Developmental regulation of nerve growth factor and its receptor in the rat caudate-putamen

Mobley, William C.; Woo, James E.; Edwards, Robert H.; Riopelle, Richard J.; Longo, Frank M.; Weskamp, Gisela; Often, Uwe; Valletta, J; Johnston, Michael V.

doi:10.1016/0896-6273(89)90276-6

Cited by 124 publications

(67 citation statements)

References 57 publications

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“…Loss of BFCNs in developing trkA (Ϫ/Ϫ) mice would be consistent with observations of BFCN cell death on depletion of target-derived trophic support between the first and fourth postnatal weeks (Burke et al, 1994a,b;Cooper et al, 1996). It is during this time (P7-P21) that NGF levels in the target of BFCNs as well as the striatum are increasing (Large et al, 1986;Whittemore et al, 1986;Lu et al, 1989;Mobley et al, 1989). Thus NGF, whether derived from local sources (Lu et al, 1989;Lauterborn et al, 1995) or from the target region, likely regulates these cholinergic systems by activating TrkA.…”

Section: Role Of Trka In Cholinergic Neuronal Maturation And/or Survisupporting

confidence: 68%

“…Striatal cholinergic neurons are large interneurons involved in the control of movement (Schwarz et al, 1986). Studies have shown that both populations of neurons express TrkA Steininger et al, 1993;Sobreviela et al, 1994;Li et al, 1995) and that NGF is expressed in the target regions of these cells (Large et al, 1986;Whittemore et al, 1986;Lu et al, 1989;Mobley et al, 1989). Furthermore, the expression levels of NGF are low at birth in the target of both populations and then increase substantially in the postnatal period (Large et al, 1986;Whittemore et al, 1986;Lu et al, 1989;Mobley et al, 1989), correlating with the maturation of both striatal cholinergic neurons and BFCNs.…”

Section: Ntrmentioning

confidence: 99%

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A Role for TrkA during Maturation of Striatal and Basal Forebrain Cholinergic NeuronsIn Vivo

et al. 1997

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Nerve growth factor (NGF), acting via the TrkA receptor, has been shown to regulate the survival and maturation of specific neurons of the peripheral nervous system. Furthermore, exogenous NGF has potent actions on TrkA-expressing cholinergic neurons of the basal forebrain (BFCNs) and striatum. However, initial analysis of mice lacking NGF or TrkA revealed that forebrain cholinergic neurons were present in these animals through the fourth postnatal week. Because of the potential effects of NGF/TrkA interactions on these developing neurons, we have analyzed quantitatively the striatal and basal forebrain cholinergic neurons in trkA knock-out mice. By postnatal day (P) 7/8, forebrain cholinergic neurons are smaller in trkA (Ϫ/Ϫ) mice than those in wild-type littermate controls. However, cholinergic neuron number and fiber density in the hippocampus, a target region of BFCNs, are grossly intact. Interestingly, by P20-P25 trkA knock-outs contain significantly fewer (20-36%) and smaller cholinergic neurons in both the striatum and septal regions, as compared with controls. Cholinergic fiber density within the hippocampus also is depleted in knock-outs by the end of the second postnatal week. Contrary to some predictions, despite expression of p75 NTR in the absence of trkA in BFCNs of these knock-out mice, many cells, although smaller, are still alive at P25. Our data suggest that, in the absence of NGF/TrkA signaling, striatal cholinergic neurons and BFCNs do not mature fully and that BFCNs begin to atrophy and/or die surrounding the time of target innervation.

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Section: Role Of Trka In Cholinergic Neuronal Maturation And/or Survisupporting

confidence: 68%

Section: Ntrmentioning

confidence: 99%

A Role for TrkA during Maturation of Striatal and Basal Forebrain Cholinergic NeuronsIn Vivo

et al. 1997

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“…Sandwich ELISA for human apoE was performed as described (Mobley et al, 1989), except that the coating antibody was a mouse monoclonal antibody (WU E-4) raised against human apoE (Krul et al, 1988), and the detection antibody was a goat polyclonal antibody (Calbiochem, San Diego, CA) raised against human apoE. Each antibody recognizes apoE2, apoE3, and apoE4 equally.…”

Section: Apoe Elisamentioning

confidence: 99%

Production and characterization of astrocyte-derived human apolipoprotein E isoforms from immortalized astrocytes and their interactions with amyloid-β

Morikawa

Fryer

Sullivan

et al. 2005

Neurobiology of Disease

119

127

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The apolipoprotein E (apoE) genotype is an important genetic risk factor for Alzheimer's disease (AD). In the central nervous system (CNS), most apoE is produced by astrocytes and is present in unique high-density lipoprotein (HDL)-like particles that have distinct properties from apoE derived from other sources. To develop an efficient system to produce astrocyte-derived apoE in large quantities, we produced and characterized immortalized cell lines from primary astrocyte cultures derived from human APOE knock-in mice. APOE2, APOE3, and APOE4 expressing cell lines were established that secrete apoE in HDL-like particles at similar levels, cholesterol composition, and size as those produced by primary astrocytes. In physiological buffers, astrocyte-secreted apoE3 and E4 associated equally well with amyloid-B. Under the same conditions, only a small fraction of AB formed sodium dodecyl sulfate (SDS)-stable complexes with apoE (E3 N E4). These immortalized astrocytes will be useful for studying mechanisms underlying the isoform-specific effects of apoE in the CNS. D 2004 Elsevier Inc. All rights reserved.

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“…NGF ELISA. Immunoassay for NGF levels was performed according to a previously published two-site NGF ELISA method (Mobley et al, 1989). Hippocampus, cingulate cortex, retrosplenial cortex, and the medial septal area, which contains both the medial septal nucleus and diagonal band (MS/ DB), were dissected and immediately frozen on dry ice and stored at Ϫ70°C.…”

Section: Generation Of P75mentioning

confidence: 99%

Absence of p75^NTRCauses Increased Basal Forebrain Cholinergic Neuron Size, Choline Acetyltransferase Activity, and Target Innervation

et al. 1997

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Emerging evidence suggests that the p75 neurotrophin receptor (p75 NTR ) mediates cell death; however, it is not known whether p75NTR negatively regulates other neuronal phenotypes. We found that mice null for p75 NTR displayed highly significant increases in the size of basal forebrain cholinergic neurons, including those that are TrkA-positive. Cholinergic hippocampal target innervation also was increased significantly. Activity of the cholinergic neurotransmitter synthetic enzyme choline acetyltransferase (ChAT) was increased in both the medial septum and hippocampus. Upregulation of these cholinergic features was not associated with increased basal forebrain or hippocampal target NGF levels. In contrast, striatal cholinergic neurons, which do not express p75 NTR , showed no difference in neuronal number, size, or ChAT activity between wild-type and p75NTR null mutant mice. These findings indicate that p75 NTR negatively regulates cholinergic neuronal phenotype of the basal forebrain cholinergic neurons, including cell size, target innervation, and neurotransmitter synthesis.

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Developmental regulation of nerve growth factor and its receptor in the rat caudate-putamen

Cited by 124 publications

References 57 publications

A Role for TrkA during Maturation of Striatal and Basal Forebrain Cholinergic NeuronsIn Vivo

A Role for TrkA during Maturation of Striatal and Basal Forebrain Cholinergic NeuronsIn Vivo

Production and characterization of astrocyte-derived human apolipoprotein E isoforms from immortalized astrocytes and their interactions with amyloid-β

Absence of p75^NTRCauses Increased Basal Forebrain Cholinergic Neuron Size, Choline Acetyltransferase Activity, and Target Innervation

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Developmental regulation of nerve growth factor and its receptor in the rat caudate-putamen

Cited by 124 publications

References 57 publications

A Role for TrkA during Maturation of Striatal and Basal Forebrain Cholinergic NeuronsIn Vivo

A Role for TrkA during Maturation of Striatal and Basal Forebrain Cholinergic NeuronsIn Vivo

Production and characterization of astrocyte-derived human apolipoprotein E isoforms from immortalized astrocytes and their interactions with amyloid-β

Absence of p75NTRCauses Increased Basal Forebrain Cholinergic Neuron Size, Choline Acetyltransferase Activity, and Target Innervation

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Absence of p75^NTRCauses Increased Basal Forebrain Cholinergic Neuron Size, Choline Acetyltransferase Activity, and Target Innervation