Biomedical subjects

Manuel Aldegunde

Publications and source records attributed to Manuel Aldegunde.

2 recordsLinked to original sources

PubMed2002

Somatodendritic action of pindolol to attenuate the paroxetine-induced decrease in serotonin release from the rat ventral hippocampus: a microdialysis study.

We used intracerebral microdialysis to study the role of raphe and presynaptic serotonin (5-HT) autoreceptors in the effect of the selective 5-HT reuptake inhibitor, paroxetine, on 5-HT release from ventral hippocampus of anaesthetised rats. In addition, we have tested the ability of pindolol, a non-selective beta-adrenergic/5-HT(1A) receptor antagonist, to alter the response of hippocampal 5-HT to paroxetine. Doses of paroxetine with maximal effects were near to three-fold less effective when administered systemically than after local infusion at increasing extracellular 5-HT in ventral hippocampus. Moreover, systemic paroxetine treatment resulted in a marked decrease of the extracellular 5-HT in the hippocampus when 5-HT reuptake was blocked with paroxetine 3 microM applied locally, thereby evidencing that systemic treatment induced a decrease of 5-HT release in the neuronal terminal. A similar drop was observed when paroxetine 3 microM was perfused into the median raphe, a region that contains the cell bodies of the neurons innervating the ventral hippocampus. Racemic (+/-)-pindolol (10 mg/kg, s.c.) completely blocked the paroxetine-induced decrease in 5-HT release from rat hippocampus. In addition, the infusion into median raphe of (-)-pindolol, the isoform with highest antagonist activity, at concentrations of 10 microM and 100 microM was able to partially block the decrease of hippocampal 5-HT release after systemic paroxetine. However, perfusion of (-)-pindolol into the hippocampus was without effect on local 5-HT release. These data suggest that pindolol acts preferentially through the blockade of somatodendritic 5-HT(1A) autoreceptors to restore the decline in 5-HT outflow in rat forebrain following systemic administration of selective 5-HT reuptake inhibitors.

Adrenergic beta-Antagonists↗

PubMed2002

Energy metabolism of fish brain.

This review focuses on recent research on the metabolic function of fish brain. Fish brain is isolated from the systemic circulation by a blood-brain barrier that allows the transport of glucose, monocarboxylates and amino acids. The limited information available in fishes suggests that oxidation of exogenous glucose and oxidative phosphorylation provide most of the ATP required for brain function in teleosts, whereas oxidation of ketones and amino acids occurs preferentially in elasmobranchs. In several agnathans and benthic teleosts brain glycogen levels rather than exogenous glucose may be the proximate glucose source for oxidation. In situations when glucose is in limited supply, teleost brains utilize other fuels such as lactate or ketones. Information on use of lipids and amino acids as fuels in fish brain is scarce. The main pathways of brain energy metabolism are changed by several effectors. Thus, several parameters of brain energy metabolism have been demonstrated to change post-prandially in teleostean fishes. The absence of food in teleosts elicits profound changes in brain energy metabolism (increased glycogenolysis and use of ketones) in a way similar to that demonstrated in mammals though delayed in time. Environmental factors induce changes in brain energy parameters in teleosts such as the enhancement of glycogenolysis elicited by pollutants, increased capacity for anaerobic glycolysis under hypoxia/anoxia or changes in substrate utilization elicited by adaptation to cold. Furthermore, several studies demonstrate effects of melatonin, insulin, glucagon, GLP-1, cortisol or catecholamines on energy parameters of teleost brain, although in most cases the results are quite preliminary being difficult to relate the effects of those hormones to physiological situations. The few studies performed with the different cell types available in the nervous system of fish allow us to hypothesize few functional relationships among those cells. Future research perspectives are also outlined.

Animals↗