RESUMEN
Sterol composition and content and their seasonal variations over 18 months were investigated in adductor muscle, digestive gland and gonads of Pecten maximus. Sterols were isolated by Silicagel 60 thin layer chromatography and identified by gas chromatography/mass spectrometry. Eleven sterols were identified, with cholesterol, brassicasterol, 24-methylenecholesterol and 22-trans-dehydrocholesterol being the principal components. The same sterols were found in all three tissues independent of season. The relative amounts of each sterol present in each tissue differed. Total sterol levels in gonad and muscle were higher than in digestive gland. Statistically significant differences (P<0.05) were found between the concentrations of each of the sterols isolated from the gonad or muscle and digestive gland. The seasonal variations in the sterol content of the gonad seem be related to the reproductive cycle, while the sterol content of the digestive gland appears to be linked to diet, mainly diatoms or dinoflagellates. The muscle sterol content showed minor changes throughout the year.
Asunto(s)
Colesterol/análogos & derivados , Moluscos/química , Esteroles/análisis , Animales , Colestadienoles/análisis , Colesterol/análisis , Cromatografía en Capa Delgada , Deshidrocolesteroles/análisis , Sistema Digestivo/química , Cromatografía de Gases y Espectrometría de Masas , Gónadas/química , Isomerismo , Moluscos/anatomía & histología , Músculo Esquelético/química , Fitosteroles , Estaciones del Año , España , Esteroles/química , Esteroles/aislamiento & purificaciónRESUMEN
Previous cerebral ischemia studies have reported the limitations of restricted periods of postischemic hypothermia in producing long-term neuroprotection. The present experiment attempts to determine whether delayed treatment with the free radical scavenger N-tert-butyl-a-phenylnitrone (PBN) is protective at 2 months following transient global forebrain ischemia, and whether additive effects can be observed when PBN is administered in combination with moderate hypothermia. For this aim rats were subjected to 10 min of two-vessel forebrain ischemia followed by (a) 3 h of postischemic normothermia (37 degrees C); (b) 3 h of postischemic hypothermia (30 degrees C); (c) normothermic procedures combined with delayed injections of PBN (100 mg/kg) on days 3, 5 and 7 post-insult; (d) postischemic hypothermia combined with delayed PBN treatment; or (e) sham procedures. Outcome measures included cognitive behavioral testing and quantitative histopathological analysis at 2 months. Postischemic PBN injections induced a systemic hypothermia (1.5 degrees C-2.0 degrees C) that lasted for 2-2.5 h. Water maze testing revealed significant performance deficits relative to shams in the normothermic ischemic group, with the postischemic hypothermia and PBN groups showing intermediate values. A significant attenuation of cognitive deficits was observed in the animal group receiving the combination postischemic hypothermia and delayed PBN treatment. Quantitative CA1 hippocampal cell counts indicated that each of the ischemia groups exhibited significantly fewer viable CA1 neurons compared to sham controls. However, in rats receiving either delayed PBN treatment or 3 h of postischemic hypothermia, significant sparing of CA1 neurons relative to the normothermic ischemia group was observed. These data indicate that hypothermia combined with PBN treatment provides long-term cognitive improvement compared to nontreatment groups. PBN-induced mild hypothermia could contribute to the neuroprotective effects of this pharmacological strategy.
Asunto(s)
Conducta Animal/fisiología , Hipotermia Inducida , Ataque Isquémico Transitorio/tratamiento farmacológico , Ataque Isquémico Transitorio/patología , Óxidos de Nitrógeno/farmacología , Animales , Conducta Animal/efectos de los fármacos , Temperatura Corporal , Óxidos N-Cíclicos , Depuradores de Radicales Libres/farmacología , Masculino , Aprendizaje por Laberinto/efectos de los fármacos , Aprendizaje por Laberinto/fisiología , Memoria/efectos de los fármacos , Memoria/fisiología , Fármacos Neuroprotectores/farmacología , Prosencéfalo/irrigación sanguínea , Prosencéfalo/patología , Prosencéfalo/fisiología , Ratas , Ratas Wistar , Percepción Espacial/efectos de los fármacos , Percepción Espacial/fisiología , Factores de TiempoRESUMEN
Gonadotropin-releasing hormones (GnRH) constitute a family of neuropeptides which are important regulators of reproduction in vertebrates. The effect of mammalian GnRH (mGnRH), salmon GnRH, chicken GnRH-I, chicken GnRH-II, and lamprey GnRH-I on [3H]thymidine incorporation into DNA of dissociated gonadal cells of marine bivalves has been studied. The incorporation of [3H]thymidine is linear between 1.5 and 8 h of incubation. All five GnRHs significantly increased DNA synthesis in gonial cells of Crassostrea gigas. The maximal activation was about of 135-140% above control. The activation is dose dependent, over the range 10(-11) to 10(-6) M, but is modulated by the physiological condition of the cells and the stage of sexual maturity of the gonad. mGnRH has also a mitogenic effect in dissociated mantle cells of Mytilus edulis. The effect of mGnRH is blocked by a GnRH antagonist ([D-pGlu1,D-Phe2, D-Trp3,6]GnRH, 5 x 10(-6)M) in C. gigas as well as in M. edulis, suggesting that the GnRH action in the gonad is mediated by specific receptors for GnRH or GnRH-like peptides. The existence of GnRH-immunoreactive neurons and fibers in the cerebral and pedal ganglia of M. edulis was demonstrated by immunocytochemistry. They are located principally in the anterior internal area of the cerebral ganglia, close to the cerebral commissure and in the posterior part of the pedal ganglia. The presence of GnRH-responsive cells and GnRH-like immunoreactive material suggests that peptides of the GnRH-like family are present and functional in bivalve molluscs.
Asunto(s)
Bivalvos/fisiología , ADN/biosíntesis , Hormona Liberadora de Gonadotropina/farmacología , Gónadas/citología , Ostreidae/fisiología , Animales , Relación Dosis-Respuesta a Droga , Femenino , Ganglios de Invertebrados/citología , Ganglios de Invertebrados/efectos de los fármacos , Ganglios de Invertebrados/metabolismo , Inmunohistoquímica , Técnicas In Vitro , Cinética , Masculino , Estimulación Química , Timidina/metabolismoRESUMEN
The present study was designed to determine whether postischemic hypothermia, delayed MK-801 (dizocilpine) administration, or a combination of these treatments can provide lasting neurobehavioral protection following transient global ischemia in rats. Rats were subjected to 10 min of normothermic (37 degrees C) ischemia induced by 2-vessel occlusion and hypotension (50 mmHg) or sham procedures. Ischemia was followed by either: (a) 3 h at normothermic brain temperatures, (b) 3 h of postischemic brain hypothermia at 30 degrees C, (c) hypothermia coupled with MK-801 (4 mg/kg, i.p.) on postischemic days 3, 5 and 7, or (d) postischemic MK-801 treatment alone. Neurobehavioral evaluation 6-8 weeks following surgery showed that normothermic ischemia (NI) was associated with water maze navigational deficits, including performance on a simple place task involving finding a hidden platform maintained in one position for 6 days, and a learning set task in which the platform was moved to a different location each day (both P's < 0.02 vs. sham). NI was also associated with increased locomotion in an open field (P < 0.01 vs. sham). A combination of postischemic hypothermia and delayed MK-801 injections provided partial protection from ischemic-associated hyperactivity in the open field (P < 0.02 vs. NI), and robust protection from simple place task deficits (P < 0.02 vs. NI). Evidence for significant protective effects of MK-801 or hypothermia alone was observed in the learning set, during the final trial blocks each day. These results provide further evidence for neuroprotective effects of these treatments at chronic survival intervals, and indicate that the therapeutic window for attenuating ischemic damage is considerably longer than has heretofore been appreciated.
Asunto(s)
Isquemia Encefálica/fisiopatología , Maleato de Dizocilpina/farmacología , Hipotermia/fisiopatología , Locomoción/efectos de los fármacos , Animales , Conducta Animal/efectos de los fármacos , Conducta Animal/fisiología , Recuento de Células/efectos de los fármacos , Corteza Cerebral/efectos de los fármacos , Modelos Animales de Enfermedad , Hipocampo/efectos de los fármacos , Masculino , Ratas , Ratas WistarRESUMEN
Previous work has demonstrated that damage to the primary somatosensory cortex produces substantial deficits in a vibrissal cue-dependent discrimination task which recover gradually over the course of post-injury testing. The present study was designed to evaluate the possible site(s) and mechanisms underlying behavioral recovery in this task. Wistar rats were trained under red light in a T-maze to produce ipsilateral turns depending upon the presence of a vibrissal cue. Animals were then subjected to photothrombotic infarctions of either the ipsilateral medial parietal cortex, the ipsilateral primary and secondary somatosensory cortex (SI/SII), the primary and secondary somatosensory cortices of both hemispheres (bilateral SI/SII) or sham surgical procedures. Behavioral testing resumed 24 hours following surgery, and continued for a total of 60 days. The performance of animals with infarcts restricted to the medial parietal cortex did not differ from that of sham-operated controls. Animals with either unilateral or bilateral SI/SII infarcts exhibited a significant decrease in percent correct responding as compared to shams and rats in the medial parietal group. These deficits recovered to pre-infarct levels over approximately 35-40 days. This rate of recovery was slower than the recovery exhibited by animals given medial parietal infarcts which spared the primary barrelfield cortex. The results of this study suggest that neither the contralateral somatosensory cortex nor the vibrissal representation within ipsilateral SII cortex play a critical role in the recovery process. The possibility that subcortical structures underlie the deficits observed following barrelfield cortical damage is discussed.
Asunto(s)
Conducta Animal/fisiología , Corteza Somatosensorial/lesiones , Vibrisas/fisiología , Animales , Infarto Cerebral/patología , Discriminación en Psicología/fisiología , Masculino , Aprendizaje por Laberinto/fisiología , Ratas , Ratas Wistar , Corteza Somatosensorial/patología , Corteza Somatosensorial/fisiopatología , Factores de Tiempo , Vibrisas/inervaciónRESUMEN
Rats with one olfactory bulb removed were trained to detect 0.5%-0.005% concentrations of amyl acetate. These rats had only a slight decrement in performance when the naris ipsilateral to the intact olfactory bulb was closed. Thus, vapors inhaled through one naris can stimulate olfactory receptor neurons in the contralateral nasal vault. This internasal stimulation is probably mediated by the nasopharyngeal canal or nasopharynx.