Biomedical subjects

J Ciriello

Publications and source records attributed to J Ciriello.

At least 19 recordsLinked to original sources

PubMed1999

Co-localization of estrogen and angiotensin receptors within subfornical organ neurons.

A double-staining immunocytochemical study was done in ovariectomized (OVX) female rats that were either treated with 17beta-estradiol (E(2)) (OVX+E(2)) to produce an approximate circulating level of 30 pg/ml plasma, or not-treated with E(2) (OVX), to investigate the distribution of subfornical organ (SFO) neurons that contained estrogen receptors (ER), and to determine whether these neurons also contained the angiotensin II AT(1)-receptor (AT(1)R). Neurons that contained either ER-like immunoreactivity only, AT(1)R-like immunoreactivity only, or both ER and AT(1)R immunoreactivity were found throughout the extent of the SFO in both the OVX+E(2) and OVX rats. However, some regional differences were apparent in both groups of female rats. Neurons containing the ER were predominantly found in the peripheral regions of the SFO, near large blood vessels and the ependymal layer of the third ventricle. A number of lightly stained ER containing neurons was also observed scattered throughout the central core region of the SFO. OVX only animals were found to have a larger number of ER containing neurons in the SFO compared to the E(2) treated animals. Neurons containing AT(1)R were also found throughout the SFO, but without a distinct distribution pattern in either group of rats, although there were more neurons that exhibited AT(1)R immunoreactivity in the OVX animals. Finally, a distinct group of SFO neurons was found that exhibited both ER and AT(1)R immunoreactivity in both groups of animals, although a larger number of these double labelled neurons was found in the OVX animal. Most of these neurons were also found along the peripheral border of the SFO in close proximity to blood vessels and the ventricular lining. These data have demonstrated the co-existence of ER and AT(1)R in SFO neurons of the female rat, and suggest that circulating level of E(2) alter the expression of both the ER and AT(1)R in these neurons. In addition, these data suggest that E(2) may alter the physiological responses of SFO neurons to angiotensin II by down regulating the number of AT(1)R.

Animals↗

PubMed1999

Effect of noradrenergic inputs on the cardiovascular depressor responses to stimulation of central nucleus of the amygdala.

Experiments were done in chloralose anesthetized, paralyzed and artificially ventilated male Wistar rats to investigate the effects of microinjections of either norepinephrine (NE) or tyramine into the central nucleus of the amygdala (ACe) on the arterial pressure (AP) and heart rate (HR) responses elicited by glutamate (Glu) stimulation of the ACe. Microinjections of Glu into the ACe elicited decreases in mean AP (-23+/-3 mmHg) and HR (-11+/-3 bpm). Microinjections of NE or tyramine into these sites did not elicit cardiovascular responses. However, Glu into the ACe in the presence of NE or tyramine elicited depressor or bradycardic response that were significantly smaller (70-100%) in magnitude than to Glu alone. These data suggest that noradrenergic mechanisms in the ACe alter the excitability of ACe neurons involved in mediating changes in systemic AP and HR.

Amygdala↗

PubMed1999

GABAergic effects on the depressor responses elicited by stimulation of central nucleus of the amygdala.

GABAergic inputs have been demonstrated in the central nucleus of the amygdala (ACe). However, the contribution of these inhibitory inputs to the cardiovascular responses elicited from the ACe is not known. Experiments were done in chloralose-anesthetized, paralyzed, and artificially ventilated male Wistar rats to investigate the effects of microinjections of GABA, the selective GABAA-receptor antagonist bicuculline, or the GABAB-receptor antagonist phaclofen, in the ACe on the mean arterial pressure (MAP) and heart rate (HR) responses elicited by L-glutamate (Glu) stimulation of the ACe. Microinjections of Glu in the ACe elicited decreases in MAP (-13.7 +/- 1.6 mmHg) and HR (-5.3 +/- 1.9 beats/min). The MAP and HR responses elicited by Glu stimulation of the ACe were significantly reduced (89%) by the prior microinjection of GABA in the same ACe site. In addition, at some sites in the ACe at which microinjection of Glu did not elicit depressor responses, Glu injections in the presence of phaclofen elicited decreases in MAP (-9.5 +/- 1.0 mmHg) and variable changes in HR. On the other hand, the magnitude of the depressor responses elicited during stimulation of the ACe site in the presence of bicuculline was significantly attenuated (60%), whereas phaclofen had no effect on the magnitude of the depressor responses elicited by Glu stimulation of the ACe. These data suggest that GABAergic mechanisms in the ACe alter the excitability of ACe neurons involved in mediating changes in systemic arterial pressure and HR.

Amygdala↗

PubMed1999

c-Fos induction in spinal cord neurons after renal arterial or venous occlusion.

Experiments were done in the anesthetized rat to identify the dorsal root ganglia (DRG) and the spinal cord segments that contain neurons activated by either renal venous occlusion (RVO) or by renal arterial occlusion (RAO). Fos induction, detected immunohistochemically in DRG and the spinal cord neurons, was used as a marker for neuronal activation. RVO induced Fos immunoreactivity in neurons in the DRG of spinal segments T8-L2 on the side ipsilateral to that of occlusion. The largest number of Fos-labeled neurons was found in the T11 DRG. In the spinal cord the largest number of Fos-labeled neurons was found in the ipsilateral dorsal horn of spinal segments T11-T12, predominantly in a cluster near the dorsomedial edge of laminae I-II. A few additional Fos-labeled neurons were observed in laminae IV and V. After RAO Fos-labeled neurons were found in the ipsilateral DRG of spinal segments similar to those observed to contain neurons after RVO. However, most of the Fos-labeled neurons were observed within the T12-L1 DRG. In the spinal cord Fos-labeled neurons were scattered throughout lamina I-II of the ipsilateral dorsal horn of spinal segments T8-L2, although the largest number was observed at the T13 level. Additionally, a distinct cluster of Fos-labeled neurons was observed predominantly in the region of the ipsilateral intermediolateral cell column, although a few neurons were found scattered throughout the nucleus intercalatus, central autonomic areas, and laminae IV and V of the cord bilaterally. No Fos labeling was observed in the complementary contralateral DRG or dorsal horns after either RVO or RAO. In addition, renal nerve transection prevented Fos labeling in the ipsilateral DRG and dorsal horns after RVO or RAO. Taken together, these data suggest that functionally different renal afferent fibers activate DRG neurons that may have distinct projections in the spinal cord.

Animals↗

PubMed1998

Afferent renal inputs to paraventricular nucleus vasopressin and oxytocin neurosecretory neurons.

Extracellular single-unit recording experiments were done in pentobarbital sodium-anesthetized rats to investigate the effects of electrical stimulation of afferent renal nerves (ARN) and renal vein (RVO) or artery (RAO) occlusion on the discharge rate of putative arginine vasopressin (AVP) and oxytocin (Oxy) neurons in the paraventricular nucleus of the hypothalamus (PVH). PVH neurons antidromically activated by electrical stimulation of the neurohypophysis were classified as either AVP or Oxy secreting on the basis of their spontaneous discharge patterns and response to activation of arterial baroreceptors. Ninety-eight putative neurosecretory neurons in the PVH were tested for their response to electrical stimulation of ARN: 44 were classified as putative AVP and 54 as putative Oxy neurons. Of the 44 AVP neurons, 52% were excited, 7% were inhibited, and 41% were nonresponsive to ARN stimulation. Of the 54 Oxy neurons, 43% were excited, 6% inhibited, and 51% were not affected by ARN. An additional 45 neurosecretory neurons (29 AVP and 16 Oxy neurons) were tested for their responses to RVO and/or RAO. RVO inhibited 42% of the putative AVP neurons and 13% of the putative Oxy neurons. On the other hand, RAO excited 33% of the AVP and 9% of the Oxy neurons. No AVP or Oxy neurons were found to be excited by RVO or inhibited by RAO. These data indicate that sensory information originating in renal receptors alters the activity of AVP and Oxy neurons in the PVH and suggest that these renal receptors contribute to the hypothalamic control of AVP and Oxy release into the circulation.

Afferent Pathways↗

PubMed1997

Fos induction in central structures after afferent renal nerve stimulation.

Experiments were done in the conscious and unrestrained rat to identify central structures activated by electrical stimulation of afferent renal nerves (ARN) using the immunohistochemical detection of Fos-like proteins. Fos-labelled neurons were found in a number of forebrain and brainstem structures bilaterally, but with a contralateral predominance. Additionally, Fos-labelled neurons were found in the lower thoracolumbar spinal cord predominantly ipsilateral to the side of ARN stimulation. Within the forebrain, neurons containing Fos-like immunoreactivity after ARN stimulation were primarily found along the outer edge of the rostral organum vasculosum of the laminae terminalis, in the medial regions of the subfornical organ, in the median preoptic nucleus, in the ventral subdivision of the bed nucleus of the stria terminalis, along the lateral part of the central nucleus of the amygdala, throughout the deeper layers of the dysgranular insular cortex, in the parvocellular component of the paraventricular nucleus of the hypothalamus (PVH), and in the paraventricular nucleus of the thalamus. Additionally, a smaller number of Fos-labelled neurons was observed in the supraoptic nucleus, in the magnocellular component of the PVH and along the lateral border of the arcuate nucleus. Within the brainstem, Fos-labelled neurons were found predominantly in the commissural and medial subnuclei of the nucleus of the solitary tract and in the external subnucleus of the lateral parabrachial nucleus. A smaller number were observed near the caudal pole of the locus coeruleus, and scattered throughout the ventrolateral medullary and pontine reticular formation in the regions known to contain the A1, C1 and A5 catecholamine cell groups. The final area observed to contain Fos-labelled neurons in the central nervous system was the thoracolumbar spinal cord (T9-L1) which contained cells in laminae I-V of the dorsal horn ipsilateral to side of stimulation and in the intermediolateral cell column at the same levels bilaterally, but with an ipsilateral predominance. Few, if any Fos-labelled neurons were observed in the same structures of control animals in which the ARN were stimulated, but the renal nerves proximal to the site of stimulation were transected, or in the sham operated animals. These data indicate that ARN information originating in renal receptors is conveyed to a number of central areas known to be involved in the regulation of body fluid balance and arterial pressure, and suggest that this afferent information is an important component of central mechanisms regulating these homeostatic functions.

Afferent Pathways↗

PubMed1997

Cardiovascular effects of neurotensin microinjections into the nucleus of the solitary tract.

Neurotensin (NT) immunoreactivity and binding sites have been demonstrated to be extensively distributed throughout the caudal nucleus of the solitary tract (NTS). In this study, the cardiovascular effects of microinjecting the tridecapeptide neurotensin (NT) or its analogues NT 1-8 and [D-Trp11]NT into NTS were investigated in the chloralose-anesthetized, paralyzed and artificially ventilated rat. Microinjection of NT (10 pmol) elicited decreases in arterial pressure (AP) (-34 +/- 3 mm Hg) and heart rate (HR) (-28 +/- 2 beats/min), whereas microinjection of equimolar amounts of the NT fragment NT 1-8 elicited a significantly smaller depressor response (-14 +/- 3 mm Hg), but the bradycardic (-22 +/- 4 beats/min) response was similar in magnitude to that elicited by NT. On the other hand, microinjection of [D-Trp11]NT did not elicit cardiovascular responses from sites in NTS. In addition, the prior injection of [D-Trp11]NT into cardiovascular responsive sites in the NTS did not significantly reduce the AP or HR response to NT. The depressor response elicited by NT was not affected by bilateral vagotomy but was abolished by either C1-C2 spinal cord transection or the i.v. administration of the nicotinic receptor blocker hexamethonium bromide. The cardiac slowing was partially attenuated by either bilateral vagotomy (-19 +/- 2 beats/min), i.v. administration of atropine methyl bromide (-17 +/- 4 beats/min), i.v. administration of hexamethonium bromide (-11 +/- 4 beats/min) or by spinal cord transection (-12 +/- 3 beats/min), and completely abolished after total autonomic blockade or by combined bilateral vagotomy and spinal cord transection. These data have demonstrated that within a restricted region of the caudal NTS NT activates neurons that contribute to vasodepressor responses as a result of sympatho-inhibition and to bradycardia responses as a result of vagal excitation and sympatho-inhibition. Furthermore, these data suggest that NT may act as a neurotransmitter or modulator in central cardiovascular reflex pathways.

Animals↗

PubMed1997

Cardiovascular responses to glutamate stimulation of diagonal band of Broca.

Experiments were done in alpha-chloralose-anesthetized, paralyzed, and artificially ventilated rats to investigate the effect of L-glutamate stimulation of the diagonal band of Broca (DBB) on arterial pressure (AP) and heart rate (HR). Stimulation of the horizontal limb of the DBB (hDB) elicited decreases in both mean AP (MAP; -32.3 +/- 2.5 mmHg; n = 37) and HR (-32.5 +/- 3.8 beats/min; n = 33) at 84% of the sites stimulated. Stimulation of the vertical limb of the DBB (vDB) elicited significantly smaller decreases in MAP (-9.7 +/- 1.0 mmHg; n = 19) and HR (-13.5 +/- 1.8 beats/min; n = 7) at approximately 13% of the sites stimulated. Intravenous administration of the muscarinic receptor blocker atropine methylbromide had no effect on the magnitude of the MAP and HR responses to stimulation of the hDB. In contrast, administration of the nicotinic receptor blocker hexamethonium bromide abolished both the depressor and the bradycardic responses elicited by stimulation of the hDB. These data indicate that the hDB contains neurons that exert cardiovascular depressor effects and that these circulatory effects are mediated by the inhibition of sympathetic vasoconstrictor fibers to the vasculature, and cardioacceleratory fibers to the heart.

Animals↗

PubMed1997

Cardiovascular depressor responses to stimulation of substantia nigra and ventral tegmental area.

Experiments were done in alpha-chloralose-anesthetized, paralyzed, and artificially ventilated rats to investigate the effect of L-glutamate (Glu) stimulation of the substantia nigra (SN) and ventral tegmental area (VTA) on arterial pressure (AP) and heart rate (HR). Glu stimulation of the SN pars compacta (SNC) elicited decreases in both mean AP (MAP; -18.9 +/- 1.3 mmHg; n = 52) and HR (-26.1 +/- 1.6 beats/min; n = 46) at 81% of the sites stimulated. On the other hand, stimulation of the SN pars lateralis or pars reticulata did not elicit cardiovascular responses. Stimulation of the adjacent VTA region elicited similar decreases in MAP (-18.0 +/- 2.6 mmHg; n = 20) and HR (-25.4 +/- 3.8 beats/min; n = 17) at approximately 74% of the sites stimulated. Intravenous administration of the dopamine D2-receptor antagonist raclopride significantly attenuated both the MAP (70%) and the HR (54%) responses elicited by stimulation of the transitional region where the SNC merges with the lateral VTA (SNC-VTA region). Intravenous administration of the muscarinic receptor blocker atropine methyl bromide had no effect on the magnitude of the MAP and HR responses to stimulation of the SNC-VTA region, whereas administration of the nicotinic receptor blocker hexamethonium bromide significantly attenuated both the depressor and the bradycardic responses. These data suggest that dopaminergic neurons in the SNC-VTA region activate a central pathway that exerts cardiovascular depressor effects that are mediated by the inhibition of sympathetic vasoconstrictor fibers to the vasculature and cardioacceleratory fibers to the heart.

Analysis of Variance↗

PubMed1997

Medullary pathways mediating depressor responses from Na(+)-sensitive sites in nucleus of the solitary tract.

Two series of experiments were done in male Wistar rats to investigate the medullary pathways that mediate the depressor responses from sodium-sensitive sites in the nucleus of the solitary tract (NTS). In the first series, the anterograde tract tracer Phaseolus vulgaris leucoagglutinin (PHA-L) was iontophoresed unilaterally at sites in the NTS at which microinjections (20 nl) of a 154-175 mM NaCl solution elicited depressor responses. PHA-L injection sites were found to be localized within the medial subnucleus of the NTS (Sm). In the medulla, PHA-L-labeled fibers and presumptive terminal boutons were observed bilaterally, but with an ipsilateral predominance, throughout the rostrocaudal extent of the NTS the dorsal motor nucleus of the vagus, area postrema, the ventrolateral medulla (VLM), and nucleus ambiguus. The pontine region, containing the A5 catecholaminergic cell group and the parabrachial nucleus, also received projections from Sm. In the second series of experiments, the effect of blocking synaptic transmission in VLM with cobalt chloride (CoCl2; 5 mM, 100 nl) on the cardiovascular response elicited by microinjection (20 nl) of hypertonic saline (154-175 mM) into the ipsilateral Sm was investigated in the alpha-chloralose-anesthetized, paralyzed, and artificially ventilated rat. Microinjection of CoCl2 into VLM, at sites shown in the previous study to receive efferent projections from Sm, significantly attenuated the depressor (60%) and bradycardic (80%) responses to stimulation of Sm. These data indicate that the sodium-sensitive region of the caudal Sm innervates VLM neurons and suggest that these VLM neurons are involved in mediating the depressor and bradycardic responses elicited by changes in the extracellular concentration of sodium.

Animals↗

PubMed1997

Afferent renal inputs onto subfornical organ neurons responsive to angiotensin II.

Experiments were done in pentobarbital sodium-anesthetized rats to investigate the effect of electrical stimulation of afferent renal nerves (ARN) on the discharge rate of subfornical organ (SFO) neurons that responded to changes in plasma levels of angiotensin II (ANG II) and projected directly to the paraventricular nucleus of the hypothalamus (PVH). Extracellular recordings were made from 76 histologically verified single neurons in the SFO that were excited by intracarotid infusions of ANG II. Of these units, 54.8% (23 of 42) responded with excitation to ARN stimulation (mean onset latency, 125 +/- 35 ms). None of the SFO units excited by plasma ANG II were found to be inhibited by ARN stimulation. An additional 34 units in the SFO that were excited by plasma ANG II were also antidromically activated by stimulation of the PVH. Of these neurons, 17.8% (6 of 34) were also excited by stimulation of ARN. The results indicate that inputs from ARN converge onto SFO neurons that alter their discharge rate during changes in plasma concentration of ANG II and project directly to the PVH. These data suggest that ARN may play an important role in body fluid balance and circulatory regulation by modulating the activity of SFO neurons that function in the detection of blood-borne signals resulting from the decrease in extracellular fluid volume and arterial pressure and that influence the activity of hypothalamic nuclei that contain neurosecretory neurons.

Action Potentials↗

PubMed1997

Cardiovascular afferent inputs to ventral tegmental area.

Extracellular single-unit recording experiments were done in alpha-chloralose-anesthetized, paralyzed, and artificially ventilated rats to investigate the effect of selective activation of arterial baroreceptors and stimulation of cardiovascular depressor sites in the nucleus of the solitary tract (NTS) on the discharge rate of neurons in the ventral tegmental area (VTA). Electrical stimulation of the aortic depressor nerve (ADN), which is known to carry aortic baroreceptor afferent fibers only, excited 12 of 21 (mean onset latency 42.4 +/- 8.8 ms) and inhibited 2 of 21 (mean onset latency 42.5 +/- 6.5 ms) single units in the VTA. The discharge rate of VTA units was also altered during the reflex activation of arterial baroreceptors by the acute rise in arterial pressure (AP) to systemic injections of phenylephrine (10 micrograms/kg i.v.): 12 of 44 units were excited and 15 of 44 were inhibited. Units that responded to either ADN stimulation or the reflex activation of the baroreflex also responded to stimulation of depressor sites in the NTS. An additional 12 units that were found in barodenervated controls to be responsive to NTS stimulation were nonresponsive to selective activation of arterial baroreceptors. These data indicate that cardiovascular afferent inputs modulate the activity of neurons in the VTA and suggest that changes in systemic AP may exert an effect on the activity of neurons involved in mesolimbic and mesocortical function.

Animals↗

PubMed1997

Medullary inputs to nucleus accumbens neurons.

Extracellular single-unit recording experiments were done in alpha-chloralose-anesthetized, paralyzed, and artificially ventilated rats to investigate the effect of stimulation of the nucleus of the solitary tract (NTS) and the ventrolateral medulla (VLM) in the region of the A1 noradrenergic cell group on the activity of neurons in the nucleus accumbens (NA). In addition, the response of NA neurons to activation of the arterial baroreceptors was investigated. Electrical or glutamate (Glu) stimulation of the ipsilateral NTS excited 47 of 99 (48%) and inhibited 10 of 99 (10%) of the units tested in the NA. Similarly, electrical or Glu stimulation of the ipsilateral VLM excited 24 of 97 (24.7%) or inhibited 7 of 97 (7.2%) of the units tested. Approximately 22% (17 of 77) of these units responded to stimulation of both the NTS and VLM. Simultaneous stimulation of both the NTS and VLM potentiated the response of the NA neuron tested. CoCl2 injection into the ipsilateral NTS did not alter the response of NA neurons to stimulation of the VLM. Similarly, CoCl2 injections into the ipsilateral VLM did not alter the response of NA neurons to NTS stimulation. The discharge rate of some of the units (6 of 49) that were activated by both NTS and VLM was also increased during the activation of arterial baroreceptors by the acute rise in systemic arterial pressure to phenylephrine injection. Units that responded to stimulation of the NTS and VLM and to baroreceptor activation were located in the shell region of the NA. These data indicate that afferent inputs from the NTS and VLM converge onto NA neurons and suggest that visceral and cardiovascular afferent inputs may influence the output of neurons in the shell region of the NA.

Animals↗

PubMed1996

Effect of aortic baroreceptor deafferentation on plasma vasopressin and oxytocin in the conscious rat.

Experiments were done in conscious, unrestrained rats to investigate the effects of selective aortic baroreceptor deafferentation (ABD) on circulating levels of the neurohypophysial hormones arginine vasopressin (AVP) and oxytocin (OXY). Plasma concentration of AVP and OXY were measured by radioimmunoassay before and 1-13 days after cutting the aortic depressor nerves, bilaterally. Arterial pressure was significantly elevated by approximately 12-39 mmHg above control levels after ABD. On day one after ABD, plasma AVP increased from control levels of 3.21 +/- 1.56 pg/ml to 8.29 +/- 4.66 pg/ml (258%) and plasma OXY increased from 2.53 +/- 4.24 pg/ml to 8.16 +/- 1.49 pg/ml (323%). However, by the third day after ABD, plasma AVP and OXY levels had returned to pre-ABD control levels. On days 8 and 13 after ABD, AVP levels were elevated again by approximately 2- and 9-fold, respectively, whereas the OXY levels remained at control levels. These data suggest that in the awake rat, the release of AVP and OXY is modulated differentially after ABD and that the increased circulating levels of AVP may be one of the mechanisms that contributes to the elevated arterial pressure in neurogenic hypertension.

Afferent Pathways↗

PubMed1996

Direct projections to subfornical organ from catecholaminergic neurons in the caudal nucleus of the solitary tract.

Experiments were done to investigate the distribution of neurons within the nucleus of the solitary tract (NTS) that projected directly to the subfornical organ (SFO) and to determine whether these neurons were components of the catecholaminergic cell groups in the dorsal medial medulla. Microinjection of the fluorescent tract-tracers fluorogold or rhodamine latex micro-beads were made into the SFO of the rat. Brainstem sections were then processed immunocytochemically for the identification of neuronal cell bodies containing the catecholamine biosynthetic enzymes tyrosine hydroxylase (TH), dopamine beta-hydroxylase (DBH) or phenylethanolamine-N-methyltransferase (PNMT). Retrogradely labelled cell bodies that projected to the SFO were found in the NTS, bilaterally, extending from approximately the level of the rostral aspect of the area postrema (obex) caudally to the calamus scriptorius. These neurons were located predominantly in the medial, lateral and dorsolateral subdivisions of NTS. Approximately one-third of these retrogradely labelled neurons were immunoreactive to TH and DBH. On the other hand, less than 7% of the retrogradely labelled neurons were found to contain TH and PNMT immunoreactivity. These data have demonstrated that noradrenergic neurons of the A2 cell group in the caudal NTS innervate the SFO and suggest that these neurons may be involved in relaying cardiovascular afferent information directly to a forebrain circumventricular organ involved in arterial pressure and body fluid homeostasis.

Afferent Pathways↗

PubMed1996

Effect of lesions of forebrain circumventricular organs on c-fos expression in the central nervous system to plasma hypernatremia.

Experiments were carried out on conscious adult male Wistar rats to investigate the effect of selective ablation of the subfornical organ (SFO), and/or the anteroventral third ventricular (AV3V) region on the induction of Fos in central structures in response to plasma hypernatremia. Fos induction, detected immunohistochemically, was used as a marker for neuronal activation. Intravenous infusions of hypertonic saline resulted in dense Fos-like immunoreactivity in several forebrain (paraventricular nucleus of the hypothalamus (PVH), supraoptic nucleus (SON), median preoptic nucleus (MnPO), medial preoptic nucleus, organum vasculosum of the laminae terminalis and (SFO) and brainstem (nucleus of the solitary tract, ventrolateral medulla, and parabrachial nucleus) structures. Intravenous infusions of the hypertonic saline solution into animals with lesions of either the SFO, the AV3V or both resulted in a decreased number of Fos-like immunoreactive neurons in the MnPO, PVH and SON. In addition, the number of Fos-labeled neurons in the SON after lesions of both the SFO and the AV3V was significantly greater than that observed in isotonic saline infused controls. Finally, lesions of the forebrain circumventricular structures did not alter the Fos labeling in brainstem structures as a result of the infusion of the hypertonic solution. These data suggest that changes in plasma osmolality and/or concentration of sodium alter the activity of SON and brainstem neurons in the absence of afferent inputs from the SFO and AV3V.

Animals↗

PubMed1996

Changes in NADPH diaphorase activity in forebrain structures of the laminae terminalis after chronic dehydration.

The effect of 3-day chronic dehydration on nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-diaphorase) histochemical staining in forebrain circumventricular structures was investigated in the rat. Increased number and/or intensity of staining of NADPH-diaphorase positive neurons was observed in subfornical organ, organum vasculosum of the laminae terminalis, and median preoptic nucleus. In addition, dense punctate NADPH-diaphorase reaction product was found throughout the internal portion of median eminence. These data suggest the involvement of nitric oxide synthase producing neurons in homeostatic mechanisms controlling body fluid balance and the circulation.

Animals↗

PubMed1996

Arcuate nucleus inputs onto subfornical organ neurons that respond to plasma hypernatremia and angiotensin II.

Experiments were done in urethane anesthetized rats to investigate the effect of electrical and glutamate stimulation of arcuate nucleus (Arc) on the discharge rate of subfornical organ (SFO) neurons that responded to either plasma hypernatremia or angiotensin II (ANG II). Extracellular recordings were made from 253 histologically verified single neurons in SFO. Of these, 40.3% (102/253) responded with excitation and 10% (25/253) with inhibition to Arc stimulation. Thirty-five (34.3%) of the units excited by Arc were also excited by intracarotid infusion of hypertonic (0.5 M) NaCl. In addition, 37 (36.3%) of the units excited by Arc were also excited by intracarotid infusion of ANG II. Furthermore, 10 (40.0%) of the units inhibited by Arc were found to be excited by ANG II. None of the units inhibited by Arc stimulation were responsive to plasma hypernatremia. These data indicate that inputs from Arc neurons converge onto SFO neurons that alter their discharge rate during changes in plasma concentration of Na+ or ANG II. These results suggest that Arc may be involved in body fluid balance and circulatory regulation by modulating the activity of SFO neurons that function in the detection of blood-borne signals from the depletion of intra- and extra-cellular fluid volumes.

Angiotensin II↗