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A Adell

Publications and source records attributed to A Adell.

At least 19 recordsLinked to original sources
PubMed2001

How does pindolol improve antidepressant action?

Since 1994, the beta-adrenoceptor and 5-HT(1A/1B) receptor ligand pindolol has been used to accelerate or enhance the clinical effects of antidepressant drugs, such as the selective 5-HT reuptake inhibitors (SSRIs), that act primarily on 5-HT-containing neurones. Pindolol was initially thought to act by preventing the inhibition of 5-HT release, elicited by SSRIs and other 5-HT-acting drugs, as a result of its ability to antagonize the action of 5-HT at midbrain raphe 5-HT(1A) autoreceptors that control the activity of ascending 5-HT-mediated pathways. However, the partial agonist properties of pindolol at 5-HT(1A) receptors and beta-adrenoceptors suggest that other explanations for its action are also possible. In this article, recent controversial data on the mechanism of action of pindolol, which are crucial for the development of more rapid and efficient antidepressant therapies, will be discussed.

Adrenergic beta-Antagonists↗
PubMed2001

The role of 5-HT1B receptors in the regulation of serotonin cell firing and release in the rat brain.

The release of 5-HT in terminal areas of the rodent brain is regulated by 5-HT1B receptors. Here we examined the role of 5-HT1B receptors in the control of 5-HT output and firing in the dorsal raphe nucleus (DR), median raphe nucleus (MnR) and forebrain of the rat in vivo. The local perfusion (30-300 microM) of the selective 5-HT1B receptor agonist CP-93,129 to freely moving rats decreased 5-HT release in the DR and more markedly in the MnR. Likewise, 300 microM CP-93,129 reduced 5-HT output in substantia nigra pars reticulata, ventral pallidum, lateral habenula and the suprachiasmatic nucleus. The effect of CP-93,129 was prevented by SB-224289, but not by WAY-100635, selective 5-HT1B and 5-HT1A receptor antagonists, respectively. SB-224289 did not alter dialysate 5-HT in any raphe nuclei. The intravenous administration of the brain-penetrant selective 5-HT1B receptor agonist CP-94,253 (0.5-2.0 mg/kg) to anesthetized rats decreased dialysate 5-HT in dorsal hippocampus and globus pallidus, increased it in MnR and left it unaltered in the DR and medial prefrontal cortex. SB-224289, at a dose known to block 5-HT1B autoreceptor-mediated effects (5 mg/kg), did not prevent the effect of CP-94,253 on MnR 5-HT. The intravenous administration of CP-94,253 (0.05-1.6 mg/kg) to anesthetized rats increased the firing rate of MnR, but not DR-5-HT neurons. The local perfusion of CP-94,253 in the MnR showed a biphasic effect, with 5-HT reductions at 0.3-3 microM and increase at 300 microM. These results suggest that 5-HT cell firing and release in midbrain raphe nuclei (particularly in the MnR) are under control of 5-HT1B receptors. The activation of 5-HT1B autoreceptors (possibly located on 5-HT nerve endings and/or varicosities within DR and MnR) reduces 5-HT release. The effects of higher concentrations of 5-HT1B receptor agonists seem more compatible with the activation of 5-HT1B heteroreceptors on inhibitory neurons.

Animals↗
PubMed2000

On the Applicability of DLVO Theory to the Prediction of Clay Colloids Stability.

The stability behavior of Na-montmorillonite colloids has been studied by combining the analysis of their surface charge properties and time-resolved dynamic light scattering experiments. The chemical surface model for several types of clays, including montmorillonite, has to take into account the double surface charge contribution due to their permanent structural charge and to their pH-dependent charge, which is developed at the edge sites, therefore, these stability studies were carried out as a function of both ionic strength and pH. DLVO theory is largely applied for the prediction of the stability of many colloidal systems, including the natural ones. This work shows that the stability behavior of Na-montmorillonite colloids cannot be satisfactorily reproduced by DLVO theory, using the surface parameters experimentally obtained. Particularly, this theory is unable to explain their pH-dependent stability behavior caused by the small charge at the edge sites. Based on these results, a literature review of DLVO stability prediction of clay colloids was performed. It confirmed that this theory is not capable of taking into account the double contribution to the total surface charge and, at the same time, pointed out the main uncertainties related to the appropriate use of the input parameters for the calculation as, for example, the Hamaker constant or the surface potential. Copyright 2000 Academic Press.

Journal Article↗
PubMed2000

GABAB-RI receptors in serotonergic neurons: effects of baclofen on 5-HT output in rat brain.

The activation of GABAB receptors hyperpolarizes 5-HT neurons and reduces cell firing. In situ hybridization showed the presence of the GABAB-RI receptor transcript in virtually all 5-HT neurons of the dorsal and median raphe nuclei (DR and MnR, respectively) whereas the GAD transcript was present mainly outside these nuclei. The systemic administration of baclofen increased the in vivo 5-HT release in the DR, MnR and several projection areas. As shown previously in the DR, the application of baclofen in the MnR increased the local 5-HT output. Thus, although 5-HT neurons contain inhibitory GABAB-RI receptors, baclofen increased 5-HT release in some brain areas, likely by a preferential action on terminal GABAB autoreceptors in inhibitory inputs to 5-HT neurons. The scarcity of GAD-expressing cells in the DR and MnR suggests that these inputs originate mainly outside these nuclei.

Animals↗
PubMed2000

Role of uptake inhibition and autoreceptor activation in the control of 5-HT release in the frontal cortex and dorsal hippocampus of the rat.

1. Using brain microdialysis, we compared the relative role of 5-hydroxytryptamine (5-HT; serotonin) blockade and somatodendritic 5-HT(1A) and/or terminal 5-HT(1B) autoreceptor activation in the control of 5-HT output. 2. Fluoxetine (10 mg kg(-1) i.p.) doubled the 5-HT output in frontal cortex and dorsal hippocampus. The 5-HT(1A) receptor antagonist WAY 100635, (0.3 mg kg(-1) s.c.) potentiated the effect of fluoxetine only in frontal cortex (to approximately 500 % of baseline). 3. Methiothepin (10 mg kg(-1) s.c.) further enhanced the 5-HT rise induced by fluoxetine+WAY 100635, to 835+/-179% in frontal cortex and 456+/-24% in dorsal hippocampus. Locally applied, methiothepin potentiated the fluoxetine-induced 5-HT rise more in the former area. 4. The selective 5-HT(1B) receptor antagonist SB-224289 (4 mg kg(-1) i.p.) enhanced the effect of fluoxetine (10 mg kg(-1) i.p.) in both areas. As with methiothepin, SB-224289 (4 mg kg(-1) i.p.) further enhanced the 5-HT increase produced by fluoxetine+WAY 100635 more in frontal cortex (613+/-134%) than in dorsal hippocampus (353+/-59%). 5. Locally applied, fluoxetine (10 - 300 microM; EC(50)=28 - 29 microM) and citalopram (1 - 30 microM; EC(50)=1.0 - 1.4 microM) increased the 5-HT output two to three times more in frontal cortex than in dorsal hippocampus. These data suggest that the comparable 5-HT increase produced by systemic fluoxetine in frontal cortex and dorsal hippocampus results from a greater effect of reuptake blockade in frontal cortex that is offset by a greater autoreceptor-mediated inhibition of 5-HT release. As a result, 5-HT autoreceptor antagonists preferentially potentiate the effect of fluoxetine in frontal cortex.

Animals↗
PubMed1999

Regulation of the release of 5-hydroxytryptamine in the median raphe nucleus of the rat by catecholaminergic afferents.

The present study was conducted in order to examine the influence of catecholaminergic afferents on the release of serotonin in the median raphe nucleus in vivo. To this aim, selective dopamine D1 and D2, and alpha1- and alpha2-adrenergic agonists and antagonists were administered locally (1, 10 and 100 microM) through a dialysis probe implanted in the median raphe nucleus of freely moving rats. The D1 and D2 agonists, (+/-)-1-phenyl-2,3,4, 5-tetrahydro-(1H)-3-benzazepine-7,8-diol (SKF-38393) and quinpirole, respectively, and the D1 and D2 antagonists, R-(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4, 5-tetrahydro-1H-3-benzazepine (SCH-23390) and raclopride, respectively, did not alter the release of serotonin in the median raphe nucleus. The alpha1-adrenoceptor agonist phenylephrine did not modify the release of serotonin in this nucleus, although an increased release was observed when the more potent alpha1-adrenoceptor agonist cirazoline was used. In contrast, the alpha1-adrenoceptor antagonist prazosin reduced the release of 5-hydroxytryptamine (5-HT) in a concentration-dependent manner. The release of 5-HT was also reduced by the alpha2-adrenoceptor agonist clonidine and increased by the alpha2-adrenoceptor antagonist 2-methoxy-idazoxan (RX821002). These results indicate that the release of serotonin in the median raphe nucleus does not appear to be regulated by dopaminergic afferents through the activation of dopamine D1 or D2 receptors. On the contrary, it is suggested that endogenous noradrenaline exerts a direct tonic stimulatory control on the release of serotonin through alpha1-adrenoceptors, and an indirect tonic inhibitory influence through alpha2-adrenoceptors located probably in noradrenergic nerve terminals within the median raphe nucleus.

Adrenergic alpha-Agonists↗
PubMed1998

Simultaneous comparison of cerebral dialysis and push-pull perfusion in the brain of rats: a critical review.

Over the last 30 years, studies of the in vivo activity of neurotransmitters and other endogenous factors in the brain have comprised a major effort in the neurosciences. Historically, the technology of push-pull perfusion was utilized as a major approach to investigations in this field. In the last 10 years, cerebral dialysis has been used as an alternative method essentially for the same scientific purpose, since the perfusion technique was viewed as difficult and excessively damaging to tissue. This review considers the representative literature in which both systems have been used to study local neurochemical responses to a drug or other chemical factor, a physiological condition or other situation. In addition, new experiments have been undertaken to compare, in the same animal and at the same time, the utility and properties inherent in the techniques of push-pull perfusion and cerebral dialysis in terms of the profile of a neurotransmitter activity and their local histopathological effects. A miniaturized 33/26 ga push-pull needle and a 24 ga dialysis probe were implanted simultaneously in the left and right caudate nuclei, respectively, in the anesthetized rat. An artificial cerebrospinal fluid (CSF) was perfused simultaneously through both devices at a rate of 10 microliters/min in the push-pull cannula and at 1.0 or 2.0 microliters/min in the dialysis probe. Within a series of 8-10 successive perfusions, excess K+ ions in a concentration of either 30 or 60 mM were incorporated in the CSF and delivered simultaneously to both the push-pull cannula and dialysis probe. Samples of perfusate and dialysate were assayed chromatographically by coulometric HPLC detector and quantitated in terms of the pg/min efflux of dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA). The results showed that the resting level of DA was almost undetectable in dialysate samples from either structure; in push-pull perfusates the recovery of DA ranged between 7.0 to 10.0 pg/min, which was increased threefold by excess K+ ions. The recovery of DA and the three metabolites in samples of push-pull perfusate was two to four times that in samples of dialysate during the condition of excess K+ ions. Post-mortem histological analysis of the sites of perfusion and dialysis revealed little or no differences in the cytological damage induced by either the perfusion needle or dialysis probe. Finally, the advantages and limitations of each of these two experimental approaches to in vivo analysis of neurotransmitter efflux are reviewed in relation to the selection of an open or closed system for the on-line study of in vivo neurochemical events.

Animals↗
PubMed1998

A microdialysis study of the in vivo release of 5-HT in the median raphe nucleus of the rat.

The present study has examined several characteristics of the release of 5-HT in the median raphe nucleus in terms of its dependence of nerve impulse, provenance of a vesicular storage fraction as well as the regulatory role played by 5-HT1A receptors. Tetrodotoxin (1 microM) and reserpine (5 mg kg(-1), i.p.) virtually suppressed the output of 5-HT. The administration of EEDQ (10 mg kg(-1), i.p.) did not alter the basal release of 5-HT but abolished the reduction of 5-HT release induced by 8-OH-DPAT (0.1 mg kg(-1), s.c.). The perfusion of 1-100 microM of 8-OH-DPAT or the novel 5-HT1A agonist BAY x 3702 decreased the efflux of 5-HT, whereas the perfusion of the 5-HT1A antagonist WAY-100635 failed to alter 5-HT release. The decrease in dialysate 5-HT induced by 100 microM 8-OH-DPAT was reversed by the concurrent perfusion of 100 microM WAY-100635. Also, the perfusion of 100 microM WAY-100635 for 2 h inhibited partly the reduction of 5-HT release evoked by the systemic administration of 8-OH-DPAT (0.1 mg kg(-1)). These results indicate that extracellular 5-HT in the median raphe nucleus is stored in vesicles and released in an impulse-dependent manner. Also, the basal release of 5-HT in the median raphe nucleus does not appear to be under the tonic control of somatodendritic 5-HT1A receptors by endogenous 5-HT. Instead, this feedback mechanism seems to be triggered when an excess of the transmitter or a 5-HT1A agonist is present in the extracellular space of the median raphe nucleus.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1996

Lesioning of midbrain raphe nuclei with 5,7-DHT fails to alter ethanol intake in the low alcohol drinking (LAD) rat.

1. The effect of 10 g 5,7-dihydroxytryptamine (5,7-DHT) micro-injected into both the dorsal (DRN) and the median raphe nuclei (MRN) on the intake of ethanol in the low alcohol drinking (LAD) rat was measured using a standard 3-30% ethanol preference test. 2. The combined lesion of both midbrain structures depleted the levels of serotonin (5-HT) and its metabolite 5-hydroxyindoleacetic acid (5-HIAA) significantly in each of eight major regions of the brain. The levels of norepinephrine, dopamine, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) remained unchanged after the lesion. 3. The effects of the neurotoxin lesions on the intakes of ethanol, food, water and total amount of fluid consumed were not significant. 4. The results corroborate our previous findings with the Sprague-Dawley strain of rat and suggest that although brain 5-HT may play a role in the maintenance of basal patterns of ethanol drinking, this monoamine may not be able to modify further the consumption of this fluid after lesioning with 5,7-DHT.

5,7-Dihydroxytryptamine↗
PubMed1996

Action of harman (1-methyl-beta-carboline) on the brain: body temperature and in vivo efflux of 5-HT from hippocampus of the rat.

Harman (1-methyl-beta-carboline) has been shown previously to act on the hippocampus of the rat in terms of its evocation of anxiogenic responses and induction of alcohol preference. In the present experiments, the localized perfusion of 200 microM harman in the dorsal hippocampus of freely moving rats increased the levels of serotonin (5-HT) but not 5-hydroxyindoleacetic acid (5-HIAA) in cerebral dialysates. The systemic administration of 5.0-20 mg/kg harman also enhanced 5-HT in the perfusates but reduced the levels of 5-HIAA in a dose-dependent manner, probably as a result of the inhibition of the enzyme monoamine oxidase type A (MAO-A). Harman given systemically in doses of 2.5-20 mg/kg induced an intense hypothermia, with a maximum fall produced by the 5.0 mg/kg dose. This fall in body temperature (Tb) induced by 5.0 mg/kg harman was not antagonized by 5.0 mg/kg of (+/-)-pindolol. Further, pretreatment of the rats with parachlorophenylalanine (pCPA) also failed to alter the harman-induced hypothermia. The systemic administration of 10 mg/kg of the MAO-A inhibitor, clorgyline, also lowered Tb significantly. Overall, the present experiments show that harman apparently influences 5-HT systems in the brain by its action in inhibiting MAO-A. This property is likely responsible also for the harman-induced increase of 5-HT in the hippocampus of the rats.

Adrenergic beta-Antagonists↗
PubMed1995

Selective destruction of midbrain raphe nuclei by 5,7-DHT: is brain 5-HT involved in alcohol drinking in Sprague-Dawley rats?

Since serotonin (5-HT) reportedly is involved in aberrant drinking of ethyl alcohol, the present study examined a possible role of the concentration of 5-HT in systems originating in the dorsal raphe nucleus (DRN), median raphe nucleus (MRN) or both nuclei. The preference for alcohol offered in concentrations increased over 10 days from 3% to 30% was determined for each Sprague-Dawley rat. After the rats were anesthetized with sodium pentobarbital, either 10 microg 5,7-DHT or artificial cerebrospinal fluid (CSF) was micro-injected stereotaxically into the DRN, MRN or both nuclei. After 10 days, a second alcohol preference test was offered to the animals. Then the rats were decapitated, each brain removed, and the block of tissue containing injection sites was saved for histological analysis. The remaining portion was dissected into separate regions for analysis by HPLC of 5-HT, 5-hydroxyindoleacetic-acid (5-HIAA), norepinephrine (NE), dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA). The 5,7-DHT lesion of the DRN depleted the levels of 5-HT and 5-HIAA by 50-55% in the midbrain and pons and by 70-80% in the frontal cortex, whereas, the 5,7-DHT lesion of MRN reduced 5-HT in all regions except the corpus striatum. The depletion of 5-HT was lower in MRN-lesioned than in DRN-lesioned rats in the frontal cortex and nucleus accumbens. The combined lesion of both DRN and MRN produced a massive decline of >90% of 5-HT and 5-HIAA in all structures except the pons where 5-HT was reduced by 70%. Whereas the level of NE was reduced mainly in the frontal cortex, the levels of DA and its metabolites were essentially unaffected by the 5,7-DHT lesions. Although single or combined lesions of the DRN and MRN failed to alter the intake of alcohol of the rats, the combined serotonergic lesions increased significantly the ingestion of water but not food. Correlational analyses in the sham groups showed a negative association between the intake of alcohol and cortical dopamine and possible hippocampal 5-HT and NE as well as between the ingestion of food and of 5-HT in the frontal cortex. Taken together, these observations in the Sprague-Dawley rat suggest that lower levels of these monoamines in certain regions of the brain may play a role in the maintenance of the basal intake of alcohol but not in the drinking after the injection of 5,7-DHT. Explanations of our findings include: (1) a compensatory neurochemical change in pre- or postsynaptic 5-HT receptors subsequent to the dysfunction of serotonergic neurons in the forebrain; (2) a unique characteristic of the Sprague-Dawley strain of rat; and (3) residual quanta of 5-HT which sustains the pattern of alcohol drinking.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1995

5-HT, dopamine, norepinephrine, and related metabolites in brain of low alcohol drinking (LAD) rats shift after chronic intra-hippocampal infusion of harman.

Harman (1-methyl-beta-carboline) has been shown to induce preference for alcohol in the genetically bred, low alcohol drinking (LAD) rat. This study was undertaken in the LAD rat to determine whether monoamines and their metabolites in different regions of the brain are altered by harman infused chronically into the dorsal hippocampus. For this purpose, a cannula was implanted stereotaxically into the dorsal hippocampus. The cannula was attached to an osmotic minipump implanted subcutaneously within the intrascapular space. The pump was filled with either an artificial cerebrospinal fluid (CSF) vehicle or harman, which was delivered at a rate of 1.0 or 3.0 micrograms/h (i.e., 5.5 or 16.5 nmol/h, respectively) for a period of 14 days. Four days after surgery, a standard preference test for ethyl alcohol was given to the rats over 10 days in which concentrations were increased daily from 3%-30%. The higher concentration of harman infused into the hippocampus elevated the level of serotonin (5-HT), both ipsilateral and contralateral to the hippocampal site of infusion, as well as in the midbrain, frontal cortex, striatum and nucleus accumbens. Similarly, this treatment resulted in a rise in the levels of norepinephrine in the hippocampus and midbrain but decreases in dopamine levels in the pons. The levels of 5-hydroxyindoleacetic acid (5-HIAA) and 3,4-dihydroxyphenylacetic acid (DOPAC) were diminished in the pons of rats given 3.0 micrograms/h harman, whereas both concentrations of the beta-carboline reduced the level of homovanillic acid (HVA) in the frontal cortex.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dihydroxyphenylacetic Acid↗
PubMed1995

Synthesis of dopamine and 5-HT in anatomical regions of the rat's brain is unaffected by sustained infusion of amperozide.

The 5-HT2A antagonist, amperozide, is considered to be a potentially useful drug for the treatment of substance abuse. The effects of this drug on the Sprague-Dawley rat were examined on the synthesis of dopamine and serotonin (5-HT) as well as on the intakes of food and water and the level of body weight. Amperozide was delivered subcutaneously by osmotic minipump in doses of 2.5 mg/kg or 5.0 mg/kg per day for 7 days. After injection of 100 mg/kg NSD-1015, each brain was dissected post mortem into midbrain, pons, hypothalamus, septum, nucleus accumbens, striatum, frontal cortex and the hippocampus. Neither concentration of amperozide altered the synthesis of dopamine or 5-HT, as measured in terms of the formation of 1-3,4-dihydroxyphenylalanine (L-DOPA) and 5-hydroxytryptophan (5-HTP), respectively, in any of the 8 brain regions analyzed. Both doses of amperozide reduced food intake by 20% within 24 hr after implantation of the pumps, but feeding resumed postoperatively at the control level within 48 hr. Amperozide affected neither the intake of water nor the level of body weight. The lack of effect on the synthesis of dopamine and 5-HT and the absence of side effects on the intakes of food and water suggest that amperozide may be a specific agent for suppressing alcohol drinking.

Alcoholism↗
PubMed1994

Increased alcohol intake in low alcohol drinking rats after chronic infusion of the beta-carboline harman into the hippocampus.

Harman (1-methyl-beta-carboline) has been shown to induce volitional drinking of ethyl alcohol in the rat. The purpose of this study was to examine the long-term effect of sustained delivery of harman into the dorsal hippocampus on the subsequent preference for alcohol in the genetically bred low alcohol drinking (LAD) rat. The individual pattern of preference for alcohol was first determined following a standard 3-30% alcohol self-selection test for 10 days. Thereafter, a cerebral cannula for constant infusion was implanted stereotaxically into the dorsal hippocampus. The cannula was attached to an osmotic minipump implanted subcutaneously, which was filled with either an artificial cerebrospinal fluid (CSF) vehicle or harman. Harman was delivered at a rate of 1.0 or 3.0 micrograms/h (i.e., 5.5 or 16.5 nmol/h, respectively) for a period of 14 days. Four days after surgery, the rats underwent a second 3-30% alcohol preference test for 10 days. Both doses of harman induced a threefold increase in the voluntary consumption of alcohol, expressed as g/kg per day. This effect of the beta-carboline seems to be specific for ethanol because its intake by the LAD rats was increased significantly only when concentrations from 11% to 30% were presented. Harman also enhanced the daily intake of food in a dose-dependent manner, but did not affect body weights or the volumes of water and total fluid consumed. These results, thus, demonstrate that the long-term exposure of hippocampal neurons to harman induces a preference for high concentrations of alcohol even in a line of rats lacking such a genetic predisposition.

Alcohol Drinking↗
PubMed1993

In vivo brain dialysis study of the somatodendritic release of serotonin in the Raphe nuclei of the rat: effects of 8-hydroxy-2-(di-n-propylamino)tetralin.

The characteristics of the serotonin (5-HT) output in the dorsal and median raphe nuclei of the rat were studies using in vivo microdialysis. The basal output of 5-HT increased after KCl was added to the perfusion fluid. In contrast, neither the omission of calcium ions nor the addition of 0.5 microM tetrodotoxin affected dialysate 5-HT or 5-hydroxyindoleacetic acid (5-HIAA). Reserpine did not decrease the output of 5-HT and 5-HIAA 24 h later and p-chloroamphetamine increased 5-HT in both vehicle- and reserpine-treated rats severalfold. 8-Hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), at 1 or 10 microM, perfused into the raphe did not change the outputs of 5-HT or 5-HIAA. Higher doses (0.1, 1, and 10 mM) increased extracellular 5-HT in the raphe, probably via an inhibition of uptake. In animals bearing two probes (raphe nuclei and ventral hippocampus), only the 10 mM dose of 8-OH-DPAT perfused into the raphe decreased the hippocampal output of 5-HT and 5-HIAA. The systemic injection of 0.1 mg/kg 8-OH-DPAT decreased dialysate 5-HT and 5-HIAA in the raphe and hippocampus. These results suggest that extracellular 5-HT in raphe nuclei originates from a cytoplasmic pool and is not dependent on either nerve impulse of 5-HT neurons or local activation of 5-HT1A receptors.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1991

Differential effects of clomipramine given locally or systemically on extracellular 5-hydroxytryptamine in raphe nuclei and frontal cortex. An in vivo brain microdialysis study.

The antidepressant drug clomipramine (CIM) blocks 5-hydroxytryptamine (5-HT) uptake in vitro. Electrophysiological studies have shown that CIM also reduces the firing of serotonergic neurons in the dorsal raphe nucleus. In order to assess the effects of CIM on serotonergic transmission in vivo, the technique of intracerebral microdialysis was used. CIM was administered either through the dialysis probe or i.p., and dialysate 5-HT and 5-hydroxyindoleacetic acid (5-HIAA) were determined in frontal cortex and/or raphe nuclei. In addition, the action of extracellular 5-HT in raphe nuclei on the release of 5-HT in frontal cortex was studied. The administration of CIM through the dialysis probe increased dialysate 5-HT in frontal cortex in a dose-dependent fashion. An actual ED50 of 3.15 microM CIM for the in vivo inhibition of 5-HT uptake can be calculated in this brain area. When given systemically (10 or 20 mg/kg i.p.), CIM did not increase dialysate 5-HT in the frontal cortex. The occurrence of extracellular 5-HT in the the raphe area was demonstrated. This pool of 5-HT increased markedly after local (10 or 40 microM) or systemic (20 mg/kg i.p.) administration of CIM. We also examined the effect of CIM applied locally in the raphe nuclei on extracellular 5-HT in the frontal cortex. The increased dialysate 5-HT in raphe after 10 or 40 microM CIM paralleled a decrease of dialysate 5-HT in the two areas correlated negatively. The administration of CIM through the dialysis probe slightly decreased dialysate 5-HIAA in the frontal cortex.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Evaluation of oxygen saturation monitoring by pulse oximetry in neonates in the delivery system.

The pulse oximeter was evaluated for use in neonates in the delivery room. One hundred neonates, delivered vaginally or by Caesarean section with general or epidural anaesthesia, were studied. After delivery, pulse oximetry probes were placed simultaneously on the ulnar side of the right hand and on the right Achilles tendon to determine whether there was a difference in arterial oxygenation (SpO2). Measurements of SpO2 were taken at 1, 5, 10 min, and 24 hr after delivery. At one and five minutes, SpO2 recorded from the right hand was higher than that recorded from the lower extremities (71.9% +/- 6.5% vs 63.4% +/- 4.3% and 83.3% +/- 4.2% vs 76% +/- 4.1%, mean +/- SD, respectively). At ten minutes these differences diminished, and had almost completely disappeared after 24 hr. These results can be explained by the presence of R-L shunting at the ductus arteriosus level, producing reduced SaO2 in the lower extremities. Oxygen saturation did not differ between neonates delivered vaginally or by Caesarean section, regardless of the presence or type of anaesthesia. We concluded that neonates remain relatively desaturated in the immediate postpartum period and that the SpO2 obtained from the right hand is a better index of neonatal oxygenation than that obtained from the heel.

Achilles Tendon↗