Biomedical subjects

I López-Coviella

Publications and source records attributed to I López-Coviella.

9 recordsLinked to original sources

PubMed2001

Estrogen modulates norepinephrine-induced accumulation of adenosine cyclic monophosphate in a subpopulation of immortalized luteinizing hormone-releasing hormone secreting neurons from the mouse hypothalamus.

A subpopulation of luteinizing hormone-releasing hormone (LHRH)-producing cells that express the intermediate filament protein vimentin and the neuronal marker neurofilament 145, but not neurofilament 200 nor glial fibrillary acidic protein, has been isolated from GT1-7 cultures. These cells express the mRNA encoding estrogen receptor alpha (ERalpha) and respond to physiological concentrations of 17beta-estradiol (E2) by reducing the accumulation of cyclic adenosine monophosphate induced by norepinephrine, but not that induced by direct activation of adenylate cyclase. These results indicate that the activity of LHRH-producing neurons may be directly modulated by estrogen. In addition, they are suggestive of an estrogen-dependent desensitization of the beta-adrenoceptor in these cells.

Animals↗

PubMed2001

Sex steroids modulate luteinizing hormone-releasing hormone secretion in a cholinergic cell line from the basal forebrain.

The function of a particular neuronal population is in part determined by its neurotransmitter phenotype. We have found that a neuronal-derived septal cell line (SN56), known for its cholinergic properties, also synthesizes and releases luteinizing hormone-releasing hormone. In addition, these cells express the messenger RNAs encoding estrogen and progesterone receptors. The activation of these receptors by their respective ligands cooperatively modulates the depolarization-induced release of luteinizing hormone-releasing hormone in these cells. We have also found that a number of septal neurons in postnatal (1-week-old) mice are immunoreactive to both choline acetyltransferase and luteinizing hormone-releasing hormone. These results indicate that both neurotransmitters, acetylcholine and luteinizing hormone-releasing hormone, may co-exist in septal neurons of the CNS and that they could be modulated by gonadal hormones, and suggest that luteinizing hormone-releasing hormone could be involved in some of the actions of sex steroids on cholinergic neurotransmission.

Animals↗

PubMed2001

Estrogen modulates alpha(1)/beta-adrenoceptor- induced signaling and melatonin production in female rat pinealocytes.

Nocturnal rise in pineal melatonin output is due to the night-induced acceleration of noradrenergic transmission and alpha(1)- and beta-adrenoceptor activation. In addition, in female animals, cyclic oscillations in circulating levels of sex steroid hormones are accompanied by changes in the rate of pineal melatonin secretion. To investigate whether estrogen directly affects pineal adrenoceptor responsiveness, pinealocytes from 21-day-old ovariectomized rats were exposed to physiological concentrations of 17beta-estradiol (17beta-E(2)) and treated with noradrenergic agonists. Direct exposure to 17beta-E(2) reduced alpha(1)/beta-adrenoceptor-induced stimulation of melatonin synthesis and release. This effect was mediated by an estrogen-dependent inhibition of both beta-adrenoceptor-induced accumulation of cAMP and alpha(1)-adrenoceptor-induced phosphoinositide hydrolysis. Furthermore, estrogen reduced transient Ca(2+) signals elicited in single pinealocytes by alpha(1)-adrenoceptor activation or by potassium-induced depolarization. In the case of beta-adrenoceptor responsiveness, neither forskolin- nor cholera toxin-induced accumulation of cAMP were affected by previous exposure to 17beta-E(2). This indicates that estrogen effects must be exerted upstream from adenylylcyclase activation, and independent of modifications in G protein expression, therefore suggesting changes in either adrenoceptor expression or receptor-effector coupling mechanisms. Since estrogen effects upon adrenoceptor responsiveness in pineal cells was not mimicked by 17beta-E(2) coupled to bovine serum albumin and showed a latency of 48 h, this effect could be compatible with a genomic action mechanism. This is also consistent with the presence of two estrogen receptor proteins, alpha- and beta-subtypes, in female rat pinealocytes under the present experimental conditions.

Action Potentials↗

PubMed2000

Induction and maintenance of the neuronal cholinergic phenotype in the central nervous system by BMP-9.

Bone morphogenetic proteins (BMPs) have multiple functions in the developing nervous system. A member of this family, BMP-9, was found to be highly expressed in the embryonic mouse septum and spinal cord, indicating a possible role in regulating the cholinergic phenotype. In cultured neurons, BMP-9 directly induced the expression of the cholinergic gene locus encoding choline acetyltransferase and the vesicular acetylcholine transporter and up-regulated acetylcholine synthesis. The effect was reversed upon withdrawal of BMP-9. Intracerebroventricular injection of BMP-9 increased acetylcholine levels in vivo. Although certain other BMPs also up-regulated the cholinergic phenotype in vitro, they were less effective than BMP-9. These data indicate that BMP-9 is a differentiating factor for cholinergic central nervous system neurons.

Acetylcholine↗

PubMed1998

Gonadal steroids and neuronal function.

Gonadal steroid hormones may affect, simultaneously, a wide variety of neuronal targets, influencing the way the brain reacts to many external and internal stimuli. Some of the effects of these hormones are permanent, whereas others are short lasting and transitory. The ways gonadal steroids affect brain function are very versatile and encompass intracellular, as well as, membrane receptors. In some cases, these compounds can interact with several neurotransmitter systems and/or transcription factors modulating gene expression. Knowledge about the mechanisms implicated in steroid hormone action will facilitate the understanding of brain sexual dimorphism and how we react to the environment, to drugs, and to certain disease states.

Animals↗

PubMed1996

Gonadal steroid modulation of neuroendocrine transduction: a transynaptic view.

1. Steroid hormones act on neuronal communication through different mechanisms, ranging from transynaptic modulation of neurotransmitter synthesis and release to development and remodeling of synaptic circuitry. Due the wide distribution of putative brain targets for steroid hormones, acute or sustained elevations of their circulating levels may affect, simultaneously, a variety of neuronal elements. In an elementary mode of interaction, steroids are able to modulate both the synthesis and release of a neurotransmitter at a particular synapse, and the response of its target postsynaptic cells. Using two neuroendocrine transducing systems-the rat pineal gland and the GT1-7 cell line-we have examined these interactions and the following findings are discussed in this article. 2. In the rat, pineal melatonin production is partially controlled by gonadal hormones. In females, melatonin synthesis and secretion is reduced during the night of proestrus, apparently as a consequence of elevated estradiol and progesterone levels. In males, circulating testosterone seems to be necessary to maintain the amplitude of the nocturnal melatonin peak. 3. Some gonadal effects on pineal activity are exerted on its noradrenergic input, since changes in circulating steroid hormone levels are able to induce acute modifications of tyrosine hydroxylase activity in pineal sympathetic nerve terminals. 4. Gonadal steroids are also able to regulate the response of pineal cells to adrenergic stimulation, since in vivo treatment of both male and female rats with steroid hormone blockers induces profound modifications in adrenergically-induced accumulation of cyclic AMP (cAMP) in dispersed pinealocytes. 5. Direct exposure of pineal cells from gonadectomized female and male rats to estradiol (E2) or testosterone (T), respectively, potentiates pinealocyte response to adrenergic activation. In addition, short-term (15 min) exposure to either progesterone (Pg) or progesterone coupled to bovine serum albumin (P-3-BSA) suppresses the E2-dependent potentiation of adrenergic response in female rat pinealocytes. 6. Exposure of GT1-7 cells to E2 completely blocked the norepinephrine (NE)-induced elevation of cAMP content. In E2-treated GT1-7 cells, additional exposure (15 min) to either Pg or P-3-BSA abolished E2-dependent inhibition of NE responsiveness. In addition, P-3-BSA alone increased basal cAMP levels in GT1-7 cells, regardless previous exposure to E2. 7. In conclusion, there are evidences, both from the current literature and from the present results, supporting the view that in some neuroendocrine systems gonadal hormones modulate neurotransmission by acting, simultaneously, at pre- and postsynaptic sites. The models presented here constitute appropriate examples of this transynaptic mode of steroid and, therefore, may offer a useful approach to investigate steroid hormone actions on the brain.

Adrenergic Fibers↗

PubMed1995

Evidence that 5'-cytidinediphosphocholine can affect brain phospholipid composition by increasing choline and cytidine plasma levels.

We examined the effects of orally administered 5'-cytidinediphosphocholine (CDP-choline) on arterial plasma choline and cytidine levels and on brain phospholipid composition in rats. Animals receiving a single oral dose of 100, 250, or 500 mg/kg showed peak plasma choline levels 6-8 h after drug administration (from 12 +/- 1 to 17 +/- 2, 19 +/- 2, and 24 +/- 2 microM, respectively). The area under the plasma choline curve at > 14 microM, i.e., at a concentration that induces a net influx of choline into the brain, was significantly correlated with CDP-choline dose. In rats receiving 500 mg/kg this area was 2.3 times that of animals consuming 250 mg/kg, which in turn was 1.8 times that of rats receiving 100 mg/kg. Plasma cytidine concentrations increased 5.4, 6.5, and 15.1 times baseline levels, respectively, 8 h after each of the three doses. When the oral CDP-choline treatment was prolonged for 42 and 90 days, brain phosphatidylcholine concentrations increased significantly (by 22-25%; p < 0.05) in rats consuming 500 mg/kg/day. Brain phosphatidylethanolamine and phosphatidylserine concentrations also increased significantly under some experimental conditions; levels of other phospholipids were unchanged.

Animals↗

PubMed1994

Tyrosine hydroxylase activity in peripherally denervated rat pineal gland.

The presence of tyrosine hydroxylase (TH) in the rat pineal gland was studied using a combination of immunochemical and biochemical methods. In superior cervical ganglionectomized (SCGx) animals and in isolated pineals incubated for 72 h, both TH immunoreactive (TH-IR) fibers and TH biochemical activity were still present but reduced. Conversely, in dispersed pinealocytes incubated for only 24 h we were unable to detect either TH activity or TH-positive cells. Since in the pineal gland of intact rats total 3-methoxy-4-hydroxy phenylglycol (MHPG) was undetectable, and only traces of norepinephrine (NE) were present in the pineal of ganglionectomized animals, the results suggest a central pinealopetal catecholaminergic pathway which could use dopamine as a neurotransmitter.

Animals↗

PubMedDate not supplied

[Bone morphogenetic proteins and cholinergic neurons in the central nervous system].

INTRODUCTION: The discovery and characterization of factors that induce and maintain specific neurotransmitter phenotypes has profound clinical implications, and continues to be one of the major objectives in the neurosciences. DEVELOPMENT: Although much progress has been realized in this area, we still understand little of how cholinergic neurons acquire and maintain their neurotransmitter characteristics, nor do we fully comprehend why these neurons in some circumstances degenerate and loose their neurotransmitter specificity. There is evidence that some members of the bone morphogenetic protein (BMP) family have profound organizing and differentiating actions in the developing nervous system, and recent studies indicate an important role in determining the cholinergic neuronal phenotype. CONCLUSIONS: BMP may act to differentiate neuronal precursor cells into cholinergic neurons and upregulate the cholinergic phenotype of already differentiated neurons in the central nervous system. This could suggest their potential use in the treatment of certain types of brain disorders.

Bone Morphogenetic Proteins↗