Inhibition of paraventricular neurons by subfornical organ and AV3V in cats

1988 ◽  
Vol 255 (6) ◽  
pp. R961-R967 ◽  
Author(s):  
T. Osaka ◽  
H. Yamashita ◽  
K. Koizumi
Keyword(s):  
Electrical Stimulation ◽  
Action Potentials ◽  
Subfornical Organ ◽  
Chemical Stimulation ◽  
Large Animal ◽  
Lamina Terminalis ◽  
Sodium Glutamate ◽  
Pentobarbital Sodium ◽  
Single Action ◽  
Stimulation Of

The study was designed to examine, by electrophysiological techniques, influences of rostral periventricular structures on neurons in the hypothalamic paraventricular nucleus (PVN) in a large animal (the cat) in which stimulating and recording sites could be precisely identified. Extracellular single action potentials were recorded from the PVN in pentobarbital sodium-anesthetized and hemispherectomized cats. Of 246 neurons tested, 24-47% were inhibited and 9-21% were excited by electrical stimulation of the subfornical organ (SFO), the nucleus preopticus medianus (POMn), and the organum vasculosum of the lamina terminalis (OVLT). The onset latencies of inhibition (19-26 ms) were shorter than those of excitation (28-80 ms). Responses of both neurosecretory and nonneurosecretory neurons were similar to the stimulation of all sites tested. Among these sites, the POMn had the strongest influence on the PVN in view of the proportion of the responsive neurons. Moreover, antidromically evoked action potentials in the PVN neurons (n = 10) were only observed after stimulation of the POMn. Chemical stimulation of POMn and SFO by microinjection of sodium glutamate (50-100 nl, 0.5 M) also inhibited 16 of 38 PVN cells; the remaining neurons were unaffected. These results suggest that activation of the POMn, OVLT, and the SFO neurons mainly inhibits the PVN neurons in the cat.

Midline medullary depressor responses are mediated by inhibition of RVLM sympathoexcitatory neurons in rats

1999 ◽  
Vol 276 (4) ◽  
pp. R1054-R1062 ◽  
Author(s):  
Anthony J. M. Verberne ◽  
Daniela M. Sartor ◽  
Ayse Berke
Keyword(s):  
Blood Pressure ◽  
Electrical Stimulation ◽  
Chemical Stimulation ◽  
Ventrolateral Medulla ◽  
Unit Discharge ◽  
Pentobarbital Sodium ◽  
Sympathetic Response ◽  
Long Latency ◽  
Stimulation Of ◽  
Nerve Discharge

Mechanisms underlying the depressor and sympathoinhibitory responses evoked from the caudal medullary raphe (MR) region were investigated in pentobarbital sodium-anesthetized, paralyzed rats. Intermittent electrical stimulation (0.5 Hz, 0.5-ms pulses, 200 μA) of the MR elicited a mixed sympathetic response that consisted of a long-latency sympathoexcitatory (SE) peak (onset = 146 ± 7 ms) superimposed on an inhibitory phase (onset = 59 ± 10 ms). Chemical stimulation of the MR (glutamate; Glu) most frequently elicited depressor responses accompanied by inhibition of sympathetic nerve discharge. Occasionally, these responses were preceded by transient pressor and SE responses. We examined the influence of intermittent electrical stimulation (0.5 Hz, 0.5-ms pulses, 25–200 μA) and Glu stimulation of the MR on the discharge of rostral ventrolateral medulla (RVLM) premotor SE neurons. Peristimulus-time histograms of RVLM unit discharge featured a prominent inhibitory phase in response to MR stimulation (onset = 20 ± 2 ms; duration = 42 ± 4 ms; n = 12 units). Glu stimulation of the MR reduced blood pressure (−37 ± 2 mmHg, n = 19) and inhibited the discharge of RVLM SE neurons (15 of 19 neurons). Depressor and sympathoinhibitory responses elicited by chemical and electrical stimulation of the MR region are mediated by inhibition of RVLM premotor SE neurons and withdrawal of sympathetic vasomotor discharge.

Electronmicroscopic and electrophysiological studies of the teat branch of the XIII thoracic nerve: relationship with lactation in the rat

1988 ◽  
Vol 118 (3) ◽  
pp. 471-483 ◽  
Author(s):  
L. M. Voloschin ◽  
E. Décima ◽  
J. H. Tramezzani
Keyword(s):  
Electrical Stimulation ◽  
Conduction Velocity ◽  
Action Potentials ◽  
Silent Period ◽  
High Amplitude ◽  
Milk Ejection ◽  
Nerve Activity ◽  
Thoracic Nerve ◽  
Myelinated Fibres ◽  
Stimulation Of

ABSTRACT Electrical stimulation of the XIII thoracic nerve (the 'mammary nerve') causes milk ejection and the release of prolactin and other hormones. We have analysed the route of the suckling stimulus at the level of different subgroups of fibres of the teat branch of the XIII thoracic nerve (TBTN), which innervates the nipple and surrounding skin, and assessed the micromorphology of the TBTN in relation to lactation. There were 844 ± 63 and 868 ± 141 (s.e.m.) nerve fibres in the TBTN (85% non-myelinated) in virgin and lactating rats respectively. Non-myelinated fibres were enlarged in lactating rats; the modal value being 0·3–0·4 μm2 for virgin and 0·4–0·5 μm2 for lactating rats (P > 0·001; Kolmogorov–Smirnov test). The modal value for myelinated fibres was 3–6 μm2 in both groups. The compound action potential of the TBTN in response to electrical stimulation showed two early volleys produced by the Aα- and Aδ-subgroups of myelinated fibres (conduction velocity rate of 60 and 14 m/s respectively), and a late third volley originated in non-myelinated fibres ('C') group; conduction velocity rate 1·4 m/s). Before milk ejection the suckling pups caused 'double bursts' of fibre activity in the Aδ fibres of the TBTN. Each 'double burst' consisted of low amplitude action potentials and comprised two multiple discharges (33–37 ms each) separated by a silent period of around 35 ms. The 'double bursts' occurred at a frequency of 3–4/s, were triggered by the stimulation of the nipple and were related to fast cheek movements visible only by watching the pups closely. In contrast, the Aα fibres of the TBTN showed brief bursts of high amplitude potentials before milk ejection. These were triggered by the stimulation of cutaneous receptors during gross slow sucking motions of the pup (jaw movements). Immediately before the triggering of milk ejection the mother was always asleep and a low nerve activity was recorded in the TBTN at this time. When reflex milk ejection occurred, the mother woke and a brisk increase in nerve activity was detected; this decreased when milk ejection was accomplished. In conscious rats the double-burst type of discharges in Aδ fibres was not observed, possibly because this activity cannot be detected by the recording methods currently employed in conscious animals. During milk ejection, action potentials of high amplitude were conveyed in the Aα fibres of the TBTN. During the treading time of the stretch reaction (SR), a brisk increase in activity occurred in larger fibres; during the stretching periods of the SR a burst-type discharge was again observed in slow-conducting afferents; when the pups changed nipple an abrupt increase in activity occurred in larger fibres. In summary, the non-myelinated fibres of the TBTN are increased in diameter during lactation, and the pattern of suckling-evoked nerve activity in myelinated fibres showed that (a) the double burst of Aδ fibres, produced by individual sucks before milk ejection, could be one of the conditions required for the triggering of the reflex, and (b) the nerve activity displayed during milk-ejection action may result, at least in part, from 'non-specific' stimulation of cutaneous receptors. J. Endocr. (1988) 118, 471–483

Structure and Function of the Lateral Giant Neurone of the Primitive Crustacean Anaspides Tasmaniae

1979 ◽  
Vol 78 (1) ◽  
pp. 121-136
Author(s):  
GERALD E. SILVEY ◽  
IAN S. WILSON
Keyword(s):  
Action Potentials ◽  
Tactile Stimulation ◽  
Large Diameter ◽  
Whole Body ◽  
Giant Fibre ◽  
Single Action ◽  
Giant Neurone ◽  
And Function ◽  
Thoracic And Abdominal ◽  
Stimulation Of

The syncarid crustacean Anaspides tasmaniae rapidly flexes its free thoracic and abdominal segments in response to tactile stimulation of its body. This response decrements but recovers in slightly more than one hour. The fast flexion is evoked by single action potentials in the lateral of two large diameter fibres (40 μm) which lie on either side of the cord. The lateral giant fibre is made up of fused axons of 11 neurones, one in each of the last 5 thoracic and 6 abdominal ganglia. The soma of each neurone lies contralateral to the axon. Its neurite crosses that of its counterpart in the commissure and gives out dendrites into the neuropile of each hemiganglion. The lateral giant neurone receives input from the whole body but fires in response only to input from the fourth thoracic segment posteriorly. Both fibres respond with tactile stimulation of only one side. Since neither current nor action potentials spread from one fibre to the other, afferents must synapse with both giant neurones. The close morphological and physiological similarities of the lateral giant neurone in Anaspides to that in the crayfish (Eucarida) suggest that the lateral giant system arose in the ancestor common to syncarids and eucarids, prior to the Carboniferous.

Respiratory responses to aortic and carotid chemoreceptor activation in the dog

1991 ◽  
Vol 70 (6) ◽  
pp. 2539-2550 ◽  
Author(s):  
F. A. Hopp ◽  
J. L. Seagard ◽  
J. Bajic ◽  
E. J. Zuperku
Keyword(s):  
Electrical Stimulation ◽  
Carotid Body ◽  
Carotid Sinus ◽  
Chemical Stimulation ◽  
Respiratory Drive ◽  
Carotid Sinus Nerve ◽  
Nerve Activity ◽  
Respiratory Reflexes ◽  
Respiratory Responses ◽  
Stimulation Of

Respiratory responses arising from both chemical stimulation of vascularly isolated aortic body (AB) and carotid body (CB) chemoreceptors and electrical stimulation of aortic nerve (AN) and carotid sinus nerve (CSN) afferents were compared in the anesthetized dog. Respiratory reflexes were measured as changes in inspiratory duration (TI), expiratory duration (TE), and peak averaged phrenic nerve activity (PPNG). Tonic AN and AB stimulations shortened TI and TE with no change in PPNG, while tonic CSN and CB stimulations shortened TE, increased PPNG, and transiently lengthened TI. Phasic AB and AN stimulations throughout inspiration shortened TI with no changes in PPNG or the following TE; however, similar phasic stimulations of the CB and CSN increased both TI and PPNG and decreased the following TE. Phasic AN stimulation during expiration decreased TE and the following TI with no change in PPNG. Similar stimulations of the CB and CSN decreased TE; however, the following TI and PPNG were increased. These findings differ from those found in the cat and suggest that aortic chemoreceptors affect mainly phase timing, while carotid chemoreceptors affect both timing and respiratory drive.

Comparison of gene expression of 2-mo denervated, 2-mo stimulated-denervated, and control rat skeletal muscles

2005 ◽  
Vol 22 (2) ◽  
pp. 227-243 ◽  
Author(s):  
Tatiana Y. Kostrominova ◽  
Douglas E. Dow ◽  
Robert G. Dennis ◽  
Richard A. Miller ◽  
John A. Faulkner
Keyword(s):  
Gene Expression ◽  
Electrical Stimulation ◽  
Mrna Expression ◽  
Action Potentials ◽  
Skeletal Muscles ◽  
Microarray Study ◽  
Number Of Genes ◽  
Denervated Muscles ◽  
And Control ◽  
Stimulation Of

Loss of innervation in skeletal muscles leads to degeneration, atrophy, and loss of force. These dramatic changes are reflected in modifications of the mRNA expression of a large number of genes. Our goal was to clarify the broad spectrum of molecular events associated with long-term denervation of skeletal muscles. A microarray study compared gene expression profiles of 2-mo denervated and control extensor digitorum longus (EDL) muscles from 6-mo-old rats. The study identified 121 genes with increased and 7 genes with decreased mRNA expression. The expression of 107 of these genes had not been identified previously as changed after denervation. Many of the genes identified were genes that are highly expressed in skeletal muscles during embryonic development, downregulated in adults, and upregulated after denervation of muscle fibers. Electrical stimulation of denervated muscles preserved muscle mass and maximal force at levels similar to those in the control muscles. To understand the processes underlying the effect of electrical stimulation on denervated skeletal muscles, mRNA and protein expression of a number of genes, identified by the microarray study, was compared. The hypothesis was that loss of nerve action potentials and muscle contractions after denervation play the major roles in upregulation of gene expression in skeletal muscles. With electrical stimulation of denervated muscles, the expression levels for these genes were significantly downregulated, consistent with the hypothesis that loss of action potentials and/or contractions contribute to the alterations in gene expression in denervated skeletal muscles.

Electrical Stimulation of the Rat Lumbar Spine Induces Reflex Action Potentials in the Nerves to the Lower Abdomen

Spine ◽  
2000 ◽  
Vol 25 (4) ◽  
pp. 411-417 ◽  
Author(s):  
Yuzuru Takahashi ◽  
Jiro Hirayama ◽  
Yoshio Nakajima ◽  
Seiji Ohtori ◽  
Kazuhisa Takahashi
Keyword(s):  
Electrical Stimulation ◽  
Lumbar Spine ◽  
Action Potentials ◽  
Lower Abdomen ◽  
Reflex Action ◽  
Stimulation Of

Acute electrical stimulation of the subfornical organ induces feeding in satiated rats

2010 ◽  
Vol 99 (4) ◽  
pp. 534-537 ◽  
Author(s):  
Pauline M. Smith ◽  
Gabriela Rozanski ◽  
Alastair V. Ferguson
Keyword(s):  
Electrical Stimulation ◽  
Subfornical Organ ◽  
Stimulation Of

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.

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