Injection of muscimol into posterior hypothalamus blocks stress-induced tachycardia

1989 ◽  
Vol 257 (1) ◽  
pp. R246-R251 ◽  
Author(s):  
M. Lisa ◽  
E. Marmo ◽  
J. H. Wible ◽  
J. A. DiMicco
Keyword(s):  
Gaba Receptors ◽  
Potential Role ◽  
Hypothalamic Nucleus ◽  
Gamma Aminobutyric Acid ◽  
Similar Treatment ◽  
Cardiovascular Changes ◽  
Vehicle Treatment ◽  
Response To Stress ◽  
Posterior Hypothalamic Nucleus

We have previously shown that the physiological and behavioral manifestations of emotional stress are produced when drugs impairing gamma-aminobutyric acid (GABA)-mediated synaptic inhibition are injected into the posterior hypothalamic nucleus in rats [Wible, J.H., Jr., F.C. Luft, and J.A. DiMicco. Am. J. Physiol. 254 (Regulatory Integrative Comp. Physiol. 23): R680-R687, 1988]. The purpose of this study was to assess further the potential role of GABA receptors in this region in the response to stress using muscimol, a GABAA receptor agonist. In six chronically instrumented conscious rats, air stress after vehicle treatment evoked marked and sustained tachycardia (+130 +/- 14 beats/min at +10 min) accompanied by a less dramatic increase in arterial pressure (+14 +/- 3 mmHg). Microinjection of muscimol (10 ng; 88 pmol) at the same posterior hypothalamic site in which GABA blockade causes cardiovascular changes similar to those seen in stress produced a modest depression of cardiovascular function in unstressed animals (-28 +/- 5 beats/min and -6 +/- 3 mmHg). However, similar treatment with muscimol virtually abolished the stress-induced tachycardia in the same rats (+9 +/- 8 beats/min), while having no significant effect on baroreflex-evoked increases in heart rate caused by intravenous infusion of sodium nitroprusside (4 micrograms). These findings support a role for activation of neurons in the posterior nucleus of the hypothalamus in the generation of stress-induced cardiovascular changes and for control of this mechanism by local GABA receptors.

scholarly journals Autophagy is activated in the ovarian tissue of polycystic ovary syndrome

Reproduction ◽  
2018 ◽  
Vol 155 (1) ◽  
pp. 85-92 ◽  
Author(s):  
Da Li ◽  
Yue You ◽  
Fang-Fang Bi ◽  
Tie-Ning Zhang ◽  
Jiao Jiao ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Potential Role ◽  
Polycystic Ovary ◽  
Ovarian Tissue ◽  
Ovary Syndrome ◽  
Cellular Processes ◽  
Transmission Electron ◽  
Wide Range ◽  
Response To Stress

The importance of autophagy in polycystic ovary syndrome (PCOS)-related metabolic disorders is increasingly being recognized, but few studies have investigated the role of autophagy in PCOS. Here, transmission electron microscopy demonstrated that autophagy was enhanced in the ovarian tissue from both humans and rats with PCOS. Consistent with this, ovarian granulosa cells from PCOS rats showed increases in the autophagy marker protein light chain 3B (LC3B), whereas levels of the autophagy substrate SQSTM1/p62 were decreased. In addition, the ratio of LC3-II/LC3-I was markedly elevated in human PCOS ovarian tissue compared with normal ovarian tissue. Real-time PCR arrays indicated that 7 and 34 autophagy-related genes were down- and up-regulated in human PCOS , Signal-Net, and regression analysis suggested that there are a wide range of interactions among these 41 genes, and a potential network based on EGFR, ERBB2, FOXO1, MAPK1, NFKB1, IGF1, TP53 and MAPK9 may be responsible for autophagy activation in PCOS. Systematic functional analysis of 41 differential autophagy-related genes indicated that these genes are highly involved in specific cellular processes such as response to stress and stimulus, and are linked to four significant pathways, including the insulin, ERBB, mTOR signaling pathways and protein processing in the endoplasmic reticulum. This study provides evidence for a potential role of autophagy disorders in PCOS in which autophagy may be an important molecular event in the pathogenesis of PCOS.

Involvement of Corticotrophin-Releasing Factor and Orexin-A in Chronic Migraine and Medication-Overuse Headache: Findings From Cerebrospinal Fluid

Cephalalgia ◽  
2008 ◽  
Vol 28 (7) ◽  
pp. 714-722 ◽  
Author(s):  
P Sarchielli ◽  
I Rainero ◽  
F Coppola ◽  
C Rossi ◽  
ML Mancini ◽  
...  
Keyword(s):  
Chronic Migraine ◽  
Potential Role ◽  
Medication Overuse ◽  
Medication Overuse Headache ◽  
Orexin A ◽  
Compensatory Response ◽  
Corticotrophin Releasing Factor ◽  
Response To Stress ◽  
The Brain

The study set out to investigate the role of corticotrophin-releasing factor (CRF) and orexin-A in chronic migraine (CM) and medication-overuse headache (MOH). Twenty-seven patients affected by CM and 30 with MOH were enrolled. Control CSF specimens were obtained from 20 age-matched subjects who underwent lumbar puncture for diagnostic purposes, and in all of them CSF and blood tests excluded central nervous system or systemic diseases. Orexin-A and CRF were determined by radioimmunoassay methods. Significantly higher levels of orexin-A and CRF were found in the CSF of MOH and to a lesser extent in patients with CM compared with control subjects (orexin-A: P < 0.001 and P < 0.02; CRF: P < 0.002 and P < 0.0003). A significant positive correlation was also found between CSF orexin-A values and those of CRF ( R = 0.71; P < 0.0008), monthly drug intake group ( R = 0.39; P < 0.03) and scores of a self-completion 10-item instrument to measure dependence upon a variety of substances, the Leeds Dependence Questionnaire (LDQ) in the MOH group ( R = 0.68; P < 0.0003). The significantly higher orexin-A levels found in CM and MOH can be interpreted as a compensatory response to chronic head pain or, alternatively, as an expression of hypothalamic response to stress due to chronic pain. A potential role for orexin-A in driving drug seeking in MOH patients through activation of stress pathways in the brain can also be hypothesized.

scholarly journals Ionotropic GABA Receptors and Distal Retinal ON and OFF Responses

Scientifica ◽  
2014 ◽  
Vol 2014 ◽  
pp. 1-23 ◽  
Author(s):  
E. Popova
Keyword(s):  
Gaba Receptors ◽  
Time Course ◽  
Light Adaptation ◽  
Current Knowledge ◽  
Relative Sensitivity ◽  
Bipolar Cells ◽  
Visual Signals ◽  
Gamma Aminobutyric Acid ◽  
Large Populations

In the vertebrate retina, visual signals are segregated into parallel ON and OFF pathways, which provide information for light increments and decrements. The segregation is first evident at the level of the ON and OFF bipolar cells in distal retina. The activity of large populations of ON and OFF bipolar cells is reflected in the b- and d-waves of the diffuse electroretinogram (ERG). The role of gamma-aminobutyric acid (GABA), acting through ionotropic GABA receptors in shaping the ON and OFF responses in distal retina, is a matter of debate. This review summarized current knowledge about the types of the GABAergic neurons and ionotropic GABA receptors in the retina as well as the effects of GABA and specific GABAAand GABACreceptor antagonists on the activity of the ON and OFF bipolar cells in both nonmammalian and mammalian retina. Special emphasis is put on the effects on b- and d-waves of the ERG as a useful tool for assessment of the overall function of distal retinal ON and OFF channels. The role of GABAergic system in establishing the ON-OFF asymmetry concerning the time course and absolute and relative sensitivity of the ERG responses under different conditions of light adaptation in amphibian retina is also discussed.

Studies of the role of gamma-aminobutyric acid in the hypothalamic control of feed intake in sheep

1985 ◽  
Vol 63 (10) ◽  
pp. 1297-1301 ◽  
Author(s):  
C. L. Girard ◽  
J. R. Seoane ◽  
J. J. Matte
Keyword(s):  
Dose Response ◽  
Feed Intake ◽  
Gaba Receptors ◽  
Response Curve ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Gaba Antagonists ◽  
Gaba Agonist ◽  
Hypothalamic Control

Fourteen sheep were used to study the role of gamma-aminobutyric acid (GABA) on the hypothalamic control of feed intake. Injections (1 μL) of pentobarbital (262 nmol) into preoptic and paraventricular areas induced feeding in satiated sheep. Injections of GABA into the same loci gave variable results, probably because the neuronal and glial uptake of GABA limits its effects. Muscimol, a GABA agonist with a higher affinity for postsynaptic GABA receptors than GABA, injected at doses from 0 to 0.750 nmol, gave a cubic dose–response curve; the highest feed intake was measured at 0.5 nmol. The response induced by muscimol was blocked by preinjections of two GABA antagonists, picrotoxin and bicuculline, with picrotoxin being more effective than bicuculline. Muscimol responsive loci were identified mainly in the preoptic, paraventricular, and anterior hypothalamus. The data suggests that neurons sensitive to gamma-aminobutyric acid may be implicated in the control of feed intake in sheep.

New aspects in the pathophysiology of rapid eye movement sleep behavior disorder: the potential role of glutamate, gamma-aminobutyric acid, and glycine

2013 ◽  
Vol 14 (8) ◽  
pp. 714-718 ◽  
Author(s):  
Pierre-Hervé Luppi ◽  
Olivier Clément ◽  
Sara Valencia Garcia ◽  
Frédéric Brischoux ◽  
Patrice Fort
Keyword(s):  
Eye Movement ◽  
Potential Role ◽  
Behavior Disorder ◽  
Aminobutyric Acid ◽  
Rapid Eye Movement ◽  
Gamma Aminobutyric Acid ◽  
Rapid Eye Movement Sleep ◽  
Sleep Behavior

scholarly journals Role of VMH ketone bodies in adjusting caloric intake to increased dietary fat content in DIO and DR rats

2015 ◽  
Vol 308 (10) ◽  
pp. R872-R878 ◽  
Author(s):  
Christelle Le Foll ◽  
Ambrose A. Dunn-Meynell ◽  
Henry M. Miziorko ◽  
Barry E. Levin
Keyword(s):  
Food Intake ◽  
Potential Role ◽  
Ketone Bodies ◽  
Caloric Intake ◽  
High Energy ◽  
Leptin Resistance ◽  
Hypothalamic Nucleus ◽  
Diet Intake ◽  
Body Production

The objective of this study was to determine the potential role of astrocyte-derived ketone bodies in regulating the early changes in caloric intake of diet induced-obese (DIO) versus diet-resistant (DR) rats fed a 31.5% fat high-energy (HE) diet. After 3 days on chow or HE diet, DR and DIO rats were assessed for their ventromedial hypothalamic (VMH) ketone bodies levels and neuronal ventromedial hypothalamic nucleus (VMN) sensing using microdialysis coupled to continuous food intake monitoring and calcium imaging in dissociated neurons, respectively. DIO rats ate more than DR rats over 3 days of HE diet intake. On day 3 of HE diet intake, DR rats reduced their caloric intake while DIO rats remained hyperphagic. Local VMH astrocyte ketone bodies production was similar between DR and DIO rats during the first 6 h after dark onset feeding but inhibiting VMH ketone body production in DR rats on day 3 transiently returned their intake of HE diet to the level of DIO rats consuming HE diet. In addition, dissociated VMN neurons from DIO and DR rats were equally sensitive to the largely excitatory effects of β-hydroxybutyrate. Thus while DR rats respond to increased VMH ketone levels by decreasing their intake after 3 days of HE diet, this is not the case of DIO rats. These data suggest that DIO inherent leptin resistance prevents ketone bodies inhibitory action on food intake.

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