Time course of the elevation of nerve growth factor (NGF) content in the hippocampus and septum following lesions of the septohippocampal pathway in rats

Gasser, U.E.; Weskamp, Gisela; Otten, U.; Dravid, A. R.

doi:10.1016/0006-8993(86)90198-8

Cited by 135 publications

(39 citation statements)

References 28 publications

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“…The latter are consistent with reports of AD-related decreases in the number of NGF receptorbearing neurons and decreased retrograde transport of NGF to the CBFNs (Hefti and Mash, 1989;Mufson et al, 1989;Allen et al, 1991;Loy et al, 1990;Strada et al, 1992). These observations are consistent with reports of accumulated NGF protein in the hippocampus of young rats after fimbria-fornix transections together with cell losses and degeneration of CBFNs in the medial septum and vertical limb of the diagonal band of Broca Korsching et al, 1986;Weskamp et al, 1986;Gasser et al, 1986;Larkfors et al, 1987;Scott et al, 1994). In the aged rat, fimbria-fornix transections also do not stimulate hippocampal NGF-protein levels (Scott et al, 1994).…”

Section: Introductionsupporting

confidence: 92%

Responses in the aged rat brain after total immunolesion

Perez‐Polo

1998

J. Neurosci. Res.

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In the present study, we compare the effects of cholinergic deafferentation of the hippocampus, cortex, and olfactory bulb of young and aged rats on nerve growth factor (NGF) protein levels in these areas. We also describe glial responses to intraventricular injections of the immunotoxin, 192 IgG-saporin in the aged. Choline acetyltransferase (ChAT) activity was dramatically decreased in the basal forebrain and target areas of the cholinergic basal forebrain neurons (CBFNs) in the young immunolesioned rats and to a lesser extent in their aged counterparts. After total immunolesion, NGF protein levels significantly increased in the hippocampus, cortex, and olfactory bulb of the young rats but not of the aged rats, except for small increases in the olfactory bulb after two weeks. After immunolesion NGF protein levels in the basal forebrain increased in young rats and less so in the aged rats. The total immunolesions had no effects on NGF and BDNF mRNA levels in the hippocampus and cortex. Two weeks after injection of the immunotoxin, the profiles of AChE- and p75NTR-positive cells significantly decreased in medial septum, vertical and horizontal limbs of diagonal band and nucleus basalis of Meynert. There was also an increase in microglia while but not astrocytes in the subnuclei of basal forebrain. In conclusion, 192 IgG-saporin was effective in producing cholinergic lesions in both young and aged rat brains, the lesion-induced NGF response was partially extinguished in the aged rat brains and immunolesions induced a microglial response in aged brain.

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Section: Introductionsupporting

confidence: 92%

Responses in the aged rat brain after total immunolesion

Perez‐Polo

1998

J. Neurosci. Res.

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“…In contrast to reduced neurotrophin receptors, NGF mRNA was significantly increased throughout the brain, with pronounced increases in the hippocampus where chronic ethanol treatment increased NGF mRNA approximately twofold (4). Increased NGF expression is known to occur as a result of brain injury (28,53). The increased NGF mRNA following chronic ethanol treatment may be due to the neuronal damage caused by ethanol.…”

Section: Neurotrophic Factorsmentioning

confidence: 95%

Alcohol and Neurodegeneration

Crews

1999

CNS Drug Reviews

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“…The loss of NGF receptor 1 cholinergic axons within the denervated hippocampus, resulting in the cessation of NGF uptake at septal axonal terminals and retrograde transport by cholinergic neurons of the medial septum and diagonal band, was proposed to account for the specificity of the sprouting response (Crutcher et al, 1979(Crutcher et al, , 1981. In fact, subsequent studies demonstrated that septal denervation results in increased hippocampal NGF levels but no change in NGF mRNA (Collins and Crutcher, 1985;Gasser et al, 1986;Korsching et al, 1986;Whittemore et al, 1987). The cellular source of NGF within the hippocampus, however, is unclear.…”

Section: Sympathetic Axons In the Undamaged And Damaged Mammalian Brainmentioning

confidence: 99%

Sympathetic axons invade the brains of mice overexpressing nerve growth factor

Kawaja

Crutcher

1997

J. Comp. Neurol.

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Transgenic mice that overexpress nerve growth factor (NGF) in cells producing glial fibrillary acidic protein were used to determine whether sympathetic axons will invade the undamaged, postnatal mammalian brain. By using reverse transcriptase-polymerase chain reaction, NGF mRNA transgene expression was detectable in the hippocampi and cerebella of transgenic mice but not in age-matched, wild type mice. Elevated levels of NGF protein were detected in the hippocampi and cerebella of postnatal and adult transgenic animals as well as in conditioned media from transgenic cerebellar astrocytes in culture. The brains of these transgenic mice were found to contain postganglionic sympathetic fibers, as identified by their immunohistochemical staining for tyrosine hydroxylase and by their disappearance following superior cervical ganglionectomy. In the cerebellum, a robust plexus of sympathetic fibers was evident in the deep white matter and in the inferior cerebellar peduncles. These axons within the cerebellum were observed as early as 14 days after birth and dramatically increased in number with age. Sympathetic axons were also associated with the large blood vessels of the hippocampal fissure and were present within the hilar region of the dentate gyrus. NGF immunoreactivity was present within the sympathetic axons as well as within glial cells in the transgenic cerebellum and hippocampus. Wild type mice, however, lacked similar patterns of immunostaining. These results demonstrate that elevated expression of NGF in the intact mammalian brain results in the growth of sympathetic axons into the central nervous system in the absence of injury.

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Time course of the elevation of nerve growth factor (NGF) content in the hippocampus and septum following lesions of the septohippocampal pathway in rats

Cited by 135 publications

References 28 publications

Responses in the aged rat brain after total immunolesion

Responses in the aged rat brain after total immunolesion

Alcohol and Neurodegeneration

Sympathetic axons invade the brains of mice overexpressing nerve growth factor

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