 465 downregulated), including significant reductions in vasopressin, oxytocin, promelanin concentrating hormone, cocaine amphetamine-related transcript (CART), and the endothelin type B receptor, as well as increases in the expression of the GABA(B) receptor. Of these regulated transcripts, we identified 37 that are commonly regulated by fasting and dehydration, nine that were uniquely regulated by dehydration, and 650 that are uniquely regulated by fasting. We also found five transcripts that were differentially regulated by fasting and dehydration including BDNF and CART. In these studies we have for the first time described the transcriptome of the rat SFO and have in addition identified genes, the expression of which is significantly modified by either water or food deprivation.

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“…Neurons in the CVOs are bathed continuously by all constituents of the circulation, and amylin activates area postrema ) and SFO (Riediger et al, 1999) neurons. SFO efferents project to hypothalamic centers regulating feeding , including arcuate (Gruber et al, 1987), paraventricular, and supraoptic nuclei, and lateral hypothalamus (Miselis, 1981(Miselis, , 1982Silverman et al, 1981;Lind et al, 1982).…”

Section: Introductionmentioning

confidence: 99%

The Subfornical Organ: A Central Target for Circulating Feeding Signals

Pulman¹,

Fry²,

Cottrell³

et al. 2006

J. Neurosci.

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The mechanisms through which circulating ghrelin relays hunger signals to the CNS are not yet fully understood. In this study, we have examined the potential role of the subfornical organ (SFO), a circumventricular structure that lacks the normal blood-brain barrier, as a CNS site in which ghrelin acts to influence the hypothalamic centers controlling food intake. We report that ghrelin increased intracellular calcium concentrations in 28% (12 of 43) of dissociated SFO neurons and that the SFO expresses mRNA for the growth hormone secretagogue receptor. Whole-cell patch recordings from SFO neurons demonstrated that in 29% (9 of 31) of neurons tested ghrelin induced a mean depolarization of 7.4 Ϯ 0.69 mV, accompanied by an increase in action potential frequency. Voltage-clamp recordings revealed that ghrelin activates a putative nonselective cationic conductance.Previous reports that the satiety signal amylin exerts similar excitatory effects on SFO neurons led us to examine whether these two peptides influence different subpopulations of SFO neurons. Concentration-dependent depolarizing effects of amylin were observed in 59% (28 of 47) of SFO neurons (mean depolarization, 8.32 Ϯ 0.60 mV). In contrast to ghrelin, voltage-clamp recordings suggest that amylin influences a voltage-dependent current activated at depolarized potentials. We tested single SFO neurons with both peptides and identified cells responsive only to ghrelin (n ϭ 9) and only to amylin (n ϭ 7) but no cells that responded to both peptides. These data support a role for the SFO as a center at which ghrelin and amylin may influence separate subpopulations of neurons to influence the hypothalamic regulation of feeding.

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Forebrain and brainstem afferents to the arcuate nucleus in the rat: Potential pathways for the modulation of hypophyseal secretions

Cited by 54 publications

References 4 publications

The hypothalamic arcuate nucleus: a new site of cardiovascular action of angiotensin-(1–12) and angiotensin II

The hypothalamic arcuate nucleus: a new site of cardiovascular action of angiotensin-(1–12) and angiotensin II

Microarray analysis of the transcriptome of the subfornical organ in the rat: regulation by fluid and food deprivation

The Subfornical Organ: A Central Target for Circulating Feeding Signals

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