Mechanisms of hemodynamic responses to electrical stimulation of subfornical organ

1986 ◽  
Vol 250 (6) ◽  
pp. R1117-R1122 ◽  
Author(s):  
M. L. Mangiapane ◽  
M. J. Brody
Keyword(s):  
Electrical Stimulation ◽  
Pressor Response ◽  
Subfornical Organ ◽  
Constant Current ◽  
Pulsed Doppler ◽  
Mesenteric Circulation ◽  
Pressor Responses ◽  
Constant Current Stimulation ◽  
Vascular Beds ◽  
Stimulation Of

The rat subfornical organ (SFO) is involved in the pressor response to circulating angiotensin II, and recent evidence indicates that SFO electrical stimulation also produces a pressor response. In the present experiments we examined the hemodynamic, neural, and humoral mechanisms that underlie the pressor response to electrical stimulation of the SFO. Rats were anesthetized with urethan and instrumented with femoral arterial catheters and with pulsed Doppler flow probes on the superior mesenteric and renal arteries and on the abdominal aorta. Constant-current stimulation, delivered to the SFO via tungsten microelectrodes, resulted in stimulus-locked frequency-dependent pressor responses and vasoconstriction in all vascular beds tested. The stimulation-evoked increases in vascular resistance were greatest in the mesenteric circulation and least in the renal. Movement of the electrode away from the SFO produced significantly smaller responses. Ganglionic blockade abolished the responses to electrical stimulation, whereas vasopressin blockade significantly attenuated the responses. The responses of baroreceptor-denervated rats were qualitatively similar to but approximately double in magnitude of those of normal rats. We conclude that electrical stimulation of the SFO elicits widespread regional vasoconstriction that is most pronounced in the mesenteric circulation. The sympathetic nervous system appears responsible for these effects, but there may be facilitation of the responses by vasopressin.

Effect of paraventricular nucleus lesions on cardiovascular responses elicited by stimulation of the subfornical organ in the rat

1985 ◽  
Vol 63 (7) ◽  
pp. 816-824 ◽  
Author(s):  
Michael B. Gutman ◽  
John Ciriello ◽  
Gordon J. Mogenson
Keyword(s):  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Paraventricular Nucleus ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Subfornical Organ ◽  
Short Latency ◽  
Peak Latency ◽  
Ganglionic Blockade ◽  
Stimulation Of

It has recently been reported that stimulation of the region of the subfornical organ (SFO) elicits an increase in arterial pressure. However, the mechanisms and forebrain neural circuitry that are involved in this cardiovascular response have not been elucidated. The present study was done in urethane-anaesthetized rats to determine whether selective activation of SFO neurons elicit cardiovascular responses and whether these responses were mediated by a pathway involving the paraventricular nucleus of the hypothalamus (PVH). Stimulation sites which required the lowest threshold current (30 μA) to elicit a pressor response and at which the largest rise in mean arterial pressure (MAP; 22 ± 2 mmHg) was elicited at a constant current intensity (150 μA) were histologically localized in the region of the SFO. Short (mean peak latency; 4 ± 2 s) and long (mean peak latency; 61 ± 8 s) latency increases in MAP were observed during and after electrical stimulation of the SFO, respectively. Cardiac slowing accompanied the short latency pressor response and cardioacceleration was observed in most (57%) of the cases to accompany the late pressor response. Microinjection of L-glutamate into the SFO consistently elicited cardiovascular responses qualitatively similar to those observed during electrical stimulation. Ganglionic blockade abolished the short latency increase in MAP and the accompanying bradycardia. However, the long latency pressor and cardioacceleratory responses were not altered by ganglionic blockade and adrenalectomy. Selective bilateral electrolytic or kainic acid lesions of the region of the PVH significantly attenuated the cardiovascular responses elicited by stimulation of the SFO. These data suggest that activation of neurons in the SFO elicit cardiovascular responses partially mediated by sympathetic outflow through a neural pathway involving the PVH.

Functional identification of central pressor pathways originating in the subfornical organ

1991 ◽  
Vol 69 (7) ◽  
pp. 1035-1045 ◽  
Author(s):  
John Ciriello ◽  
Michael B. Gutman
Keyword(s):  
Spinal Cord ◽  
Electrical Stimulation ◽  
Paraventricular Nucleus ◽  
Supraoptic Nucleus ◽  
Subfornical Organ ◽  
Preoptic Nucleus ◽  
Thoracic Spinal Cord ◽  
Median Preoptic Nucleus ◽  
Pressor Responses ◽  
Stimulation Of

The functional projections from pressor sites in the subfornical organ (SFO) were identified using the 2-deoxyglucose (2-DG) autoradiographic method in urethane-anesthetized, sinoaortic-denervated rats. Autoradiographs of brain and spinal cord sections taken from rats whose SFO was continuously stimulated electrically for 45 min with stereotaxically placed monopolar electrodes (150 μA, 1.5-ms pulse duration, 15 Hz) following injection of tritiated 2-DG were compared with control rats that received intravenous infusions of pressor doses of phenylephrine to mimic the increase in arterial pressure observed during SFO stimulation. Comparisons were also made to autoradiographs from rats in which the ventral fornical commissure (CFV), just dorsal to the SFO, was electrically stimulated. The pressor responses during either electrical stimulation of the SFO or intravenous infusion of phenylephrine were similar in magnitude. On the other hand, stimulation of the CFV did not elicit a significant pressor response. Electrical stimulation of the SFO increased 2-DG uptake, in comparison to the phenylephrine-infused rats, in the nucleus triangularis, septofimbrial nucleus, lateral septal nucleus, nucleus accumbens, bed nucleus of the stria terminalis, dorsal and ventral nucleus medianus (median preoptic nucleus), paraventricular nucleus of the thalamus, hippocampus, supraoptic nucleus, suprachiasmatic nucleus, paraventricular nucleus of the hypothalamus, and the intermediolateral nucleus of and central autonomic area of the thoracic spinal cord. In contrast, in rats whose CFV was stimulated, these nuclei did not demonstrate changes in 2-DG uptake compared with control animals that received pressor doses of phenylephrine. These data have demonstrated some of the components of the neural circuitry likely involved in mediating the pressor responses to stimulation of the SFO and the corrective responses to activation of the SFO by disturbances to circulatory and fluid balance homeostasis.Key words: cardiovascular reflex pathways, drinking, median preoptic nucleus, osmoreceptors, paraventricular nucleus of the hypothalamus, supraoptic nucleus.

scholarly journals Stimulation of the paraventricular nucleus modulates firing of neurons in the nucleus of the solitary tract

1999 ◽  
Vol 277 (2) ◽  
pp. R403-R411 ◽  
Author(s):  
Yu-Fei Duan ◽  
Irwin J. Kopin ◽  
David S. Goldstein
Keyword(s):  
Electrical Stimulation ◽  
Paraventricular Nucleus ◽  
Pressor Response ◽  
Hypothalamic Paraventricular Nucleus ◽  
Solitary Tract ◽  
Defense Reaction ◽  
Neuronal Inhibition ◽  
Pressor Responses ◽  
Baroreceptor Stimulation ◽  
Stimulation Of

The present study assessed whether the baroreflex inhibition elicited by electrical stimulation of the hypothalamic paraventricular nucleus (PVN) involves altered activity in the nucleus of the solitary tract (NTS). Unit recordings were made from 107 neurons in the NTS in anesthetized rabbits. Intravenous phenylephrine was used to induce a pressor response and to activate baroreflexes. Of the neurons that responded to pressor responses, two-thirds were excited and one-third was inhibited. Stimulation of the PVN inhibited 70% of the phenylephrine-responsive NTS neurons, with or without concurrent baroreceptor stimulation. When PVN stimulation was delivered concurrently with phenylephrine injection, more NTS neuronal inhibition and less excitation occurred than with phenylephrine alone. Usually PVN stimulation inhibited NTS neurons that were excited by pressor responses; less commonly, PVN stimulation excited NTS neurons that were inhibited by pressor responses. The findings are consistent with the view that PVN activation during the defense reaction inhibits baroreflexes by altering firing of NTS neurons.

scholarly journals Tenderness of the Skin after Chemical Stimulation of Underlying Temporal and Thoracolumbar Fasciae Reveals Somatosensory Crosstalk between Superficial and Deep Tissues

Life ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 370
Author(s):  
Walter Magerl ◽  
Emanuela Thalacker ◽  
Simon Vogel ◽  
Robert Schleip ◽  
Thomas Klein ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Hypertonic Saline ◽  
Detection Threshold ◽  
Constant Current ◽  
Iliotibial Band ◽  
Deep Tissue ◽  
Test Parameter ◽  
Temporal Fascia ◽  
Sufficient Stimulus ◽  
Stimulation Of

Musculoskeletal pain is often associated with pain referred to adjacent areas or skin. So far, no study has analyzed the somatosensory changes of the skin after the stimulation of different underlying fasciae. The current study aimed to investigate heterotopic somatosensory crosstalk between deep tissue (muscle or fascia) and superficial tissue (skin) using two established models of deep tissue pain (namely focal high frequency electrical stimulation (HFS) (100 pulses of constant current electrical stimulation at 10× detection threshold) or the injection of hypertonic saline in stimulus locations as verified using ultrasound). In a methodological pilot experiment in the TLF, different injection volumes of hypertonic saline (50–800 µL) revealed that small injection volumes were most suitable, as they elicited sufficient pain but avoided the complication of the numbing pinprick sensitivity encountered after the injection of a very large volume (800 µL), particularly following muscle injections. The testing of fascia at different body sites revealed that 100 µL of hypertonic saline in the temporal fascia and TLF elicited significant pinprick hyperalgesia in the overlying skin (–26.2% and –23.5% adjusted threshold reduction, p < 0.001 and p < 0.05, respectively), but not the trapezius fascia or iliotibial band. Notably, both estimates of hyperalgesia were significantly correlated (r = 0.61, p < 0.005). Comprehensive somatosensory testing (DFNS standard) revealed that no test parameter was changed significantly following electrical HFS. The experiments demonstrated that fascia stimulation at a sufficient stimulus intensity elicited significant across-tissue facilitation to pinprick stimulation (referred hyperalgesia), a hallmark sign of nociceptive central sensitization.

Excitatory amino acid receptors within NTS mediate arterial chemoreceptor reflexes in rats

1993 ◽  
Vol 265 (2) ◽  
pp. H770-H773 ◽  
Author(s):  
W. Zhang ◽  
S. W. Mifflin
Keyword(s):  
Electrical Stimulation ◽  
Amino Acid ◽  
Receptor Antagonist ◽  
Carotid Body ◽  
Excitatory Amino Acid ◽  
Pressor Responses ◽  
Carotid Body Chemoreceptors ◽  
Arterial Chemoreceptor ◽  
Stimulation Of ◽  
Arterial Baroreceptor

The nucleus tractus solitarius (NTS) is the primary site of termination of arterial baroreceptor and chemoreceptor afferent fibers. Excitatory amino acid (EAA) receptors within NTS have been shown to play an important role in the mediation of arterial baroreceptor reflexes; however, the importance of EAA receptors within NTS in the mediation of arterial chemoreceptor reflexes remains controversial. Therefore, in chloralose-urethan-anesthetized, mechanically ventilated, paralyzed rats, 4 nmol of the broad-spectrum EAA receptor antagonist kynurenic acid (Kyn) was injected into the NTS to observe the effects of EAA receptor blockade on the pressor responses evoked by either activation of ipsilateral carotid body chemoreceptors (by close arterial injection of CO2-saturated bicarbonate) or electrical stimulation of ipsilateral carotid sinus nerve (CSN). Under control conditions, activation of carotid body chemoreceptors and CSN stimulation evoked increases in arterial pressure of 27 +/- 2 (n = 24 sites) and 28 +/- 3% (n = 8), respectively. Kyn microinjection into NTS significantly reduced the pressor responses evoked by activation of carotid body chemoreceptors and electrical stimulation of the CSN for 20 and 25 min, respectively. Attenuation of pressor responses evoked by chemoreceptor activation were maximal at 20 min post-Kyn injection (13 +/- 2%), whereas CSN-evoked pressor responses were maximally attenuated at 15 min (6 +/- 4%). Microinjection into NTS of 4 nmol of xanthurenic acid, a structural analogue of Kyn with no EAA receptor antagonist properties, had no effect on chemoreceptor reflexes. We conclude that EAA receptors within NTS play an important role in the mediation of arterial chemoreceptor reflexes.

Mechanisms of pressor response produced by stimulation of nucleus ambiguus

1990 ◽  
Vol 259 (5) ◽  
pp. R955-R962
Author(s):  
B. H. Machado ◽  
M. J. Brody
Keyword(s):  
Arterial Pressure ◽  
Vascular Resistance ◽  
Pressor Response ◽  
Nucleus Ambiguus ◽  
Ventrolateral Medulla ◽  
Pressor Responses ◽  
Regional Vascular Resistance ◽  
Parasympathetic Control ◽  
Renal Vascular ◽  
Stimulation Of

We showed previously that activation of nucleus ambiguus (NA) induced bradycardia and increased arterial pressure. In this study, we compared responses produced by electrical and chemical (glutamate) stimulation of NA and adjacent rostral ventrolateral medulla (RVLM). Equivalent pressor responses were elicited from both areas. However: 1) The response from RVLM was elicited at a lower frequency. 2) Regional vascular resistance changes were different, i.e., electrical stimulation of NA increased vascular resistance in hindquarters much more than the renal and mesenteric beds. In contrast, electrical and chemical stimulation of RVLM produced a more prominent effect on the renal vascular bed. 3) Bradycardia was elicited from NA at lower current intensity. 4) Glutamate produced bradycardia only when injected into NA. Studies in rats with sinoaortic deafferentation showed that bradycardic response to activation of NA was only partly reflex in origin. We conclude that 1) NA and RVLM control sympathetic outflow to regional vascular beds differentially and 2) the NA region involves parasympathetic control of heart rate and sympathetic control of arterial pressure.

scholarly journals Laminar Variation in Threshold for Detection of Electrical Excitation of Striate Cortex by Macaques

2005 ◽  
Vol 94 (5) ◽  
pp. 3443-3450 ◽  
Author(s):  
Edgar A. DeYoe ◽  
Jeffrey D. Lewine ◽  
Robert W. Doty
Keyword(s):  
Electrical Stimulation ◽  
Striate Cortex ◽  
Human Subjects ◽  
Human Case ◽  
Constant Current ◽  
Electrical Excitation ◽  
Detection Thresholds ◽  
Current Pulses ◽  
A Site ◽  
Stimulation Of

Macaques were trained to signal their detection of electrical stimulation applied by a movable microelectrode to perifoveal striate cortex. Trains of ≤100 cathodal, 0.2-ms, constant current pulses were delivered at 50 or 100 Hz. The minimum current that could be reliably detected was measured at successive depths along radial electrode penetrations through the cortex. The lowest detection thresholds were routinely encountered when the stimulation was applied to layer 3, particularly just at the juncture between layers 3 and 4A. On the average, there was a twofold variation in threshold along the penetrations, with the highest intracortical thresholds being in layers 4C and 6. Variations as high as 20-fold were obtained in some individual penetrations, whereas relatively little change was observed in others. The minimum detectable current was 1 μA at a site in layer 3, i.e., 10–100 times lower than that for surface stimulation. Because macaques, as do human subjects, find electrical stimulation of striate cortex to be highly similar at all loci (a phosphene in the human case), it is puzzling as to how such uniformity of effect evolves from the exceedingly intricate circuitry available to the effective stimuli. It is hypothesized that the stimulus captures the most excitable elements, which then suppress other functional moieties, producing only the luminance of the phosphene. Lowest thresholds presumably are encountered when the electrode lies among these excitable elements that can, with higher currents, be stimulated directly from some distance or indirectly by the horizontal bands of myelinated axons, the stria of Baillarger.

Adrenomedullary pressor responses to stimulation of the rostral hypothalamus in the rat: influence of adrenaline-induced vasodilation and reflex cardioinhibition

1988 ◽  
Vol 66 (2) ◽  
pp. 213-221
Author(s):  
Pierre Gauthier
Keyword(s):  
Pressor Response ◽  
Primary Phase ◽  
Anterior Hypothalamus ◽  
Plasma Noradrenaline ◽  
Current Response ◽  
Adrenergic Blockade ◽  
Hypothalamic Region ◽  
Pressor Responses ◽  
Noradrenaline And Adrenaline ◽  
Stimulation Of

Electrical stimulation (100 Hz, 1 ms, 150 μA, 10 s) of the anterior hypothalamus in chloralose-anesthetized rats evoked a biphasic pressor response consisting of an initial sharp rise in arterial pressure at the onset of stimulation, followed by a second elevation after cessation of the stimulus. This response was accompanied by an increase in plasma noradrenaline and adrenaline levels. Peripheral sympathectomy with guanethidine selectively abolished the primary phase of the biphasic pressor response, while bilateral removal of the adrenal medulla eliminated only the secondary component. After α-adrenergic blockade with phentolamine, the primary phase of the stimulation-induced response was reduced while the secondary pressor component was blocked and replaced by a significant hypotension. The intravenous administration of sotalol enhanced the secondary pressor component without affecting the stimulation-induced plasma noradrenaline and adrenaline responses. After treatment with atropine, the secondary pressor effect was also potentiated, as the reflex bradycardia normally associated with the response was eliminated. A subsequent administration of sotalol in these rats further potentiated the secondary pressor component to stimulation. In rats treated with atropine and sotalol, the sympathetic vasomotor and the adrenomedullary pressor responses could be dissociated according to thresholds and stimulus frequency or current–response characteristics. The results suggest that in intact rats, adrenaline-induced vasodilation and reflex cardiac inhibition contribute to either reduce or mask the adrenomedullary component of the biphasic pressor response evoked by stimulation of the anterior hypothalamus. The study also raises the hypothesis of a dual regulation of both components of the sympathetic system in the anterior hypothalamic region.

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