Evoked potentials as indicator of possible involvement of ventromedial hypothalamus and lateral nucleus of the amygdala in the formation of feeding behavior

2004 ◽  
Vol 138 (5) ◽  
pp. 433-436
Author(s):  
V. M. Serdyuchenko ◽  
N. S. Kositsyn
Keyword(s):  
Evoked Potentials ◽  
Feeding Behavior ◽  
Ventromedial Hypothalamus ◽  
Lateral Nucleus

scholarly journals Adeno-associated viral glutamate decarboxylase expression in the lateral nucleus of the rat hypothalamus reduces feeding behavior

Gene Therapy ◽  
2004 ◽  
Vol 11 (9) ◽  
pp. 797-804 ◽  
Author(s):  
A J Noordmans ◽  
D K Song ◽  
C J Noordmans ◽  
M Garrity-Moses ◽  
M J During ◽  
...  
Keyword(s):  
Feeding Behavior ◽  
Glutamate Decarboxylase ◽  
Rat Hypothalamus ◽  
Lateral Nucleus

scholarly journals Slow Late Component in Conditioned Stimulus-Evoked Potentials From the Amygdala After Fear Conditioning in the Rat

2002 ◽  
Vol 9 (4) ◽  
pp. 261-272 ◽  
Author(s):  
J. M. J. Knippenberg ◽  
E. L. J. M. van Luijtelaar ◽  
J. H. R. Maes
Keyword(s):  
Evoked Potentials ◽  
Fear Conditioning ◽  
Slow Component ◽  
Pavlovian Fear Conditioning ◽  
Late Component ◽  
Conditioning Procedure ◽  
Experimental Conditions ◽  
Before And After ◽  
Male Wistar Rats ◽  
Lateral Nucleus

Male Wistar rats were subjected to a differential Pavlovian fear conditioning procedure in which one of two tones (6 or 10 kHz) was followed by an electric shock (CS+) and the other was not (CS-). Before and after fear conditioning, we recorded the evoked potentials elicited byCS+andCS-from electrodes aimed at the lateral nucleus of the amygdala. Before conditioning, a slow, negative component with peak amplitude around 150 ms was present in the evoked potentials. This component was sensitive to habituation. After fear conditioning, bothCS+andCS-elicited the same late component, albeit with a larger amplitude. This enhancement was temporary: decreasing amplitude was observed in the course of CS test presentations under extinction. Prior research revealed a comparable slow component in the amygdala of the cat under similar experimental conditions. The collective results indicate that the large late component in the amygdala is enhanced by fear conditioning, suggesting that such enhancement reflects the anticipation of a biologically significant event.

Anorexia induced in rat by D-glucosamine deoxidized at C-1

1986 ◽  
Vol 251 (3) ◽  
pp. R481-R491 ◽  
Author(s):  
K. Fujimoto ◽  
T. Sakata ◽  
T. Shiraishi ◽  
K. Kurata ◽  
K. Terada ◽  
...  
Keyword(s):  
Feeding Behavior ◽  
Dark Period ◽  
Ventromedial Hypothalamus ◽  
Hydroxyl Group ◽  
Behavior Changes ◽  
Amino Group ◽  
The Third ◽  
Glucose Molecule ◽  
Endogenous Glucose ◽  
Glucose Analogue

The effects of D-glucosamine (2-amino-2-deoxy-D-glucose), an endogenous glucose analogue, and 1-deoxy-D-glucosamine on feeding behavior were clarified. Test solutions (24 mumol) were infused into the third cerebroventricle of the rat. Glucosamine induced a feeding episode within 30 min after infusion and then prolonged the ensuing postprandial intermeal interval for the first 4 h of the dark period, while glucose suppressed feeding by decreasing meal size. Ventricular injection of 1-deoxyglucosamine potently suppressed feeding in a dose-related manner by affecting all meal parameters, and oral administration of 2,400 mumol also induced anorexia. Changes in activity of glucose-sensitive neurons in the lateral hypothalamus and glucoreceptor neurons in the ventromedial hypothalamus after electrophoretic application of glucosamine and 1-deoxyglucosamine were compatible with behavior changes. The results indicate that replacement of a hydroxyl group by an amino group at C-2 of the glucose molecule affects feeding behavior and deoxidation of C-1 potently induces anorexia.

Glucagon-like peptide 1-(7–36) amide acts at lateral and medial hypothalamic sites to suppress feeding in rats

2003 ◽  
Vol 284 (6) ◽  
pp. R1427-R1435 ◽  
Author(s):  
Rafael R. Schick ◽  
Jens P. Zimmermann ◽  
Thomas vorm Walde ◽  
Volker Schusdziarra
Keyword(s):  
Food Intake ◽  
Feeding Behavior ◽  
Effective Dose ◽  
Ventromedial Hypothalamus ◽  
Brain Regions ◽  
Central Administration ◽  
Minimal Effective Dose ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Fasted Rats

Glucagon-like peptide 1-(7–36) amide (GLP-1) potently inhibits rat feeding behavior after central administration. Because third ventricular injection of GLP-1 appeared to be less effective than lateral ventricular injection, we have reexamined this issue. In addition, we attempted to identify brain regions other than the paraventricular nucleus of the hypothalamus that are sensitive toward GLP-1-induced feeding suppression. Finally, we examined the local role of endogenous GLP-1 by specific GLP-1 receptor blockade. After lateral ventricular injection, GLP-1 significantly inhibited food intake of 24-h-fasted rats in a dose-dependent fashion with a minimal effective dose of 1 μg. After third ventricular injection, GLP-1 (1 μg) was similarly effective in suppressing food intake, which extends previous findings. Intracerebral microinjections of GLP-1 significantly suppressed food intake in the lateral (LH), dorsomedial (DMH), and ventromedial hypothalamus (VMH), but not in the medial nucleus of the amygdala. The minimal effective dose of GLP-1 was 0.3 μg at LH sites and 1 μg at DMH or VMH sites. LH microinjections of exendin-(9–39) amide, a GLP-1 receptor antagonist, at 1 or 2.5 μg did not alter feeding behavior in 24-h-fasted rats. In satiated animals, however, a single LH injection of 1 μg exendin-(9–39) amide significantly augmented food intake, but only during the first 20 min (0.6 vs. 0.1 g). With three repeated injections of 2.5 μg exendin-(9–39) amide every 20 min, 1-h food intake was significantly increased by 300%. These data strongly support and extend the concept of GLP-1 as a physiological regulator of food intake in the hypothalamus.

Feeding induced by intracerebroventricular 2-deoxy-D-glucose in the rat

1975 ◽  
Vol 229 (5) ◽  
pp. 1438-1447 ◽  
Author(s):  
RR Miselis ◽  
AN Epstein
Keyword(s):  
Feeding Behavior ◽  
Core Temperature ◽  
Lateral Hypothalamus ◽  
Mode Of Action ◽  
Preoptic Area ◽  
Ventromedial Hypothalamus ◽  
Dependent Manner ◽  
Dose Dependent ◽  
The Brain ◽  
Glucose Analogue

Feeding was induced with lateral intracerebroventricular (ICV) injections of 2-deoxy-D-glucose (2-dg), a glucose analogue causing glucoprivation. Feeding increased rapidly by an average of 2.6 g following ICV 2-DG (2.9 or 5.8 mg per rat), but did not increase after ICV D-glucose or sucrose. At the same doses, 2-DG did not increase feeding when given peripherally. Core temperature dropped in a dose-dependent manner with doses of 2-DG sufficient to induce feeding after peripheral administration, but did not occur with ICV injections. The 2-DG (0.006--1.219 M) did not stimulate feeding when infused bilaterally into the lateral hypothalamus, the preoptic area, or the anterior lateral hypothalamus. Nor did it produce feeding when injected into the ventromedial hypothalamus at the same sites and in the same rats in which procaine HC1 caused increased feeding. The brain, therefore, is directly sensitive to glucoprivation in the control of feeding, and glucoprivation alone is sufficient to mobilize feeding behavior. The specific site of sensitivity to glucoprivation and the mode of action of the glucoprivic system in the brain are unknown.

Effect of urea on central nervous system activity in the cat

1959 ◽  
Vol 197 (1) ◽  
pp. 141-144 ◽  
Author(s):  
George C. Stevenson ◽  
R. Campbell Jacobs ◽  
M. William Ross ◽  
William F. Collins ◽  
Clark T. Randt
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Evoked Potentials ◽  
Reticular Formation ◽  
Operative Procedure ◽  
Cortical Activity ◽  
Nervous System Activity ◽  
Midbrain Reticular Formation ◽  
Central Nervous System Activity ◽  
Lateral Nucleus

Effects of i.v. infusion of urea were studied in 26 cats by recording spontaneous cortical activity and somatic afferent evoked potentials from the posteroventral lateral nucleus of the thalamus and periaqueductal midbrain reticular formation. Subsequent to the administration of a 20% solution of urea, spindling and seizure discharges appeared in the electrocorticogram. The evoked potentials from the posteroventral lateral nucleus of the thalamus and reticular formation remained unchanged. Control studies indicated that the operative procedure, including the insertion of subcortical electrodes, hydration incident to fluid administration, possible deterioration of the preparation and alteration of the osmolarity of the serum did not produce the observed results. It was demonstrated that urea administered intravenously, in amounts producing blood NPN values commensurate with those observed in patients with uremia, alters cortical activity and excitability.

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