PubMed Health⌕ Search

Biomedical subjects

D J Berlove

Publications and source records attributed to D J Berlove.

9 recordsLinked to original sources

Pretreatment with intraventricular basic fibroblast growth factor decreases infarct size following focal cerebral ischemia in rats.

Basic fibroblast growth factor is a polypeptide with potent multipotential trophic effects on central nervous system cells, including neurons, glia, and endothelial cells. In particular, it promotes the survival of a wide variety of brain neurons in vitro, and protects these neurons against the effects of several neurotoxins, including excitatory amino acids, hypoglycemia, and calcium ionophore. Since lack of substrate delivery, excitatory amino acid toxicity, and calcium entry into cells appear to be important processes in neuronal death after ischemia, we tested the hypothesis that pretreatment with basic fibroblast growth factor limits infarct size in a model of focal cerebral ischemia in vivo. Mature male Long-Evans rats received either continuous intraventricular infusion of basic fibroblast growth factor (1.2 micrograms/day; with or without heparin, added to stabilize the growth factor) or vehicle alone for 3 days before focal ischemic infarcts were made in the right lateral cerebral cortex by permanent distal middle cerebral artery occlusion and temporary (45-minute) bilateral carotid occlusion. Intraoperative measurements of core temperature, arterial blood pressure and blood gases, blood glucose concentration, and hematocrit, and postoperative measurements of temperature revealed no differences among vehicle- versus basic fibroblast growth factor-treated animals. Twenty-four hours later, animals were killed, brains were removed and stained to visualize cortical infarcts, and infarct volume was determined by image analysis. Overall, we found a 25% reduction in infarct volume in basic fibroblast growth factor- (N = 25) versus vehicle-treated (N = 23) animals (p < 0.01). This reduction was not enhanced by the addition of heparin.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗

Basic fibroblast growth factor protects cerebrocortical neurons against excitatory amino acid toxicity in vitro.

BACKGROUND AND PURPOSE: Previous studies have shown that basic fibroblast growth factor protects against excitatory amino acid toxicity in cultured hippocampal, striatal, and cerebellar neurons. In the current study, we examined the neuroprotective effects of this growth factor on cerebrocortical neurons, which are commonly involved in thromboembolic stroke. METHODS: Dissociated neuron-glia cultures of embryonic rat cerebral cortex (12 days in vitro) were preincubated with basic fibroblast growth factor (0.1 to 100 ng/mL) for 6 hours before incubation with glutamate (0 to 1000 mumol/L) for 16 hours. The number of phase-bright neurons was taken as an index of neuronal survival. RESULTS: Basic fibroblast growth factor protected neurons against glutamate toxicity, especially at lower (10, 25, and 50 mumol/L), but not higher (100 and 1000 mumol/L), glutamate concentrations. Neuroprotection was seen at growth factor doses as low as 1 ng/mL. CONCLUSIONS: Basic fibroblast growth factor protects cultured cerebrocortical neurons against glutamate neurotoxicity.

Analysis of Variance↗

Co-localization of putative vasopressin receptors and vasopressinergic neurons in rat hypothalamus.

Vasopressin and oxytocin are synthesized by neurons in the paraventricular and supraoptic nuclei of hypothalamus. Dense concentrations of vasopressin binding sites have also been localized in these nuclei. Using a vasopressin anti-idiotypic antiserum, a dual immunocytochemical labeling procedure has been employed to elucidate the distribution of putative vasopressin receptors in anatomical relation to vasopressin and oxytocin immunoreactive cells in rat brain. Putative vasopressin receptors are observed in relation to magnocellular neurons in hypothalamus that are vasopressin immunoreactive. They do not appear to be associated with parvocellular vasopressinergic cells or oxytocin immunoreactive neurons. The presence of these presumed autoreceptors would support evidence that vasopressin may autoregulate the activity of magnocellular vasopressinergic neurons in hypothalamus.

Animals↗

Growth factor expression after stroke.

Fibroblast growth factors are polypeptides with potent trophic effects on central nervous system cells. Both acidic and basic forms of fibroblast growth factor are found in the mammalian brain. We have examined the expression of these factors after focal brain injury or stroke. After infarction of the lateral cerebral cortex in the mature rat brain, we found a twofold to threefold increase during the first 3 weeks after stroke in levels of fibroblast growth factors in tissue surrounding infarcts. This increase persisted for at least 2 months and appeared mainly to be due to increased levels of basic, but not acidic, fibroblast growth factor. Because of its gliotrophic, angiogenic, and neuronotrophic properties, basic fibroblast growth factor may play an important role in the cascade of cellular reactions that contributes to wound healing and functional recovery after stroke.

Animals↗

Staining of magnocellular neurons of the supraoptic and paraventricular nuclei with vasopressin anti-idiotype antibody: a potential method for receptor immunocytochemistry.

A vasopressin anti-idiotype antibody was generated by immunization with a primary anti-vasopressin IgG. This antibody was capable of immunostaining vasopressinergic neurons in the supraoptic and paraventricular nuclei of the hypothalami of normal and Brattleboro rats. Staining was eliminated by preabsorption or coincubation of the antibody with a vasopressin binding protein prepared from rat neural membranes. The anti-idiotype also inhibited binding of [3H]vasopressin to this neural membrane protein in a dose-dependent manner. These experiments suggest that the anti-idiotype antibody recognizes a receptor associated with vasopressinergic neurons.

Animals↗

Immunocytochemistry of magnocellular neurons of supraoptic and paraventricular nuclei of normal and Brattleboro rats with vasopressin anti-idiotype antibody.

A vasopressin anti-idiotype antibody was generated by immunization with purified IgG of a primary vasopressin antiserum. The anti-idiotype antibody immunostained neurons in the supraoptic and paraventricular nuclei of the hypothalamus of normal and Brattleboro rats. The distribution of immunostained perikarya in these hypothalamic nuclei together with the staining of fibers in median eminence and neural lobe was similar to that observed in normal rats with anti-vasopressin and suggests strongly that vasopressinergic neurons are being stained. Absorption studies with vasopressin and a vasopressin-binding receptor protein further indicate that a receptor associated with vasopressinergic neurons is recognized by the anti-idiotype antibody.

Animals↗

Vasopressin receptor distribution in adrenalectomized rats using vasopressin anti-idiotype.

Following adrenalectomy, it has been demonstrated that parvocellular corticotropin-releasing factor-containing neurons in the paraventricular nucleus (PVN) of rat hypothalamus synthesize vasopressin. The present study examined whether putative vasopressin receptors are expressed in parallel with the appearance of vasopressin immunoreactivity in these parvocellular neurons. A vasopressin anti-idiotypic antibody which immunostains putative vasopressin receptors associated with magnocellular PVN neurons was utilized. Following adrenalectomy, antivasopressin immunostained neurons in parvocellular and magnocellular PVN, whereas the anti-idiotypic antibody immunostained magnocellular neurons only. We therefore conclude that the putative vasopressin receptor recognized by the anti-idiotype is not demonstrated in association with parvocellular vasopressin-producing neurons of the adrenalectomized rat.

Adrenalectomy↗