Cerebral infarction: time course of signal intensity changes on diffusion-weighted MR images.

Objective: The objective of this study was to determine the time course of signal intensity changes on diffusion-weighted MR images after cerebral infarction.

Materials And Methods: Echoplanar diffusion-weighted MR images were obtained at 1.5 T in 212 patients referred for suspected cerebral infarction over a 6-month period.

Mucopolysaccharidosis III (Sanfilippo syndrome) type B: cranial imaging in two cases.

We present the imaging findings in two patients with mucopolysaccharidosis III (Sanfilippo syndrome) type B, both with arachnoid cysts. We postulate that the deposition of glycosaminoglycans in the meninges may impair CSF flow and explain the development of arachnoid cysts also noted in patients with other forms of mucopolysaccharidoses.

Progesterone attenuation of alpha 1-adrenergic receptor stimulation of phosphoinositol hydrolysis in hypothalamus of estrogen-primed female rats.

These experiments examined whether the previously observed abolition by progesterone (P) of alpha 1-adrenergic potentiation of adenylyl cyclase activity in brain slices of estrogen-primed female rats is attributable to a reduced capacity of alpha 1-adrenoceptors to stimulate phosphoinositol hydrolysis. In preoptic area and hypothalamic slices from ovariectomized (OVX) female rats, both norepinephrine (NE) and the alpha 1-adrenergic agonist phenylephrine (PHE) were robust stimulators of inositol phosphate (IP) formation. The NE response was completely blocked by the alpha 1-adrenergic antagonist prazosin.

Estradiol selectively regulates alpha 1B-noradrenergic receptors in the hypothalamus and preoptic area.

We previously demonstrated that estradiol administered in vivo elevates the number of alpha 1-adrenoceptors in preoptic area (POA) and hypothalamic membranes from ovariectomized female rats and potentiates alpha 1 receptor augmentation of beta-adrenoceptor-stimulated cAMP formation in slices from these brain regions. Present studies examined (1) if estradiol selectively regulates any alpha 1-adrenoceptor subtype, and (2) which alpha 1 receptor subtype mediates the augmentation of cAMP synthesis. Hypothalamic and POA membranes from estradiol-treated rats, when compared to ovariectomized rats, had modestly (30-50%) but significantly elevated numbers of 3H-prazosin (alpha 1) binding sites.

Progesterone promotes rapid desensitization of alpha 1-adrenergic receptor augmentation of cAMP formation in rat hypothalamic slices.

We previously demonstrated that norepinephrine (NE) induction of cAMP accumulation in slices of the preoptic area (POA) and middle hypothalamus (MH) is reduced by in vivo administration of progesterone to estradiol-primed rats, apparently by eliminating alpha 1-receptor augmentation of beta-receptor-stimulated cAMP formation. The present studies examined whether in vitro exposure to progesterone would also depress NE-stimulated cAMP synthesis. POA and MH slices from estradiol-primed females were incubated with 20 nM progesterone for 5-30 min prior to addition of 100 microM NE.

Protein kinase C and phospholipase C mediate alpha 1- and beta-adrenoceptor intercommunication in rat hypothalamic slices.

These experiments examined the mechanism by which phenylephrine enhances beta-adrenoceptor-stimulated cyclic AMP formation in rat hypothalamic and preoptic area slices. To this end we manipulated phospholipase C. phospholipase A2, and protein kinase C activity in slices and assessed the effects of these manipulations on phenylephrine augmentation of isoproterenol-stimulated cyclic AMP generation.

Alpha 1-adrenoceptor augmentation of beta-stimulated cAMP formation is enhanced by estrogen and reduced by progesterone in rat hypothalamic slices.

These experiments examined the influence of estradiol and progesterone given in vivo on norepinephrine (NE) regulation of cAMP synthesis in hypothalamic and preoptic area slices in vitro. Administration of progesterone to estrogen-primed female rats attenuated NE-induced slice cAMP accumulation. This hormone-dependent reduction in NE-stimulated cAMP synthesis was observed in slices incubated with TTX and in slices prepared from hypophysectomized rats, suggesting that progesterone effects on NE receptor activation of cAMP-generating systems are not secondary to the release of neurotransmitters that inhibit adenylyl cyclase or to changes in pituitary hormone secretion.

Progesterone depression of norepinephrine-stimulated cAMP accumulation in hypothalamic slices.

The present experiments examined the effects of progesterone on adrenergic receptor coupling to adenylate cyclase in hypothalamic and preoptic area slices by monitoring norepinephrine (NE)-stimulated increases in cAMP accumulation. Progesterone treatment of estrogen-primed rats decreased NE-induced slice cAMP accumulation. The reduced cAMP response was estrogen-dependent since it was not demonstrable in slices from rats exposed to progesterone without prior estrogen priming.

Mediation of norepinephrine-stimulated cyclic AMP accumulation by adrenergic receptors in hypothalamic and preoptic area slices: effects of estradiol.

Adrenergic receptor agonists and antagonists were employed to establish (a) which receptor subtypes mediate the cyclic AMP response to norepinephrine in hypothalamic and preoptic area slices from gonadectomized female rats and (b) which receptor subtypes might be modulated by the steroid hormone estradiol. Slice cyclic AMP levels were elevated by the beta receptor agonist isoproterenol, but not by alpha 1 (phenylephrine, methoxamine) or alpha 2 (clonidine) agonists. However, the alpha agonist phenylephrine potentiated the effect of the beta agonist isoproterenol on slice cyclic AMP accumulation.

Norepinephrine-stimulated cyclic AMP accumulation in rat hypothalamic slices: effects of estrous cycle and ovarian steroids.

Hypothalamic slices prepared from female rats in various hormonal conditions were incubated in vitro in the presence or absence of 10 microM norepinephrine (NE), and cyclic AMP content was measured. Slices from animals in late diestrus or with exogenous estrogen treatment responded to NE with marked elevations of cyclic AMP in all but the posterior hypothalamus. Slices from rats sacrificed in late proestrus or following estrogen plus progestin administration showed little or no NE-stimulated cyclic AMP accumulation.