Development of Oxytocinergic Neurons in Monolayer Cultures Derived from Embryonic, Fetal and Postnatal Rat Hypothalami

Madarász, Emı́lia; Környei, Zsuzsanna; Poulain, Daniel; Theodosis, Dionysia T.

doi:10.1111/j.1365-2826.1992.tb00190.x

Cited by 14 publications

(9 citation statements)

References 32 publications

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“…In rat, primary fetal brain cultures from the hypothalamus, vasopressin mRNA and peptide can be detected, but oxytocin cannot (Di Scala-Guenot et al, 1990a, b) without stimulation by potassium or thyroid hormone (Madarasz et al, 1992). This difference is consistent with in vivo results that vasopressin emerges earlier than oxytocin and is also consistent with the hypothesis that developmental oxytocin is activity dependent (Zheng et al, 2014).…”

Section: Dynamic Developmental Profiles: When and Where Are The Factosupporting

confidence: 81%

Developmental Perspectives on Oxytocin and Vasopressin

Hammock

2014

Neuropsychopharmacol

164

146

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The related neuropeptides oxytocin and vasopressin are involved in species-typical behavior, including social recognition behavior, maternal behavior, social bonding, communication, and aggression. A wealth of evidence from animal models demonstrates significant modulation of adult social behavior by both of these neuropeptides and their receptors. Over the last decade, there has been a flood of studies in humans also implicating a role for these neuropeptides in human social behavior. Despite popular assumptions that oxytocin is a molecule of social bonding in the infant brain, less mechanistic research emphasis has been placed on the potential role of these neuropeptides in the developmental emergence of the neural substrates of behavior. This review summarizes what is known and assumed about the developmental influence of these neuropeptides and outlines the important unanswered questions and testable hypotheses. There is tremendous translational need to understand the functions of these neuropeptides in mammalian experience-dependent development of the social brain. The activity of oxytocin and vasopressin during development should inform our understanding of individual, sex, and species differences in social behavior later in life.

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Section: Dynamic Developmental Profiles: When and Where Are The Factosupporting

confidence: 81%

Developmental Perspectives on Oxytocin and Vasopressin

Hammock

2014

Neuropsychopharmacol

164

146

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“…The remainincg neurons represent y-aminobutyric (GABA)-producing neurons (Masuko, Nakajimia & Nakajima, 1992) and other unidentified neuronal phenotypes. The hypothalamic cultures also contain a variety of neuronal phenotypes, including neurons producing the hypothalamic hormones, GABA and dopamnine (Aladarasz, Kornyei, Poulain & Theodosis, 1992;. Therefore, we are not sure whether a subpopulation of neurons possess these K+ channels or whether K+ channels are present in all types of neuron.…”

Section: Discussionmentioning

confidence: 99%

Arachidonic acid activation of a new family of K+ channels in cultured rat neuronal cells.

Kim¹,

Sladek²,

Aguado-Velasco³

et al. 1995

The Journal of Physiology

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1. The presence and properties of K+ channels activated by arachidonic acid were studied in neuronal cells cultured from the mesencephalic and hypothalamic areas of rat brain.2. Arachidonic acid produced a concentration-dependent (5-50 #UM) and reversible activation of whole-cell currents. 3. In excised membrane patches, arachidonic acid applied to the cytoplasmic or extracellular side of the membrane caused opening of three types of channels whose current-voltage relationships were slightly outwardly rectifying, inwardly rectifying and linear, and whose single channel slope conductances at +60 mV were 143, 45 and 52 pS, respectively.4. All three currents were K+ selective and blocked by 2 mm Ba2+ but not by other K+ channel blockers such as tetraethylammonium chloride, 4-aminopyridine and quinidine. The outwardly and inwardly rectifying currents were slightly voltage dependent with higher channel activity at more depolarized potentials.5. Arachidonic acid activated the K+ channels in cells treated with cyclo-oxygenase and lipoxygenase inhibitors (indomethacin and nordihydroguaiaretic acid), indicating that arachidonic acid itself can directly activate the channels. Alcohol and methyl ester derivatives of arachidonic acid failed to activate the K+ channels, indicating that the charged carboxyl group is important for activation. 6. Certain unsaturated fatty acids (linoleic, linolenic and docosahexaenoic acids), but not saturated fatty acids (myristic, palmitic, stearic acids), also reversibly activated all three types of K+ channel. 7. All three K+ channels were activated by pressure applied to the membrane (i.e. channels were stretch sensitive) with a half-maximal pressure of -18 mmHg. The K+ channels were not blocked by 100 ,UM GdCl3. 8. A decrease in intracellular pH (over the range 5 6-7 2) caused a reversible, pH-dependent increase in channel activity whether the channel was initially activated by arachidonic acid or stretch.9. Glutamate, a neurotransmitter reported to generate arachidonic acid in striatal neurons, did not cause activation of the K+ channels when applied extracellularly in cell-attached patches. 10. It is suggested that the K+ channels described here belong to a distinct family of ion channels that are activated by either fatty acids or membrane stretch. Although the physiological roles of these K+ channels are not yet known, they may be involved in cellular processes such as cell volume regulation and ischaemia-induced elevation of K+ loss.

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“…Immunocytochemical staining of intermediate filaments. Visualization of glial fibrillary acidic protein (GFAP) and neurofilament (NF) proteins was done as described previously (Madarász et al, 1992). The same protocol was used to demonstrate nestin immunoreactivity.…”

Section: Immunocytochemical Methodsmentioning

confidence: 99%

Retinoic acid induced neural differentiation in a neuroectodermal cell line immortalized by p53 deficiency

Schlett

Madarász

1997

J. Neurosci. Res.

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Neuroepithelial cell lines were established from cerebral vesicles of 9‐day‐old mouse embryos lacking functional p53 genes (Livingstone et al: Cell 70:923–935, 1992). All‐trans retinoic acid (RA) induced bulk formation of neurons both in several p53‐deficient neuroepithelial cell lines and in wild‐type neural cells derived from early embryonic (E9–E12) forebrain vesicles. Forty‐eight‐hour treatment with 10−6 MRA was necessary and sufficient to initiate neuron formation by p53‐/‐‐progenitors, but neuronal characteristics appeared with a delay of 3–4 days. The first appearance of cells with astroglial features followed that of neurons with a further delay of 4–5 days. The establishment of neuronal phenotypes involved minimally three rounds of cell cycle. Future neurons were sorted out from substrate‐attached cells and were characterized by a specific rearrangement of nestin‐immunoreactive filaments. The formation of neuronal phenotypes was not synchronized within the RA‐treated cell populations. The data indicate that RA, which promotes the initiation of neural differentiation, cannot function as a direct regulator of cell‐fate decisions made by neural progenitor cells. J. Neurosci. Res. 47:405–415, 1997. © 1997 Wiley‐Liss, Inc.

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Development of Oxytocinergic Neurons in Monolayer Cultures Derived from Embryonic, Fetal and Postnatal Rat Hypothalami

Cited by 14 publications

References 32 publications

Developmental Perspectives on Oxytocin and Vasopressin

Developmental Perspectives on Oxytocin and Vasopressin

Arachidonic acid activation of a new family of K+ channels in cultured rat neuronal cells.

Retinoic acid induced neural differentiation in a neuroectodermal cell line immortalized by p53 deficiency

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