Interaction of taurine and related compounds with GABAergic neurones in the nucleus raphe dorsalis

Liljequist, R.

doi:10.1016/0091-3057(93)90286-3

Cited by 17 publications

(9 citation statements)

References 27 publications

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“…For this purpose, we microinjected very low doses of recombinant human leptin directly into the VMH and compared the effects on eating to those of similar small doses delivered into the lateral ventricle or into the dorsal raphe nucleus, another brain region believed to play a role in feeding behavior (10).…”

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The Effect of Leptin Is Enhanced by Microinjection Into the Ventromedial Hypothalamus

et al. 1997

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To determine whether changes in food intake produced by leptin involve targeting the hormone to distinct central nervous system regions, guide cannulas were positioned stereotaxically into three brain regions-the ventromedial hypothalamus (VMH) (bilaterally, n = 6), the dorsal raphe nucleus (/i = 3), and the lateral ventricle (w = 3)-of nonobese male rats (400-500 g). Daily food intake and body weight changes were measured during twice-daily injections of saline (0.1 ul) followed by recombinant human leptin (0.05 ug) for 3 days via the brain cannulas. VMH-injected rats also were followed during a postleptin saline recovery interval. This small dose of leptin did not change food intake or body weight from that during the preceding saline injection period in ventricle-injected or dorsal raphe-injected rats. In sharp contrast, VMH-injected rats ate much less food (56 ± 8% basal) and lost 9 + 3 g/day or 5% of their body weight during 3 days of leptin administration. VMH-injected animals fully recovered from leptin-induced effects within 3 days. We conclude that small doses of leptin that do not effect eating behavior when delivered to the ventricle or the dorsal raphe (another brain region believed to regulate feeding), suppress food intake when injected into the VMH. These data suggest that the VMH or a brain region in close proximity to it is a key target for the biological actions of leptin. Diabetes 46:150-152, 1997 O besity and its resulting complications, such as heart disease, hypertension, dyslipidemia, and diabetes, have become increasingly significant public health concerns. The existence of a circulating satiety factor that contributes to the development of obesity has been suggested since the early parabiotic experiments of Coleman (1) showing reversal of obesity when the circulatory system of a morbidly obese (pb/ob) mouse was connected to that of a lean mouse. This hypothesis has been greatly strengthened by the recent cloning of the ob gene (2) From the Yale University School of Medicine, Department of Internal Medicine, New Haven, Connecticut.Address correspondence and reprint requests to Ralph J. Jacob, Yale University School of Medicine, Department of Internal Medicine/Endocrinology, 333 Cedar St., Box 208020, New Haven, CT 06520-8020.Received for publication 7 August 1996 and accepted in revised form 18 October 1996.CNS, central nervous system; VMH, ventromedial hypothalamus.and the identification of its product (leptin) as a 16-kDa protein secreted by adipose tissue into the circulation. In the ob/ob mouse, a mutation of the leptin gene results in the production of a truncated nonfunctional molecule. The importance of this genetic defect is underscored by data showing that systemic or intracerebroventricular (in smaller doses) administration of leptin produces reductions in food intake and body weight in leptin-deficient ob/ob mice (3-6). To produce similar effects in lean animals, much larger doses of leptin were required (3-6). Although a wide variety of tissues appear to express leptin recepto...

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The Effect of Leptin Is Enhanced by Microinjection Into the Ventromedial Hypothalamus

et al. 1997

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“…Performance in different types of learning tasks may depend on different attributes of the remembered experience. The results from our previous studies with adult rats showed that similarly to spatial learning, active avoidance learning performance was also facilitated with intraperitoneal GES administration (Liljequist et al 1983(Liljequist et al & 1990. Although these results together support the conclusion that the administration of GES favours learning and recalling phases in these two types of learning tasks, additional behavioural analyses are needed to characterize how learning or alternatively, performance factors are influenced.…”

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confidence: 80%

“…We have previously described facilitated learning performance of adult rats in one way active avoidance (Liljequist et a/. 1983) and spatial learning (Liljequist et al 1990) situations following the administration of guanidinoethanesulphonic acid (GES). The facilitated acquisition performance could be blocked by the N-methyl-D-aspartate (NMDA) receptor channel blocker MK-801.…”

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Guanidinoethanesulphonic Acid Facilitates Retention of Spatial Memory in Old Rats

Liljequist

Winblad

1993

Pharmacology & Toxicology

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“…Cognitive performance changes in close relation with NMDA receptors and even low concentrations of additional excitatory amino acids and modulatory compounds are able to induce variations in learning capacity (Liljequist, 1996). GES has been found to interact with the GABAergic ion-channel (Liljequist, 1993). MK-801, an antagonist at the ion-channel of NMDA preferring subtype of glutamate receptors, and GES have shown weak interactions in in vivo animal learning and activity studies and ex vivo binding experiments (Liljequist, 1990;Liljequist and Winblad, 1993).…”

Section: Discussionmentioning

confidence: 98%

Guanidinoethane sulphonic acid interferes with the binding of [3H]dizocilpine and neurotoxic action of AF64A

Liljequist

1997

Amino Acids

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Summary. The binding of [3H]dizocilpine [[3H]MK-801] to the N-methyl-D-aspartate receptor complex of well washed rat cortical membranes was reduced by guanidinoethane sulphonic acid (GES). Micromolar concentrations of GES, which were high relative to those of dizocilpine, inhibited in a concentration dependent manner the binding of [3H]dizocilpine. The inhibitory effect of GES on [3H]dizocilpine binding was slightly influenced by concentration of glutamate. The glutamate antagonist DL-2-amino-5-phosphonovaleric acid blocked the effect GES at concentrations higher relative to GES. The inhibitory effect of GES was still present during spermidine-induced stimulation of pH]dizocilpine binding. GES reduced the binding of the glycine antagonist [3H]5,7-dichlorokynurenic acid with an ICs0 of 530/~M. Intraperitoneal injections of GES (0.2mmol/kg) protected against both amnesia and decrease in the choline acetyltransferase activity following local injections of the neurotoxin AF64A into the nucleus basalis magnocellularis. GES given to lesioned rats during the training period in the spatial learning task gradually improved the performance to the level of sham operated rats. It is concluded that GES interferes with the transmitter and the dizocilpine binding sites of the NMDA receptor complex and has the capacity to protect against neurotoxic brain damage.

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Interaction of taurine and related compounds with GABAergic neurones in the nucleus raphe dorsalis

Cited by 17 publications

References 27 publications

The Effect of Leptin Is Enhanced by Microinjection Into the Ventromedial Hypothalamus

The Effect of Leptin Is Enhanced by Microinjection Into the Ventromedial Hypothalamus

Guanidinoethanesulphonic Acid Facilitates Retention of Spatial Memory in Old Rats

Guanidinoethane sulphonic acid interferes with the binding of [3H]dizocilpine and neurotoxic action of AF64A

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