Central action of glucagon in rat hypothalamus

1986 ◽  
Vol 250 (1) ◽  
pp. R120-R126 ◽  
Author(s):  
A. Inokuchi ◽  
Y. Oomura ◽  
N. Shimizu ◽  
T. Yamamoto
Keyword(s):  
Cell Membrane ◽  
Cortical Neurons ◽  
Membrane Resistance ◽  
Inhibitory Effect ◽  
Hypothalamic Nucleus ◽  
Central Action ◽  
Intracellular Recordings ◽  
Hypothalamic Area ◽  
Ventromedial Hypothalamic Nucleus ◽  
Dorsomedial Hypothalamic Nucleus

The effects of electrophoretically applied glucagon on neuronal activity in the rat lateral hypothalamic area (LHA), dorsomedial hypothalamic nucleus (DMH), and ventromedial hypothalamic nucleus (VMH) were examined. In the LHA glucagon significantly suppressed the activity of glucose-sensitive neurons compared with its effect on non-glucose-sensitive neurons. This inhibitory effect of glucagon on LHA neurons was blocked by ouabain. Intracellular recordings from LHA neurons revealed that glucagon hyperpolarized the cell membrane without a significant change in the input membrane resistance. Intra-arterial injection of glucagon suppressed the activity of some neurons that were suppressed by electrophoretically applied glucagon. Similarly, glucagon suppressed the activity of significant numbers of DMH and VMH neurons with doses higher than those that affected LHA glucose-sensitive neurons. Cortical neurons were unaffected by glucagon. The data suggest that blood-borne glucagon could suppress the activity of LHA glucose-sensitive neurons and, in addition, might contribute to the control of metabolism and the termination of feeding behavior.

Effects of hypothalamic stimulation and lesion on adrenal nerve activity

1987 ◽  
Vol 253 (3) ◽  
pp. R418-R424 ◽  
Author(s):  
H. Yoshimatsu ◽  
Y. Oomura ◽  
T. Katafuchi ◽  
A. Niijima
Keyword(s):  
Anterior Part ◽  
Sympathetic Nerves ◽  
Middle Part ◽  
Hypothalamic Nucleus ◽  
Moderate Increase ◽  
Sympathoadrenal System ◽  
Nerve Activity ◽  
Hypothalamic Area ◽  
Ventromedial Hypothalamic Nucleus ◽  
Stimulation Of

Activity changes of efferent adrenal sympathetic nerves in response to bilateral manipulations of the hypothalamus, partly after intra-third cerebroventricular injection of 2-deoxy-D-glucose (2-DG) were investigated in anesthetized rats. Stimulation of the middle part of the lateral hypothalamic area (LHAm) increased adrenal nerve activity, whereas lesion caused rapid and remarkable decrease. Stimulation of the anterior part of the LHA (LHAa) tended to decrease the activity, and lesion produced either rapid decrease or late moderate increase. Stimulation of the ventromedial hypothalamic nucleus (VMH) did not affect the nerve activity, but lesion increased it gradually and then remarkably. Cerebroventricular infusion of 2-DG caused remarkable increase in activity that was suppressed by LHAm lesion. Subsequent infusion of 2-DG during the period of suppressed activity was no longer effective. The increased firing rate after 2-DG was suppressed by stimulation of the VMH, whereas lesion caused no change. These findings indicate that the central regulation of adrenal nerve activity is connected with individual hypothalamic regions and consequently depends on the degree and mode of activation of the sympathoadrenal system.

Effects of hypothalamic stimulation on activity of dorsomedial medulla neurons that respond to subdiaphragmatic vagal stimulation

1987 ◽  
Vol 58 (4) ◽  
pp. 655-675 ◽  
Author(s):  
H. Nishimura ◽  
Y. Oomura
Keyword(s):  
Conduction Velocity ◽  
Vagal Stimulation ◽  
Hypothalamic Stimulation ◽  
Hypothalamic Nucleus ◽  
Motor Nucleus ◽  
Intracellular Recordings ◽  
Hypothalamic Area ◽  
Extracellular Recordings ◽  
Postsynaptic Potentials ◽  
The Mean

1. Effects of hypothalamic stimulation on activity of dorsomedial medulla neurons that responded to subdiaphragmatic vagal stimulation were investigated in urethan-anesthetized rats. 2. Extracellular recordings were made from 231 neurons in the nucleus of the tractus solitarius (NTS) that fired repetitively in response to single-pulse subdiaphragmatic vagal stimulation and from 320 neurons in the dorsal motor nucleus of the vagal nerve (DMV) that responded antidromically to subdiaphragmatic vagal stimulation. The mean latencies of responses to subdiaphragmatic vagal stimulation were 90.3 +/- 17.1 ms (mean +/- SD) for NTS neurons, and 90.8 +/- 11.2 ms for DMV neurons. This indicated that both afferent and efferent subdiaphragmatic vagal fibers were thin and unmyelinated and had a conduction velocity of approximately 1 m/s. 3. In extracellular recordings from 320 DMV neurons, marked inhibition preceded the antidromic response and subdiaphragmatic vagal stimulation evoked orthodromic spikes in only a few neurons. 4. Intracellular recordings from 66 DMV neurons revealed inhibitory postsynaptic potentials (IPSPs) before the antidromic responses. These IPSPs suppressed spontaneous firing and prevented excitatory postsynaptic potentials (EPSPs) from generating action potentials. 5. Stimulation in all hypothalamic loci studied, the ventromedial hypothalamic nucleus (VMH), the lateral hypothalamic area (LHA), and the paraventricular nucleus (PVN), induced responses with similar characteristics of excitation alone or excitation followed by inhibition in most NTS and DMV neurons. 6. No reciprocal effect of VMH and LHA stimulation was observed on NTS and DMV neurons. 7. Intracellular recordings from DMV neurons revealed monosynaptic EPSPs in response to stimulation of the VMH, the LHA, and the PVN. 8. PVN stimulation evoked significantly more responses in NTS and DMV neurons than VMH stimulation and more responses in DMV neurons than LHA stimulation. This suggests a difference in the number of connections between each hypothalamic site and the dorsomedial medulla. 9. The same dorsomedial medulla neurons were tested with VMH and LHA stimulation. The respective mean latencies of the antidromic and the orthodromic NTS neuron responses were 37.3 +/- 3.2 and 39.6 +/- 12.9 ms for VMH stimulation and 29.8 +/- 5.3 and 31.8 +/- 8.7 ms for LHA stimulation. The mean latencies of the orthodromic DMV neuron responses were 39.4 +/- 8.3 ms for VMH stimulation and 31.1 +/- 5.2 ms for LHA stimulation. The estimated conduction velocity from the VMH to the dorsomedial medulla was approximately 0.25 m/s and from the LHA it was approximately 0.33 m/s, which was significantly faster.(ABSTRACT TRUNCATED AT 400 WORDS)

Meal size and number: relationship to dopamine levels in the ventromedial hypothalamic nucleus

1997 ◽  
Vol 272 (6) ◽  
pp. R1925-R1930 ◽  
Author(s):  
M. M. Meguid ◽  
Z. J. Yang ◽  
A. Laviano
Keyword(s):  
Lag Time ◽  
Reciprocal Relationship ◽  
Meal Size ◽  
Hypothalamic Nucleus ◽  
Inverse Association ◽  
Dopamine Level ◽  
Hypothalamic Area ◽  
Ventromedial Hypothalamic Nucleus ◽  
Food Intake Regulation ◽  
Intake Regulation

Evidence shows a reciprocal relationship exists between the lateral hypothalamic area (LHA) and the ventromedial hypothalamic nucleus (VMN) in food intake regulation. Since a direct correlation between meal size and LHA-dopamine in Fischer rats was previously reported, we tested the hypothesis that an inverse association may exist between meal size and VMN-dopamine response. This was studied in awake 24-h food-deprived rats who were then allowed to eat freely for 20 min while the VMN-dopamine response was measured by microdialysis every 20 min for 2 h. In a second experiment, only one-half the amount freely eaten was provided during microdialysis. The following were observed. 1) Dopamine concentrations in VMN decreased during eating. 2) The degree and duration of decrease after the meal corresponded to the size of the meal. 3) When the decreased postmeal VMN-dopamine level had returned to baseline and food was available, rats ate once more. The findings show that, in normal rats, eating was associated with decreased dopamine levels in the VMN and was followed by a lag time during which no additional eating occurred. VMN dopamine levels thereby contribute to determining the duration of the intermeal interval and hence, by inference, the meal number.

A comparison of brain angiotensin II receptors during lactation and diestrus of the estrous cycle in the rat

1999 ◽  
Vol 277 (3) ◽  
pp. R904-R909 ◽  
Author(s):  
Robert C. Speth ◽  
William T. Barry ◽  
M. Susan Smith ◽  
Kevin L. Grove
Keyword(s):  
Receptor Binding ◽  
Arcuate Nucleus ◽  
Preoptic Area ◽  
Renin Angiotensin System ◽  
Hypothalamic Nucleus ◽  
Ang Ii ◽  
Hypothalamic Area ◽  
Angiotensin System ◽  
Dorsomedial Hypothalamic Nucleus ◽  
The Brain

During lactation there are many dramatic alterations in the hypothalamic-pituitary (HP) axis, as well as an increased demand for food and water. The renin-angiotensin system (RAS) is one of the major mediators of the HP axis. This study examined the receptors for ANG II in the rat brain during lactation and diestrus. Compared with diestrus, lactating rats had significant decreases in ANG II receptor binding in several forebrain regions, most notably in the arcuate nucleus/median eminence, dorsomedial hypothalamic nucleus (DMH), and lateral hypothalamic area (LHA). In contrast, there was an increase in ANG II receptor binding in the preoptic area during lactation. These significant changes in ANG II binding in the brain during lactation support the hypothesis that changes in the RAS may contribute to the dramatic changes in the HP axis during lactation. In addition, the significant reduction in ANG II binding in the DMH and LHA may be indicative of a role in the regulation of food intake, a function only recently associated with the RAS.

Adrenal sympathetic nerve activity in response to hypothalamic injections of 2-deoxy-D-glucose

1991 ◽  
Vol 261 (4) ◽  
pp. R875-R881 ◽  
Author(s):  
H. Yoshimatsu ◽  
M. Egawa ◽  
G. A. Bray
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Hypothalamic Nucleus ◽  
Nerve Activity ◽  
Hypothalamic Area ◽  
Hypothalamic Region ◽  
Hypothalamic Nuclei ◽  
The Central Nervous System ◽  
Direct Administration ◽  
Dorsomedial Hypothalamic Nucleus

Adrenal sympathetic nerve activity after microinfusion of 2-deoxy-D-glucose (2-DG) into various hypothalamic nuclei was investigated in anesthetized rats. Infusion of 2-DG into the ventrolateral portion of the lateral hypothalamic area (LHA) induced a large and long-lasting increase (greater than 60 min) in adrenal nerve activity. In contrast, infusion into the dorsal or medial portion of the LHA tended to produce a small decrease with a return to baseline within approximately 60 min after the end of the infusion. The direct administration of 2-DG into either the paraventricular nucleus or the dorsomedial hypothalamic nucleus produced a strong inhibition of adrenal nerve activity. Infusions into the ventromedial hypothalamic nucleus induced either a decrease of adrenal nerve activity or were without effect. These findings provide evidence that induction of glucoprivation in the hypothalamus with 2-DG can excite or inhibit adrenal nerve activity, depending on the hypothalamic region. These data also indicate that the ventrolateral portion of the LHA plays an important role in the regulation of adrenal catecholamine secretion in response to glucoprivic conditions in the central nervous system.

scholarly journals Glucocorticoid Maintains Pulsatile Secretion of Luteinizing Hormone under Infectious Stress Condition

Endocrinology ◽  
2003 ◽  
Vol 144 (8) ◽  
pp. 3477-3482 ◽  
Author(s):  
Takashi Matsuwaki ◽  
Erina Watanabe ◽  
Masatoshi Suzuki ◽  
Keitaro Yamanouchi ◽  
Masugi Nishihara
Keyword(s):  
Stress Condition ◽  
Pulse Generator ◽  
Suppressive Effect ◽  
Inhibitory Effect ◽  
Hypothalamic Nucleus ◽  
Ovx Rats ◽  
Lh Pulsatility ◽  
Tnf Α ◽  
Dorsomedial Hypothalamic Nucleus ◽  
Generator Activity

Abstract We have previously shown that TNF-α, a major proinflammatory cytokine, suppressed hypothalamic GnRH pulse generator activity and that this inhibitory effect was enhanced by α-helical CRH, a CRH receptor antagonist. The present study was conducted to elucidate the involvement of glucocorticoid (GC) in modulating LH pulses under infectious stress condition. Adrenalectomy (ADX) markedly enhanced the suppressive effect of TNF-α (1 μg), injected iv, on LH pulses in ovariectomized (OVX) rats. Pretreatment with a sc injection of corticosterone (10 mg) almost completely restored LH pulses after TNF-α injection in OVX/ADX animals. Injection of TNF-α increased the number of c-Fos-immunoreactive cells in the supraoptic nucleus (SON), the dorsomedial hypothalamic nucleus (DMH), and the parvocellular region of the paraventricular nucleus (PVN), which was more prominent in OVX/ADX than OVX animals except in the DMH. Pretreatment with corticosterone decreased the number of Fos-immunoreactive cells in the PVN and SON but not in the DMH. These results suggest that GC has a potent protective effect on LH pulsatility under conditions of infectious stress, the mechanism of which involves at least the suppression of the excitability of PVN and SON neurons. In addition, the DMH does not seem to mediate the central action of GC, though it may play an important role in inducing pathophysiological reactions to invasive stress.

scholarly journals Identification of a discrete neuronal circuit that relays insulin signaling into the brain to regulate glucose homeostasis

2021 ◽  
Author(s):  
Mouna El Mehdi ◽  
Saloua Takhlidjt ◽  
Mélodie Devère ◽  
Arnaud Arabo ◽  
Marie-Anne Le Solliec ◽  
...  
Keyword(s):  
Glucose Homeostasis ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Inhibitory Effect ◽  
Neuronal Population ◽  
Biologically Active ◽  
Hypothalamic Nucleus ◽  
Hypothalamic Area ◽  
Antihyperglycemic Effect ◽  
Hypothalamic Regulation

26RFa (QRFP) is a biologically active peptide that regulates glucose homeostasis by acting as an incretin and by increasing insulin sensitivity at the periphery. 26RFa is also produced by a neuronal population localized in the hypothalamus. In the present study, we have investigated whether the 26RFa neurons may be involved in the hypothalamic regulation of glucose homeostasis. Our data indicate that 26RFa, i.c.v. injected, induces a robust antihyperglycemic effect associated with an increase of insulin production by the pancreatic islets. In addition, we found that insulin strongly stimulates 26RFa expression and secretion by the hypothalamus. RNAscope experiments revealed that neurons expressing 26RFa in the lateral hypothalamic area and the ventromedial hypothalamic nucleus also express the insulin receptor and that insulin induces the expression of 26RFa in these neurons. Concurrently, we show that the central antihyperglycemic effect of insulin is abolished in presence of a 26RFa receptor (GPR103) antagonist as well as in mice deficient for 26RFa. Finally, our data indicate that the hypothalamic 26RFa neurons are not involved in the central inhibitory effect of insulin on hepatic glucose production, but mediate the central effects of the hormone on its own peripheral production. To conclude, in the present study we have identified a novel actor of the hypothalamic regulation of glucose homeostasis, the 26RFa/GPR103 system and we provide the evidence that this neuronal peptidergic system is a key relay for the central regulation of glucose metabolism by insulin.

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