Effects of intrahypothalamic injections of GABA, muscimol, pentobarbital, and L-glutamic acid on feed intake of satiated sheep

1989 ◽  
Vol 67 (1) ◽  
pp. 5-9 ◽  
Author(s):  
S. A. Wandji ◽  
J. R. Seoane ◽  
A. G. Roberge ◽  
L. Bédard ◽  
L. Thibault
Keyword(s):  
Glutamic Acid ◽  
Feed Intake ◽  
Feeding Behaviour ◽  
Ventromedial Hypothalamus ◽  
Neural Pathways ◽  
Direct Stimulation ◽  
Dorsomedial Hypothalamus ◽  
Cranial Implants ◽  
Stimulation Of

Five wethers were surgically prepared with cranial implants to study the role of gabaminergic neural pathways on the hypothalamic control of feeding behaviour in ruminants. In the first experiment, the animals were injected (1 μL) with a physiological Tyrode (0.95%) solution, muscimol (0.5 and 1.0 nmol), GABA (0.5 and 1.0 nmol), and L-glutamic acid (0.5 and 1.0 nmol). Feed intake following injections of muscimol (1.0 nmol) and L-glutamic acid (0.5 and 1.0 nmol) was twice as large as that following the Tyrode solution, at 60-min postinjections. These results, however, were not statistically significant (p = 0.12–0.15). In the second experiment, the animals were injected (1 μL) with saline, muscimol (0.8 nmol), L-glutamic acid (0.8 nmol), and pentobarbital (0.26 μmol). Fifteen minutes after the injections, pentobarbital had induced a significant feeding response when compared with control values (p < 0.01), whereas the effect of L-glutamic acid was not significant. However, 30 min after the injections, feed intake of sheep having received L-glutamic acid was higher than that obtained with the control injections (p < 0.01). The response to pentobarbital was stronger than that to either muscimol or L-glutamic acid. Histological analyses of brain tissue indicated that injections were performed in the ventromedial hypothalamus of four sheep and in the dorsomedial hypothalamus of the other. The data indicate that L-glutamic acid stimulates feed intake by acting either as a precursor of GABA or by a direct stimulation of glutaminergic neural pathways involved in the control of feed intake.Key words: Feeding behaviour, glutamic acid, GABA, sheep.

scholarly journals The Role of BMP Signaling in Osteoclast Regulation

2021 ◽  
Vol 9 (3) ◽  
pp. 24
Author(s):  
Brian Heubel ◽  
Anja Nohe
Keyword(s):  
Bone Formation ◽  
Bone Morphogenetic Proteins ◽  
Bone Diseases ◽  
Bmp Signaling ◽  
Bone Homeostasis ◽  
Direct Stimulation ◽  
Federal Drug Administration ◽  
Bmp Pathway ◽  
Stimulation Of

The osteogenic effects of Bone Morphogenetic Proteins (BMPs) were delineated in 1965 when Urist et al. showed that BMPs could induce ectopic bone formation. In subsequent decades, the effects of BMPs on bone formation and maintenance were established. BMPs induce proliferation in osteoprogenitor cells and increase mineralization activity in osteoblasts. The role of BMPs in bone homeostasis and repair led to the approval of BMP2 by the Federal Drug Administration (FDA) for anterior lumbar interbody fusion (ALIF) to increase the bone formation in the treated area. However, the use of BMP2 for treatment of degenerative bone diseases such as osteoporosis is still uncertain as patients treated with BMP2 results in the stimulation of not only osteoblast mineralization, but also osteoclast absorption, leading to early bone graft subsidence. The increase in absorption activity is the result of direct stimulation of osteoclasts by BMP2 working synergistically with the RANK signaling pathway. The dual effect of BMPs on bone resorption and mineralization highlights the essential role of BMP-signaling in bone homeostasis, making it a putative therapeutic target for diseases like osteoporosis. Before the BMP pathway can be utilized in the treatment of osteoporosis a better understanding of how BMP-signaling regulates osteoclasts must be established.

Replicating the Role of the Human Retina for a Cortical Visual Neuroprosthesis

2013 ◽  
pp. 1532-1551
Author(s):  
Samuel Romero ◽  
Christian Morillas ◽  
Antonio Martínez ◽  
Begoña del Pino ◽  
Francisco Pelayo ◽  
...  
Keyword(s):  
Visual Cortex ◽  
Significant Degree ◽  
Research Field ◽  
Human Retina ◽  
Direct Stimulation ◽  
Biologically Inspired ◽  
Visual Inputs ◽  
Response Modeling ◽  
Stimulation Of

Neuroengineering is an emerging research field combining the latest findings from neuroscience with developments in a variety of engineering disciplines to create artificial devices, mainly for therapeutical purposes. In this chapter, an application of this field to the development of a visual neuroprosthesis for the blind is described. Electrical stimulation of the visual cortex in blind subjects elicits the perception of visual sensations called phosphenes, a finding that encourages the development of future electronic visual prostheses. However, direct stimulation of the visual cortex would miss a significant degree of image processing that is carried out by the retina. The authors describe a biologically-inspired retina-like processor designed to drive the implanted stimulator using visual inputs from one or two cameras. This includes dynamic response modeling with minimal latency. The outputs of the retina-like processor are comparable to those recorded in biological retinas that are exposed to the same stimuli and allow estimation of the original scene.

Stimulation of steroid secretion by adrenocorticotropin injections and by arginine vasopressin infusions: no evidence for a direct stimulation of the human adrenal by arginine vasopressin

1991 ◽  
Vol 125 (4) ◽  
pp. 348-353 ◽  
Author(s):  
V. Bähr ◽  
J. Hensen ◽  
O. Hader ◽  
T. Bölke ◽  
W. Oelkers
Keyword(s):  
Arginine Vasopressin ◽  
Plasma Aldosterone ◽  
Regression Coefficients ◽  
Minor Importance ◽  
Cortisol Secretion ◽  
Plasma Acth ◽  
Direct Stimulation ◽  
Stimulatory Action ◽  
Stimulation Of

Abstract. Arginine vasopressin stimulates the secretion of adrenocorticotropin. A direct stimulatory effect of AVP on cortisol as well as aldosteron secretion has been postulated by several investigators. To study the possible role of a direct stimulatory action of AVP on the adrenal cortex, normal volunteers were treated with incremental injections of ACTH or with incremental infusions of AVP which raised plasma AVP levels to a maximum of 256±16 pmol/l. In both situations, a significant (p<0.001) linear correlation between plasma ACTH and plasma cortisol was observed. The regression coefficients were not different (p>0.5). Plasma aldosterone was stimulated by both treatments, but the weakly positive correlation between plasma ACTH and plasma aldosterone was not significant for either stimulus. Thus, in man, a direct stimulatory effect of AVP on cortisol secretion cannot be demonstrated. A direct effect of AVP on aldosterone cannot be definitely excluded, but is certainly of minor importance.

Ghrelin enhances gastric motility through direct stimulation of intrinsic neural pathways and capsaicin-sensitive afferent neurones in rats

2004 ◽  
Vol 39 (12) ◽  
pp. 1209-1214 ◽  
Author(s):  
H. Fukuda ◽  
Y. Mizuta ◽  
H. Isomoto ◽  
F. Takeshima ◽  
K. Ohnita ◽  
...  
Keyword(s):  
Gastric Motility ◽  
Neural Pathways ◽  
Direct Stimulation ◽  
Stimulation Of

scholarly journals ARF6 stimulates clathrin/AP-2 recruitment to synaptic membranes by activating phosphatidylinositol phosphate kinase type Iγ

2003 ◽  
Vol 162 (1) ◽  
pp. 113-124 ◽  
Author(s):  
Michael Krauss ◽  
Masahiro Kinuta ◽  
Markus R. Wenk ◽  
Pietro De Camilli ◽  
Kohji Takei ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Synaptic Membranes ◽  
Direct Stimulation ◽  
Vesicle Membranes ◽  
Phosphatidylinositol Phosphate ◽  
Presynaptic Plasma Membrane ◽  
Phosphatidylinositol 4 ◽  
Adp Ribosylation Factor ◽  
Stimulation Of

Clathrin-mediated endocytosis of synaptic vesicle membranes involves the recruitment of clathrin and AP-2 adaptor complexes to the presynaptic plasma membrane. Phosphoinositides have been implicated in nucleating coat assembly by directly binding to several endocytotic proteins including AP-2 and AP180. Here, we show that the stimulatory effect of ATP and GTPγS on clathrin coat recruitment is mediated at least in part by increased levels of PIP2. We also provide evidence for a role of ADP-ribosylation factor 6 (ARF6) via direct stimulation of a synaptically enriched phosphatidylinositol 4-phosphate 5-kinase type Iγ (PIPKIγ), in this effect. These data suggest a model according to which activation of PIPKIγ by ARF6-GTP facilitates clathrin-coated pit assembly at the synapse.

scholarly journals A hypothalamic circuit that controls body temperature

2017 ◽  
Vol 114 (8) ◽  
pp. 2042-2047 ◽  
Author(s):  
Zheng-Dong Zhao ◽  
Wen Z. Yang ◽  
Cuicui Gao ◽  
Xin Fu ◽  
Wen Zhang ◽  
...  
Keyword(s):  
Body Temperature ◽  
Gabaergic Neurons ◽  
Designer Drugs ◽  
Electrophysiological Recording ◽  
Strong Increase ◽  
Temperature Sensitive ◽  
Neural Pathways ◽  
Dorsomedial Hypothalamus ◽  
Reduced Body ◽  
Stimulation Of

The homeostatic control of body temperature is essential for survival in mammals and is known to be regulated in part by temperature-sensitive neurons in the hypothalamus. However, the specific neural pathways and corresponding neural populations have not been fully elucidated. To identify these pathways, we used cFos staining to identify neurons that are activated by a thermal challenge and found induced expression in subsets of neurons within the ventral part of the lateral preoptic nucleus (vLPO) and the dorsal part of the dorsomedial hypothalamus (DMD). Activation of GABAergic neurons in the vLPO using optogenetics reduced body temperature, along with a decrease in physical activity. Optogenetic inhibition of these neurons resulted in fever-level hyperthermia. These GABAergic neurons project from the vLPO to the DMD and optogenetic stimulation of the nerve terminals in the DMD also reduced body temperature and activity. Electrophysiological recording revealed that the vLPO GABAergic neurons suppressed neural activity in DMD neurons, and fiber photometry of calcium transients revealed that DMD neurons were activated by cold. Accordingly, activation of DMD neurons using designer receptors exclusively activated by designer drugs (DREADDs) or optogenetics increased body temperature with a strong increase in energy expenditure and activity. Finally, optogenetic inhibition of DMD neurons triggered hypothermia, similar to stimulation of the GABAergic neurons in the vLPO. Thus, vLPO GABAergic neurons suppressed the thermogenic effect of DMD neurons. In aggregate, our data identify vLPO→DMD neural pathways that reduce core temperature in response to a thermal challenge, and we show that outputs from the DMD can induce activity-induced thermogenesis.

Stimulation of metabotropic glutamate receptors in the dorsomedial hypothalamus elevates heart rate in rats

1996 ◽  
Vol 270 (5) ◽  
pp. R1115-R1121 ◽  
Author(s):  
J. DiMicco ◽  
A. J. Monroe
Keyword(s):  
Heart Rate ◽  
Glutamate Receptors ◽  
Metabotropic Glutamate Receptors ◽  
Cardiovascular Effects ◽  
Nmda Receptor Antagonist ◽  
Dorsomedial Hypothalamus ◽  
Metabotropic Glutamate ◽  
Selective Blockade ◽  
Stimulation Of

This study examined the potential role of metabotropic glutamate receptors (mGluRs) in the dorsomedial hypothalamus (DMH) by assessing the cardiovascular effects of microinjecting the agonist trans-1-aminocyclopentane-1, 3- dicarboxylate (tACPD) into this region in urethan-anesthetized rats. Dose-related tachycardia was observed after unilateral microinjection of 1S 3R-tACPD (10-200 pmol/50nl) but not after injection of 1R, 3S-tACPD, which has been reported to have little or no activity at mGluRs. Microinjection of dihydroxyphenylglycine, an agonist at mGluRs linked to phosphoinositide hydrolysis, resulted in increases in heart rate that correlated closely in magnitude to those seen after injection of the same dose of 1S, 3R-tACPD. Coinjection of the N-methyl-D-aspartate (NMDA) receptor antagonist DL-2- amino-5-phosphonopentanoic acid, given at doses shown to elicit selective blockade of NMDA ionotropic glutamate receptors, reduced the increase in heart rate evoked by 100 pmol 1S, 3R-tACPD alone. Thus the DMH contains functional mGluRs, and stimulation of these receptors activates the same sympathoexcitatory mechanism characterized previously to provoke dose-related tachycardia.

Ventromedial hypothalamic lesions impair glucoregulation in response to endotoxin

1997 ◽  
Vol 272 (5) ◽  
pp. R1525-R1531 ◽  
Author(s):  
J. P. Lynch ◽  
M. M. Wojnar ◽  
C. H. Lang
Keyword(s):  
Metabolic Response ◽  
Plasma Concentrations ◽  
Ventromedial Hypothalamus ◽  
Whole Body ◽  
Tnf Alpha ◽  
Hormone Release ◽  
Glucose Flux ◽  
Bilateral Lesions ◽  
Stimulation Of

The purpose of the present study was to determine the role of the ventromedial hypothalamus (VMH) in regulating counter-regulatory hormone release and the increase in glucose flux that is observed after injection of endotoxin [lipopolysaccharide (LPS)]. Bilateral lesions of the VMH were produced electrolytically 2 wk before the experiment; sham-operated rats served as controls. [3-3H]glucose was infused to assess whole body glucose flux before and for 4 h after intravenous injection of Escherichia coli LPS. In control rats, LPS increased the plasma concentrations of glucose and lactate and the rates of glucose appearance and disappearance. In these animals, LPS also produced sustained elevations in corticosterone, glucagon, and catecholamines. In contrast, the glucose metabolic response to LPS was attenuated by > 50% in VMH-lesioned rats. These changes were associated with a blunted increase in the plasma concentration of glucagon, epinephrine, and norepinephrine in VMH-lesioned rats compared with control animals. There was no difference in the plasma concentrations of corticosterone or TNF-alpha between the two groups after LPS or the responsiveness of sham- and VMH-lesioned rats to an infusion of either glucagon or epinephrine. These data indicate that the VMH plays a central role in regulating the secretion of glucagon and catecholamines and the stimulation of glucose flux after LPS.

Replicating the Role of the Human Retina for a Cortical Visual Neuroprosthesis

2012 ◽  
pp. 346-365
Author(s):  
Samuel Romero ◽  
Christian Morillas ◽  
Antonio Martínez ◽  
Begoña del Pino ◽  
Francisco Pelayo ◽  
...  
Keyword(s):  
Visual Cortex ◽  
Significant Degree ◽  
Research Field ◽  
Human Retina ◽  
Direct Stimulation ◽  
Biologically Inspired ◽  
Visual Inputs ◽  
Response Modeling ◽  
Stimulation Of

Neuroengineering is an emerging research field combining the latest findings from neuroscience with developments in a variety of engineering disciplines to create artificial devices, mainly for therapeutical purposes. In this chapter, an application of this field to the development of a visual neuroprosthesis for the blind is described. Electrical stimulation of the visual cortex in blind subjects elicits the perception of visual sensations called phosphenes, a finding that encourages the development of future electronic visual prostheses. However, direct stimulation of the visual cortex would miss a significant degree of image processing that is carried out by the retina. The authors describe a biologically-inspired retina-like processor designed to drive the implanted stimulator using visual inputs from one or two cameras. This includes dynamic response modeling with minimal latency. The outputs of the retina-like processor are comparable to those recorded in biological retinas that are exposed to the same stimuli and allow estimation of the original scene

scholarly journals The Role of the N-Methyl-D-Aspartate Receptors in Social Behavior in Rodents

2019 ◽  
Vol 20 (22) ◽  
pp. 5599
Author(s):  
Iulia Zoicas ◽  
Johannes Kornhuber
Keyword(s):  
Nmda Receptor ◽  
Social Behavior ◽  
Nmda Receptors ◽  
Well Being ◽  
Social Deficits ◽  
Direct Stimulation ◽  
Positive Effects ◽  
Pharmacological Stimulation ◽  
Stimulation Of

The appropriate display of social behaviors is essential for the well-being, reproductive success and survival of an individual. Deficits in social behavior are associated with impaired N-methyl-D-aspartate (NMDA) receptor-mediated neurotransmission. In this review, we describe recent studies using genetically modified mice and pharmacological approaches which link the impaired functioning of the NMDA receptors, especially of the receptor subunits GluN1, GluN2A and GluN2B, to abnormal social behavior. This abnormal social behavior is expressed as impaired social interaction and communication, deficits in social memory, deficits in sexual and maternal behavior, as well as abnormal or heightened aggression. We also describe the positive effects of pharmacological stimulation of the NMDA receptors on these social deficits. Indeed, pharmacological stimulation of the glycine-binding site either by direct stimulation or by elevating the synaptic glycine levels represents a promising strategy for the normalization of genetically-induced, pharmacologically-induced or innate deficits in social behavior. We emphasize on the importance of future studies investigating the role of subunit-selective NMDA receptor ligands on different types of social behavior to provide a better understanding of the underlying mechanisms, which might support the development of selective tools for the optimized treatment of disorders associated with social deficits.

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