Ontogeny of &lt;sup&gt;3&lt;/sup&gt;H-Diazepam Binding Sites in Different Rat Brain Area

Aldinio, C.; Balzano, Marielle; Savoini, G.; León, Andrés de; Toffano, Zeno

doi:10.1159/000112815

Cited by 22 publications

(3 citation statements)

References 17 publications

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“…The increase in [3H]-diazepam binding during development is due to a large number of binding sites rather than to a higher affinity for [3H]-diazepam. These results are in accordance with those reported by Braestrup and Nielsen [1978], Candy and Martin [1979], Mallorga et al [1980], and Aldinio, et al [1981] who have shown that benzodiazepine receptors are present in the rat brain at an early stage of development and reach a maximal concentration after about 4 weeks. The present study also establishes that methylxanthines such as caf feine and theophylline and purine compounds are able to displace the spe cific diazepam binding in cerebral membranes from adult rats as already demonstrated by Marangos et al [1979].…”

Section: Discussionsupporting

confidence: 93%

In vitro and in vivo Displacement of [^3H]-Diazepam Binding by Purine Derivatives in Developing Rat Brain

Jl¹,

Barberis²,

Vert³

1984

Dev Pharmacol Ther

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In vitro inhibiton of [^3H]-diazepam binding to developing rat brain synaptosomal membranes has been studied. Adenosine, inosine, and hypoxanthine display approximately equal potencies as inhibitors of [^3H]-diazepam binding to young rat brain membranes. In adult, inosine and hypoxanthine exhibit greater inhibitory potency. Data are also presented which show that the xanthine stimulants caffeine and theophylline competitively inhibit [^3H]-diazepam binding with an equal potency throughout the development. In vivo study is also reported which shows that [^3H]-diazepam binding to membranes from 5-day-old rats is displaced when female rats have been daily injected with caffeine or theophylline during gestation and lactation.

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Section: Discussionsupporting

confidence: 93%

In vitro and in vivo Displacement of [^3H]-Diazepam Binding by Purine Derivatives in Developing Rat Brain

Jl¹,

Barberis²,

Vert³

1984

Dev Pharmacol Ther

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“…It is further corroborated by the observation that the labeling pattern was virtually identical for FNZP and the specific BDZ antagonist Ro 15-1788 (Darragh et al, 1981;Hunkeler et al, 1981). Biochemical studies indicate that the affinity characteristics of BDZ-binding sites do not noticeably change during ontogeny (Braestrup and Nielsen, 1978;Mallorga et al, 1980;Aldinio et al, 1981). Whether there are changes in the relationship to the GABA receptor remains uncertain.…”

Section: Discussionmentioning

confidence: 87%

An autoradiographic study of the prenatal development of benzodiazepine- binding sites in rat brain

Schlumpf¹,

Richards²,

Lichtensteiger³

et al. 1983

J. Neurosci.

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The regional development of benzodiazepine-binding sites in fetal brain was studied by autoradiography. Cryostat sections through the brains of fetuses from time-pregnant rats were incubated either with r3H]flunitrazepam or with the specific benzodiazepine antagonist [3H]R015-1788. The specificity of radioligand binding was checked by co-incubation with an excess of nonradioactive antagonist or clonazepam, respectively.Labeling with either agonist or antagonist revealed a similar developmental pattern of binding sites. Specific binding was first detected on gestational day (GD) 14 in the spinal cord and lower brainstem. Between GD 14 and GD 15, labeling spread throughout the lower brainstem, mesencephalon, and parts of the diencephalon, with higher densities in ventral areas. Matrix zones remained unlabeled. On GD 16, binding was present in the developing caudate putamen, the olfactory bulb, and the frontoventral parts of the neocortex. Binding sites had spread over the remaining neocortex by GD 21 and increased in density in di-and telencephalic areas. At earlier stages of development, neocortical binding sites were restricted to the superficial (GD 16 and 18) and deep (GD 18) layers above and below the cortical plate; the latter was unlabeled. By GD 21, binding sites also occurred in the cortical plate with an inside-out density gradient. By this time, layer I exhibited the highest density of silver grains.

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“…At birth, these receptors are present at a relatively high density and they reach adult levels about 3 wk later. During postnatal development, the increase in benzodiazepine binding has been demonstrated to be due to a larger number of specific sites, rather than to a higher receptor affinity (21)(22)(23). A sequential development of benzodiazepine receptors in relation to the time course of maturation of cerebral structures could be shown, with a proliferation peak that parallels rapid brain growth in the rat (between 5 and 15 d of age).…”

Section: Development Of Central Benzodiazepine Receptorsmentioning

confidence: 99%

Autoradiographic Changes in Central Benzodiazepine Binding Sites and Their Coupling to γ-Aminobutyric Acid Receptors after Seizures in the Developing Rat

Werck

Daval

1991

Pediatr Res

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ABSTRACT. Benzodiazepines are psychoactive substances classically used for their anticonvulsant properties in neonates as well as in adults. In a previous work, we have shown that seizures lead to an age-dependent upregulation of central benzodiazepine binding sites measured in isolated rat cerebral membranes. However, information concerning regional changes in the receptor density was lacking. In our present study, the effects of bicuculline- GABA, y-aminobutyric acidNumerous neuropathologic studies have pointed out that during the neonatal period and early infancy, epileptic manifestations are relatively frequent, with peculiar characteristics. Children are more susceptible to epileptic brain damage than adults (I), and recurrent or prolonged seizures in infants and children may be followed by major neurologic sequelae (2).Benzodiazepines are psychoactive drugs with anxiolytic, anticonvulsant, and muscle relaxant properties that are widely prescribed in neonates as well as in adults (3). The mechanism of benzodiazepine central action has been attributed to a highaffinity, saturable, and specific binding site and its interaction with a GABA-regulated chloride channel (4, 5). In animals,

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Ontogeny of <sup>3</sup>H-Diazepam Binding Sites in Different Rat Brain Area

Cited by 22 publications

References 17 publications

In vitro and in vivo Displacement of [^3H]-Diazepam Binding by Purine Derivatives in Developing Rat Brain

In vitro and in vivo Displacement of [^3H]-Diazepam Binding by Purine Derivatives in Developing Rat Brain

An autoradiographic study of the prenatal development of benzodiazepine- binding sites in rat brain

Autoradiographic Changes in Central Benzodiazepine Binding Sites and Their Coupling to γ-Aminobutyric Acid Receptors after Seizures in the Developing Rat

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