Losartan improves the performance of ethanol-intoxicated rats in an eight-arm radial maze.

Results of previous research demonstrate that angiotensin II (Ang II) inhibits long-term potentiation (LTP) in medial perforant path-dentate gyrus granule cells and that the inhibition is mediated by the AT1 receptor because it can be blocked by losartan, a specific AT1 receptor antagonist. Ang II impairment of retention and ethanol inhibition of LTP can both be blocked by pretreatment with losartan. Because losartan pretreatment also prevents ethanol intoxication measured in terms of the aerial righting reflex, the purpose of the present study was to assess the effects of 2.

Blockade of hippocampal long-term potentiation following soman pretreatment in the rat.

One of the most potent toxins known is the cholinesterase inhibitor, soman, which produces severe convulsions and cell loss in the central nervous system. In these experiments the effect of multiple low doses of soman on the acquisition and maintenance of long-term potentiation (LTP) was determined in rats. LTP is a form of synaptic plasticity that has been studied as a cellular substrate for learning and memory mechanisms.

Lateral hypothalamic stimulation inhibits dentate granule cell LTP: direct connections.

We discovered that angiotensin II (Ang II) applied directly to the dentate gyrus inhibited LTP induction in medial perforant path-dentate granule cell synapses and that the inhibition can be blocked by losartan, an Ang II AT1 receptor specific antagonist. In the first part of this study we found that electrical stimulation of the lateral hypothalamus (LH) inhibits LTP in these synapses and the inhibition can be blocked by pretreating the animals with losartan, indicating that LH angiotensin-containing neurons project to the dentate gyrus. Results of the second part of the study demonstrate clearly that some angiotensin-containing LH neurons project directly to dentate granule cells.

Ethanol affects hypothalamic neurons projecting to the hippocampus and inhibits dentate granule cell LTP.

In previous studies we demonstrated that ethanol inhibition of hippocampal granule cell long-term potentiation (LTP) is mediated by angiotensin II (AII), and the inhibition can be blocked by losartan, a specific AII receptor antagonist. The purpose of the present study was to demonstrate that this low-dose ethanol inhibition of dentate granule cell LTP induction is mediated by lateral hypothalamic (LH) afferents that project to the granule cells. In urethane anesthetized rats, we compared the effects of ethanol infusion, 6.

Comparison of retinyl ester hydrolase activities in bovine liver and retinal pigment epithelium.

Various properties of retinyl ester hydrolysis in the liver and the retinal pigment epithelium (RPE) have been studied, yet the relationship between the retinyl ester hydrolase (REH) activities in these tissues of the same species is not known. In the present study, REH activities in bovine liver and RPE microsomes were compared to explore potential biochemical relationships of retinyl ester metabolism in these tissues. Rates of [3H]all-trans retinyl palmitate hydrolysis by liver and RPE were comparable (i.

Angiotensin II antagonists block ethanol effects on the aerial righting reflex.

The purpose of the present study was to determine the effects of an angiotensin II (AII) AT1 antagonist, losartan 10, 15, and 20 mg/kg IP, and the AII AT2 antagonist, PD 123319, 20 mg/kg IP on ethanol (EtOH) intoxication as measured by the aerial righting reflex in male rats. EtOH (25%), 2.0 g/kg, was administered by stomach tube under mild metaphane anesthesia and the aerial righting reflex was determined at 30-min intervals for 3.

Nicotine blocks angiotensin II inhibition of LTP in the dentate gyrus.

Angiotensin (ANG)-containing axons, terminals, and receptors have been found in the hippocampus. When angiotensin II (ANG II) is administered to the dentate gyrus, long-term potentiation (LTP) induction, in response to medial perforant path stimulation, is inhibited and it can be blocked by losartan, an ANG II AT1 receptor antagonist. ANG II has been shown to mediate impairment of the retention of an inhibitory shock avoidance response and to be involved in ethanol and diazepam inhibition of dentate gyrus LTP, all of which can be blocked by losartan.

Angiotensin II blockade of long-term potentiation at the perforant path--granule cell synapse in vitro.

Field recordings of evoked excitatory postsynaptic potentials (pEPSPs) were carried out in the granule cell stratum moleculare following stimulation of the perforant path in rat hippocampal slices. Under control conditions tetanic stimulation produced long-term potentiation (LTP) as measured by an increase in the initial slope of the pEPSPs that lasted for at least 1 h. LTP experiments were repeated with 0.

Dose and time dependency of angiotensin II inhibition of hippocampal long-term potentiation.

We previously reported that injection of 1.0 microliter of 4.78 microM angiotensin II (AII) above the hippocampus in rats inhibits long-term potentiation (LTP) induction in medial perforant path-stimulated dentate granule cells.

Light microscopic immunocytochemical evidence of converging serotonin and dopamine terminals in ventrolateral nucleus accumbens.

The mesencephalic tegmentum contains monoaminergic neurons that project to the nucleus accumbens (NAcc). These monoaminergic neurons consist of the serotonergic (5-HT) neurons of the dorsal and median raphe and the dopaminergic (DA) neurons of the ventral tegmental area (VTA). Recent neurochemical reports describe cocaine-induced alterations in dopamine and serotonin release in NAcc that has coincidental occurrence both spatially and temporally, as shown by in vivo voltammetry.

Losartan reduces ethanol intoxication in the rat.

Results of a previous study showed that ethanol inhibition of hippocampal long-term potentiation (LTP) induction was mediated by angiotensin II (AII) and the AT1 subtype receptor because it was blocked by losartan, a specific AT1 antagonist. Because LTP is an important hippocampal function involved in the memory process and other behaviors, it is possible that losartan might block some of the directly observable ethanol-induced changes in rat behavior. Results demonstrate that losartan can effectively block some of the intoxicating effects of low doses of ethanol, 2 g/kg PO or IP.

Catecholamine-CRF synaptic interaction in a septal bed nucleus: afferents of neurons in the bed nucleus of the stria terminalis.

Projections of catecholamine neurons to the bed nucleus of the stria terminalis (BST), especially its corticotropin releasing factor (CRF)-producing neurons, are implicated as being major contributors to the neurochemically mediated central regulation of the stress response. The purpose of the present study was to examine in the BST of the rat brain the morphological characteristics of interactions between two neuron populations of the brain, catecholaminergic and CRF neurons. A double-label immunocytochemical, light and electron microscopic technique allowed the demonstration of the synaptic interaction between dopamine (DA, i.

Angiotensin AII AT1 receptor mediates ethanol-diazepam inhibition of hippocampal LTP.

Within a limited range of doses, co-administration of ethanol (EtOH) and diazepam (DZ) produce enhanced anxiolytic effects. These combined effects on long-term potentiation (LTP) in the hippocampus of rats anesthetized with urethane were studied in an attempt to provide an explanation at a more fundamental neuronal level. Male Sprague-Dawley rats received 0.