alpha-1 Adrenergic Receptors in the Central Nervous System

Szabadi, E.; Bradshaw, C. M.

doi:10.1007/978-1-4612-4582-7_10

Cited by 4 publications

(5 citation statements)

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“…Estradiol-initiated increases in neuronal excitability may well be a mechanism by which estrogen and NE interact to facilitate estrous responses. Electrophysiological evidence for an excitatory role of al, receptors has been shown in the brain, spinal cord, and parasympathetic autonomic ganglia (see Szabadi and Bradshaw, 1987). Studies in slices of hypothalamus and POA also suggest that LY, agonists excite and p agonists inhibit neuronal activity (Kow and Pfaff, 1988;Condon et al, 1989;Kim et al, 1989).…”

Section: Discussionmentioning

confidence: 97%

“…Gs then activates the catalytic subunit of adenylyl cyclase, leading to the formation of CAMP. Agonist occupancy of (Y, -adrenergic receptors results in the activation of another guanyl nucleotide binding protein, Gp, which activates phospholipase C (Brown et al, 1984;Minneman and Johnson, 1984;Mahan, 1987;Szabadi and Bradshaw, 1987;Okajima et al, 1989) leading to the hydrolysis of membrane inositol phospholipids into inositol 1,4,5-trisphosphate (IP,) and diacylglycerol (see reviews in Berridge, 1987;Cockcroft and Stutchfield, 1988;Chuang, 1989).…”

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confidence: 99%

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

Petitti

Etgen

1990

J. Neurosci.

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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 suppression of NE-induced cAMP formation could be prevented by incubating slices in the presence of a phorbol ester. In additional studies, the activity of beta-NE receptors was assessed by measuring isoproterenol (ISO)-stimulated cAMP accumulation in the presence of the phosphodiesterase inhibitor RO-20-1724, and the activity of alpha 1 receptors was evaluated by measuring phenylephrine (PHE) augmentation of the ISO response. Estradiol reduced the cAMP response to ISO in both hypothalamic and preoptic area slices, and this effect was not reversed by subsequent progesterone treatment. Estradiol also enhanced PHE augmentation of ISO-stimulated cAMP synthesis. Moreover, administration of progesterone subsequent to estradiol eliminated alpha 1-receptor augmentation of the ISO response. An alpha 1 enhancement of the ISO response is observed if the progestin receptor antagonist RU 38486 is administered before progesterone. Progesterone also abolished PHE potentiation of vasoactive intestinal polypeptide-stimulated cAMP accumulation. In contrast, neither phorbol ester nor muscarinic (carbachol) potentiation of the cAMP response to ISO was affected by progesterone. The data suggest that ovarian steroids regulate the coupling of both alpha 1 and beta receptors to the membrane effector systems that generate intracellular cAMP.

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Section: Discussionmentioning

confidence: 97%

mentioning

confidence: 99%

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

Petitti

Etgen

1990

J. Neurosci.

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“…While these are the effects observed in biochemical studies, they are not the major effects seen physiologically in the CNS by activation of LY, receptors. In most studied areas of the brain, including the cerebral cortex, medial and lateral geniculate nuclei, the reticular thalamic nucleus, dorsal raphe and spinal motor neurons, (Y, receptor activation causes strictly excitatory responses both in vivo and in vitro (Baraban and Aghajanian, 1980;Bradshaw et al, 198 1, 1985;Fung and Barnes, 198 1;Aghajanian, 1985;Freedman and Aghajanian, 1987;McCormick and Prince, 1988;McCormick and Wang, 199 1;McCormick, 1992; for review, see Szabadi, 1979;Foote et al, 1983;Szabadi and Bradshaw, 1987). However, it appears that this activation is due largely to a decrease in resting K+ conductance and not to a robust increase in Ca2+ conductance (Baraban and Aghajanian, 1980;Aghajanian, 1985 shows the differential distribution of a,4 ,, and c(," mRNA in selected regions of the CNS as compared to previous ligand binding studies (Unnerstall et al, 1982(Unnerstall et al, , 1985Dashwood, 1983;Rainbow and Biegon, 1983;Palacios et al, 1987;Unnerstall, 1987;Marks et al, 1990;Cbamba et al, 1991).…”

Section: Functional Roles For Dlflerent O(~ Receptorsmentioning

confidence: 99%

Distribution of alpha 1 adrenoceptors in rat brain revealed by in situ hybridization experiments utilizing subtype-specific probes

et al. 1994

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The distribution of neurons in the rat CNS that synthesize mRNA for the alpha 1A/D and alpha 1B adrenoceptors was revealed by the in situ hybridization method. Forty-eight-mer DNA probes were synthesized to two different and unique regions of both the alpha 1A/D and alpha 1B mRNAs. Tissue sections from all levels of the CNS and some peripheral ganglia were incubated in a hybridization cocktail containing one of these four probes. The two mRNAs were expressed in a discrete and often complementary manner to each other, and identical hybridization patterns were seen for the probes directed against the same mRNA. The alpha 1A/D probes hybridized heavily with neurons in the internal granular and internal plexiform layers of the olfactory bulb, in layers II-V of most areas of the cerebral cortex, and in the lateral aspect of the lateral amygdaloid nucleus, with pyramidal neurons of CA1-CA4 regions, hilar and granular neurons of the dentate gyrus, and neurons in the reticular thalamic nucleus, cranial and spinal motor nuclei, and the inferior olivary nucleus. Light labeling was seen in a variety of other regions in the brain and spinal cord. The alpha 1B probes hybridized heavily with neurons in the mid layers of cerebral cortex and with virtually all neurons in the thalamus, except the reticular and habenular nuclei. In addition, labeling was seen in the lateral and central amygdaloid nuclei, in brainstem and spinal motor nuclei, over most neurons of the dorsal and medullary raphe nuclei and neurons of the intermediolateral cell column in the spinal cord. Light labeling was seen in the septal nucleus, the horizontal limb of the diagonal band, the paraventricular and lateral hypothalamic nuclei, the pontine and medullary reticular formation, and in most laminae in the spinal cord. The patterns of labeling obtained with the alpha 1B probes resemble the labeling seen in previous autoradiographic ligand binding studies utilizing "general" alpha 1 ligands, while the labeling patterns seen with the alpha 1A/D probes do not correspond to any published alpha 1 receptor distribution pattern, indicating that this mRNA likely encodes for a novel adrenoceptor. The present findings further expand the heterogeneity of adrenoceptor mRNAs presented in two accompanying studies (Nicholas et al., 1993a,b). This differential distribution of adrenoceptors subtypes provides a framework for the functional diversity to the apparently widespread, diffuse, and rather homogeneous noradrenergic innervation of the CNS.

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“…In contrast, up-regulation of the al-adrenoceptors of the rat cerebral cortex has been observed after treatment such as systemic injection of reserpine or intracerebroventricular injection of 6-hydroxydopamine (Bylund & U'Prichard 1983;Szabadi & Bradshaw 1987;Gross et a1 1988). In this study also, chronic treatment with a high dose of prazosin, but not with a low dose, significantly increased ul-adrenoceptor density, especially aIL subtype.…”

Section: Discussionmentioning

confidence: 99%

“…For example, the density of central fl-adrenoceptors is reduced by repeated stress and increased by chronic treatment with 8-adrenoceptor antagonist (Heal 1990;Takita et a1 1993Takita et a1 , 1995. In contrast, central al-adrenoceptors are not affected by stress (Lynch et a1 1983) but are up-regulated by systemic injection of reserpine or intracerebroventricular injection of 6-hydroxydopamine (Bylund & U'F'richard 1983;Szabadi & Bradshaw 1987;Gross et a1 1988 We have previously demonstrated that three distinct binding sites for prazosin (presumably E~A . ~I B and ~I L subtypes) occur in rat cerebral cortex (Oshita et a1 1991) and in Mongolian gerbil cerebral cortex (Kimura et a1 1993).…”

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confidence: 99%

Chronic Treatment with Prazosin Causes a Subtype-specific Increase in the α1-Adrenoceptor Density of the Stressed Rat Cerebral Cortex

Takita

Taniguchi

Zhu

et al. 1997

Journal of Pharmacy and Pharmacology

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The effects of chronic treatment with prazosin and of immobilization stress on the alpha 1-adrenoceptor subtypes in rat cerebral cortex have been examined. Prazosin-treated rats were allowed free access to tap water containing two different concentrations of prazosin (16 or 156 mg L-1) for 5 weeks. The mean plasma concentrations of prazosin were 5 ng mL-1 in groups treated with a low dose and 8 or 14 ng mL-1 in those treated with a high dose. Immobilization stress (2 h day-1, 2 weeks) or chronic treatment with a low dose of prazosin caused no significant change in the affinity for [3H]prazosin or in the maximum number of alpha 1-adrenoceptor sites (Bmax). However, treatment with prazosin (low dose) combined with stress increased the density of alpha 1-adrenoceptors with low affinity for prazosin. Treatment with a high dose of prazosin increased the density of alpha 1L-adrenoceptors, irrespective of stress loading. The densities of alpha 1A- and alpha 1B-adrenoceptors with high affinity for prazosin were increased only after treatment with a high dose of prazosin in combination with stress. These results indicate that three distinct alpha 1-adrenoceptor subtypes, alpha 1A, alpha 1B and alpha 1L, might be affected differently by treatment with prazosin and by stress.

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alpha-1 Adrenergic Receptors in the Central Nervous System

Cited by 4 publications

References 202 publications

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

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

Distribution of alpha 1 adrenoceptors in rat brain revealed by in situ hybridization experiments utilizing subtype-specific probes

Chronic Treatment with Prazosin Causes a Subtype-specific Increase in the α1-Adrenoceptor Density of the Stressed Rat Cerebral Cortex

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