Characterization and Partial Purification of AIM: A Plasma Protein That Induces Rat Cerebral Type 2 Astroglia from Bipotential Glial Progenitors

Levison, Steven W.; McCarthy, Ken D.

doi:10.1111/j.1471-4159.1991.tb08220.x

Cited by 59 publications

(45 citation statements)

References 45 publications

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“…Mouse (CD1 strain) hippocampal neurons isolated from the CA1-CA3 region were cultured on microislands as described previously (Furshpan et al, 1976;Bekkers and Stevens, 1991). Neurons were obtained from animals (age postnatal day 0-2) and plated onto a feeder layer of hippocampal astrocytes that had been laid down previously (Levison and McCarthy, 1991). Cultures were grown in high glucose (20 mM) DMEM containing 10% horse serum, without mitotic inhibitors and used for recordings after 8 days in culture and for no more than 3 hours after removal from culture medium.…”

Section: Hippocampal Culture Preparationmentioning

confidence: 99%

Cannabinoid Receptor–Interacting Protein 1a Modulates CB₁ Receptor Signaling and Regulation

et al. 2015

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Cannabinoid CB 1 receptors (CB 1 Rs) mediate the presynaptic effects of endocannabinoids in the central nervous system (CNS) and most behavioral effects of exogenous cannabinoids. Cannabinoid receptor-interacting protein 1a (CRIP 1a ) binds to the CB 1 R C-terminus and can attenuate constitutive CB 1 R-mediated inhibition of Ca 21 channel activity. We now demonstrate cellular colocalization of CRIP 1a at neuronal elements in the CNS and show that CRIP 1a inhibits both constitutive and agonist-stimulated CB 1 Rmediated guanine nucleotide-binding regulatory protein (G-protein) activity. Stable overexpression of CRIP 1a in human embryonic kidney (HEK)-293 cells stably expressing CB 1 Rs (CB 1 -HEK), or in N18TG2 cells endogenously expressing CB 1 Rs, decreased CB 1 Rmediated G-protein activation (measured by agonist-stimulated [ activation. These effects were not attributable to differences in CB 1 R expression or endocannabinoid tone because CB 1 R levels did not differ between cell lines varying in CRIP 1a expression, and endocannabinoid levels were undetectable (CB 1 -HEK) or unchanged (N18TG2) by CRIP 1a overexpression. In CB 1 -HEK cells, 4-hour pretreatment with cannabinoid agonists downregulated CB 1 Rs and desensitized agonist-stimulated [ 35 S]GTPgS binding. CRIP 1a overexpression attenuated CB 1 R downregulation without altering CB 1 R desensitization. Finally, in cultured autaptic hippocampal neurons, CRIP 1a overexpression attenuated both depolarizationinduced suppression of excitation and inhibition of excitatory synaptic activity induced by exogenous application of cannabinoid but not by adenosine A1 agonists. These results confirm that CRIP 1a inhibits constitutive CB 1 R activity and demonstrate that CRIP 1a can also inhibit agonist-stimulated CB 1 R signaling and downregulation of CB 1 Rs. Thus, CRIP 1a appears to act as a broad negative regulator of CB 1 R function.

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Section: Hippocampal Culture Preparationmentioning

confidence: 99%

Cannabinoid Receptor–Interacting Protein 1a Modulates CB₁ Receptor Signaling and Regulation

et al. 2015

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“…Mouse (CD1 strain) hippocampal neurons isolated from the CA1-CA3 region were cultured on microislands as described previously (Bekkers and Stevens 1991;Furshpan et al 1976). Neurons were obtained from animals (age postnatal days 0 -2) and plated onto a feeder layer of hippocampal astrocytes that had been laid down previously (Levison and McCarthy 1991). Cultures were grown in high-glucose (20 mM) medium containing 10% horse serum without mitotic inhibitors and used for recordings after 8 days in culture and for no more than 3 h after removal from culture medium.…”

Section: Culture Preparationmentioning

confidence: 99%

Cannabinoid CB₁ Receptor-Dependent Long-Term Depression in Autaptic Excitatory Neurons

Kellogg

Straiker²

2009

Journal of Neurophysiology

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Kellogg R, Mackie K, Straiker A. Cannabinoid CB1 receptordependent long-term depression in autaptic excitatory neurons. J Neurophysiol 102: 1160 -1171. First published June 3, 2009 doi:10.1152/jn.00266.2009. Long-term depression (LTD) of synaptic signaling-lasting from tens of minutes to hours or longer-is a widespread form of synaptic plasticity in the brain. Neurons express diverse forms of LTD, including autaptic LTD (autLTD) observed in cultured hippocampal neurons, the mechanism of which remains unknown. We have recently reported that autaptic neurons express both endocannabinoid-mediated depolarization-induced suppression of excitation (DSE) and metabotropic suppression of excitation (MSE). We now report that activating cannabinoid CB 1 receptors is necessary for the induction of autLTD. Most surprisingly, CB 1 does not induce autLTD via the G i/o proteins typically activated by this receptor nor with G s . Rather, the requirements of presynaptic phospholipase C and filled calcium stores suggest G q . In autLTD, a 3-to 4-min activation of the receptor by the endocannabinoid 2-arachidonoyl glycerol leads to prolonged inhibition while leaving short-term inhibition (e.g., DSE) intact. autLTD requires activation of both metaboand ionotropic glutamate receptors. autLTD also requires MEK/ERK activation. Under certain conditions, one or more DSE stimuli will elicit autLTD. It is becoming evident that cannabinoids mediate multiple forms of plasticity at a single synapse, stretching temporally from tens of seconds (DSE/MSE) to tens of minutes (autLTD) to hours (CB 1 desensitization). Our findings imply a remarkable flexibility for the cannabinoid signaling system whereby discrete mechanisms of CB 1 activation within a single neuron yield temporally and mechanistically distinct forms of plasticity.

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“…Previous data showed that the BzATP-evoked Ca 2 +response in rat brain astrocytes was completely abolished by removal of external Ca 2 + (6). Neither cell pretreatment with the protein kinase C (PKC) activator 4p-phorbol 12-myristate 13-acetate (PMA) (1 u M for 30 min) , to inhibit the IP3-induced release of intracellular calcium (33), nor challenging the cells with the sequisterpene lactone tumor promoter thapsigargin (Tg) (1/--lM) to inhibit the intracellular Ca 2 +-ATPase (54) , affected the BzATP-induced [Ca"], increase (Fig. 2C) .…”

Section: Effect Of P2x 7 Ac Tivation On Rat Brain Astrocyte Intra Celmentioning

confidence: 99%

P2X₇Receptor Activation in Rat Brain Cultured Astrocytes Increases the Biosynthetic Release of Cysteinyl Leukotrienes

Ballerini

Ciccarelli

Caciagli

et al. 2005

Int J Immunopathol Pharmacol

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* Equally contributed to this paperAstrocytes have been recognized as important elements in controlling inflammatory as well as immune processes in the central nervous system (CNS). Recently, glial cells have been shown to produce cysteinyl leukotrienes (CysLTs) which are known lipid mediators of inflammation and whose extracellular concentrations rise under different pathological conditions in the brain. In the same conditions also extracellular concentrations of ATP dramatically increase reaching levels able to activate P2X 7 ionotropic receptors for which an emerging role in neuroinflammation and neurodegeneration has been claimed. RT-PCR analysis showed that primary cultures of rat brain astrocytes express P2X 7 receptors. Application of the selective P2X7 agonist benzoyl-benzolyATP(BzATP) markedly increased [Ca"], which was mediated by a calcium influx from the extracellular milieu. The P2X 7 antagonist, oATP,suppressed the BzATP-induced calcium increase. Consistent with the evidence that increased calcium levels activate the leukotriene biosynthetic pathway, challenge of astrocytes with either the calcium ionophore A23187 or BzATP significantly increased CysLT production and the cell pre-treatment with EGTA abolished these effects. Again the P2X7 antagonist prevented the BzATP-mediated CysLT efflux, whereas the astrocyte pretreatment with MK-571, a CysLT I receptor antagonist, was ineffective. The astrocyte pre-treatment with a cocktail of inhibitors of ATP binding cassette (ABC) proteins reduced the BzATP-mediated CysLT production confirming that ABC transporters are involved in the release of CysLTs. The astrocyte P2X 7-evoked rise of CysLT efflux was abolished in the presence of MK-886, an inhibitor of 5-lipoxygenase activating protein (FLAP) whose expression, along with that of 5'-lipoxygenase (5-LO) was reported by Northern Blot analysis. The stimulation ofP2X 7 induced an up-regulation of FLAP mRNA that was reduced by the antagonist oATP. These data suggest that in rat brain cultured astrocytes P2X 7 ATP receptors may participate in the control of CysLT release thus further supporting a role for extracellular ATP as an integral component of the inflammatory brain response.Inflammation is involved in several neurological diseases including brain injury, cerebral ischemia, multiple sclerosis,Alzheimer's and Parkinson's diseases (31,47,35). Neuroinflammation is characterized by the activation of both microglia and astrocytes (45). Glial cells, including astrocytes, are reported to produce

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Characterization and Partial Purification of AIM: A Plasma Protein That Induces Rat Cerebral Type 2 Astroglia from Bipotential Glial Progenitors

Cited by 59 publications

References 45 publications

Cannabinoid Receptor–Interacting Protein 1a Modulates CB₁ Receptor Signaling and Regulation

Cannabinoid Receptor–Interacting Protein 1a Modulates CB₁ Receptor Signaling and Regulation

Cannabinoid CB₁ Receptor-Dependent Long-Term Depression in Autaptic Excitatory Neurons

P2X₇Receptor Activation in Rat Brain Cultured Astrocytes Increases the Biosynthetic Release of Cysteinyl Leukotrienes

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Characterization and Partial Purification of AIM: A Plasma Protein That Induces Rat Cerebral Type 2 Astroglia from Bipotential Glial Progenitors

Cited by 59 publications

References 45 publications

Cannabinoid Receptor–Interacting Protein 1a Modulates CB1 Receptor Signaling and Regulation

Cannabinoid Receptor–Interacting Protein 1a Modulates CB1 Receptor Signaling and Regulation

Cannabinoid CB1 Receptor-Dependent Long-Term Depression in Autaptic Excitatory Neurons

P2X7Receptor Activation in Rat Brain Cultured Astrocytes Increases the Biosynthetic Release of Cysteinyl Leukotrienes

Contact Info

Product

Resources

About

Cannabinoid Receptor–Interacting Protein 1a Modulates CB₁ Receptor Signaling and Regulation

Cannabinoid Receptor–Interacting Protein 1a Modulates CB₁ Receptor Signaling and Regulation

Cannabinoid CB₁ Receptor-Dependent Long-Term Depression in Autaptic Excitatory Neurons

P2X₇Receptor Activation in Rat Brain Cultured Astrocytes Increases the Biosynthetic Release of Cysteinyl Leukotrienes