Moderate lesion of the rat cholinergic septohippocampal pathway increases hippocampal nerve growth factor synthesis: evidence for long-term compensatory changes?

Hellweg, Rainer; Humpel, Christian; Löwe, Andrea; Hörtnagl, Heide

doi:10.1016/s0169-328x(96)00310-5

Cited by 32 publications

(8 citation statements)

References 24 publications

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“…Another non-exclusive possibility involves an indirect action via the septo-hippocampal cholinergic pathway. VAD reduces the activity of this pathway [18], [55], known to be under the control of NGF [56], [57]. Furthermore, immunolesion of this pathway decreases hippocampal neurogenesis [58], [59], whereas chronic treatment with NGF increases hippocampal neurogenesis [60].…”

Section: Discussionmentioning

confidence: 99%

Retinoic Acid Restores Adult Hippocampal Neurogenesis and Reverses Spatial Memory Deficit in Vitamin A Deprived Rats

et al. 2008

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A dysfunction of retinoid hippocampal signaling pathway has been involved in the appearance of affective and cognitive disorders. However, the underlying neurobiological mechanisms remain unknown. Hippocampal granule neurons are generated throughout life and are involved in emotion and memory. Here, we investigated the effects of vitamin A deficiency (VAD) on neurogenesis and memory and the ability of retinoic acid (RA) treatment to prevent VAD-induced impairments. Adult retinoid-deficient rats were generated by a vitamin A-free diet from weaning in order to allow a normal development. The effects of VAD and/or RA administration were examined on hippocampal neurogenesis, retinoid target genes such as neurotrophin receptors and spatial reference memory measured in the water maze. Long-term VAD decreased neurogenesis and led to memory deficits. More importantly, these effects were reversed by 4 weeks of RA treatment. These beneficial effects may be in part related to an up-regulation of retinoid-mediated molecular events, such as the expression of the neurotrophin receptor TrkA. We have demonstrated for the first time that the effect of vitamin A deficient diet on the level of hippoccampal neurogenesis is reversible and that RA treatment is important for the maintenance of the hippocampal plasticity and function.

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Section: Discussionmentioning

confidence: 99%

Retinoic Acid Restores Adult Hippocampal Neurogenesis and Reverses Spatial Memory Deficit in Vitamin A Deprived Rats

et al. 2008

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“…Several studies have demonstrated a significant decrease of cholinergic function and memory in ApoE-KO mice [15,31,32]. It has been postulated that cholinergic deficit correlates inversely with NGF-like activity [33,34]. The rationale behind this prediction is that the loss of cholinergic fibers leads to reduced choline acetyltransferase activity along with increased levels of NGF.…”

Section: Discussionmentioning

confidence: 99%

Low-Moderate Doses of Nicotine Decreased mRNA of NGF and BDNF and Their Receptors at 30 Min in the Frontal Cortex and Hippocampus of ApoE-KO Mice

Ruby

2013

J Neurol Res

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Background: Several studies have detected nicotine-associated increases in the mRNA and protein expression of NGF, BDNF and TrkA and TrkB receptors in multiple brain regions. Methods: We investigated the acute effects of different doses of nicotine (0.1, 0.5 and 1.0 mg/kg) on the mRNA levels of NGF, BDNF, TrkA and TrkB in the frontal cortex and hippocampus of ApoE-knockout (ApoE-KO) and wild-type (WT) mice. Results: The results demonstrated that in the frontal cortex and hippocampus, nicotine decreases NGF and BDNF mRNA levels in both ApoE-KO and WT mice. Nicotine also reduced TrkA in the frontal cortex and TrkB in both brain regions of WT mice, whereas no changes were observed in ApoE-KO mice. Interestingly, all of these effects were limited to low-intermediate doses (0.1 and 0.5 mg/kg) of nicotine, while 1.0 mg/kg of nicotine had no noticeable effect on the brain of either strain of mice. ApoE-KO mice showed a distinctly higher level of NGF mRNA expression versus the WT mice in both regions of the brain, whereas TrkA expression was lower only in the frontal cortex. Conclusions: These findings suggest that acute nicotine causes a decrease in the mRNA levels of NGF, BDNF and their receptors in the frontal cortex and hippocampus of mice depending on nicotine doses. A high level of NGF mRNA was observed in the brain of ApoE-KO mice, suggesting a role of ApoE in the expressions of neurotrophins in the hippocampus.

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“…This new pattern was similar to those described in studies of potential NGF producers after colchicine treatment: immunopositive pyramidal neurons in Layers V and III, and nonpyramidal neurons and some astrocytes in Layers II–VI (Conner and Varon, 1992; Nishio et al, 1994). It has been suggested that injury to the cholinergic neurons of the basal forebrain (Hellweg et al, 1997; Rossner et al, 1997; Gu et al, 1998), the impairment of neuritic transport mechanisms (Conner and Varon, 1992), or the dysfunction of the NGF system in AD (Scott and Crutcher, 1994) could lead to an increase in cortical cell NGF content. Neither the present data nor those reported in the literature, however, suggest that nicotine‐induced problems exist in NGF delivery, trkA binding, or NGF transport to the cytoplasm of the basalocortical forebrain neurons.…”

Section: Discussionmentioning

confidence: 99%

“…An increase in neuronal NGF has been demonstrated in many situations (Hellweg et al, 1997; Rossner et al, 1997; Rattray, 2001; Sofroniew et al, 2001), but only one study (French et al, 1999) has demonstrated this effect to be nicotine induced (after direct administration of nicotine to rat hippocampus). Astroglial cells can synthesize NGF, as demonstrated in pathological and experimental conditions (Oderfeld‐Nowak et al, 1992; Yu et al, 1996; Siegel and Chauhan, 2000), but this has not been reported previously as nicotine inducible.…”

Section: Discussionmentioning

confidence: 99%

Chronic nicotine administration increases NGF‐like immunoreactivity in frontoparietal cerebral cortex

Martínez‐Rodríguez

Toledano

Álvarez

et al. 2003

J of Neuroscience Research

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Nicotine/nicotine agonists, which have been proposed as therapeutic agents for the treatment of Alzheimer's disease and other neurodegenerative disorders, produce a wide variety of effects on the nervous system. Some mechanisms involved remain poorly understood. In this work, immunohistochemical techniques were used to determine the effect of nicotine on nerve growth factor (NGF) in the frontoparietal (motor, somatosensory) brain cortex of the albino rat. Nicotine was chronically administered intraperitoneally using osmotic pumps (0.35 mg nicotine base/kg body weight/day for 14 days). An increase in the number and the immunoreaction intensity of NGF‐like positive pyramidal and nonpyramidal neurons of these cortical areas was observed after treatment. Immunopositive astroglial cells were always seen in sections of treated animals but not in controls. The neuropil of control animals was, in general, devoid of reaction, but in treated animals, immunopositive prolongations were located randomly, some in close association with capillaries. At the electron microscopic level, these prolongations were demonstrated as belonging to neurons (dendrites and axons) and astroglial cells. Nicotinic activation of selected neurons and glial cells seems to trigger NGF/neurotrophic mechanisms, suggesting their use may be of benefit in prevention and treatment of neurodegenerative diseases. © 2003 Wiley‐Liss, Inc.

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Moderate lesion of the rat cholinergic septohippocampal pathway increases hippocampal nerve growth factor synthesis: evidence for long-term compensatory changes?

Cited by 32 publications

References 24 publications

Retinoic Acid Restores Adult Hippocampal Neurogenesis and Reverses Spatial Memory Deficit in Vitamin A Deprived Rats

Retinoic Acid Restores Adult Hippocampal Neurogenesis and Reverses Spatial Memory Deficit in Vitamin A Deprived Rats

Low-Moderate Doses of Nicotine Decreased mRNA of NGF and BDNF and Their Receptors at 30 Min in the Frontal Cortex and Hippocampus of ApoE-KO Mice

Chronic nicotine administration increases NGF‐like immunoreactivity in frontoparietal cerebral cortex

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