Effects of nerve growth factor on visual cortical plasticity require afferent electrical activity

AbstractRecent investigations have shown that cortical nerve growth factor (NGF) infusions during the critical period inhibit ocular-dominance plasticity in the binocular portion of the rat visual cortex. The mechanisms underlying the effects of NGF on visual cortical plasticity are still unclear. To investigate whether during normal development intracortical and/or extracortical cells possess uptake/transport mechanisms for the neurotrophin, we injected 125I-NGF into the occipital cortex of rats at different postnatal ages. Within the cortex, only a few labelled cells were observed. These cells were confined to the vicinity of the injection site and their number depended on the animal's age at the time of injection. Labelled cells were absent at postnatal day (PD) 10 but could be detected between PD 14 and PD 18. They then decreased in number over the following period and were not detected in adult animals. Outside the cortex, neurons of the lateral geniculate nucleus (LGN) were not observed to take up and retrogradely transport NGF at any age after birth. In contrast, retrogradely labelled neurons were found in the basal forebrain. Labelled cells were first observed here at PD 14 and then increased in number until reaching the adult pattern. Our results show that intrinsic and extrinsic neurons are labelled following intracortical injections of iodinated NGF. In both neuronal populations, the uptake and transport of NGF is present over a period corresponding to the critical period for visual cortical plasticity. These findings suggest that NGF may play a role, both intra and extracortically, in plasticity phenomena.

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Beta-nerve growth factor stimulates spontaneous electrical activity of in vitro embryonic mouse GnRH neurons through a P75 mediated-mechanism

Scientific Reports ◽

10.1038/s41598-020-67665-4 ◽

2020 ◽

Vol 10 (1) ◽

Cited By ~ 1

Author(s):

Caroline Pinet-Charvet ◽

Renaud Fleurot ◽

Flavie Derouin-Tochon ◽

Simon de Graaf ◽

Xavier Druart ◽

...

Keyword(s):

Nerve Growth Factor ◽

Growth Factor ◽

Electrical Activity ◽

Embryonic Mouse ◽

Nerve Growth ◽

Spontaneous Electrical Activity ◽

Gnrh Neurons

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Nerve growth factor (NGF) prevents the shift in ocular dominance distribution of visual cortical neurons in monocularly deprived rats

Journal of Neuroscience ◽

10.1523/jneurosci.12-12-04651.1992 ◽

1992 ◽

Vol 12 (12) ◽

pp. 4651-4662 ◽

Cited By ~ 172

Author(s):

L Maffei ◽

N Berardi ◽

L Domenici ◽

V Parisi ◽

T Pizzorusso

Keyword(s):

Nerve Growth Factor ◽

Growth Factor ◽

Cortical Neurons ◽

Ocular Dominance ◽

Nerve Growth ◽

Visual Cortical

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Basal Forebrain Cholinergic System Is Involved in Rapid Nerve Growth Factor (NGF)-Induced Plasticity in the Barrel Cortex of Adult Rats

Journal of Neurophysiology ◽

10.1152/jn.00489.2003 ◽

2004 ◽

Vol 91 (1) ◽

pp. 424-437 ◽

Cited By ~ 17

Author(s):

Neal Prakash ◽

Susana Cohen-Cory ◽

Silke Penschuck ◽

Ron D. Frostig

Keyword(s):

Nerve Growth Factor ◽

Growth Factor ◽

Basal Forebrain ◽

Cholinergic System ◽

Barrel Cortex ◽

Cortical Plasticity ◽

Nerve Growth ◽

Adult Rat ◽

Cortical Projections ◽

Imaging Results

We have previously reported that topical application of nerve growth factor (NGF) to the barrel cortex of an adult rat rapidly augmented a whisker functional representation (WFR) by increasing its area and height within minutes after NGF application. In addition, we found that TrkA, the high-affinity NGF receptor, was only found on fibers projecting into the barrel cortex. Here we use a combination of techniques including chronic intrinsic signal optical imaging, neuronal fiber tracking and immunohistological techniques, to test the hypothesis that NGF-induced rapid cortical plasticity is mediated by the cortical projections of the basal forebrain cholinergic system (BFCS). Our studies localize the source of the cells in the BFCS that project to a single WFR and also demonstrate that TrkA-immunoreactive fibers in the cortex are also cholinergic and likely arise from the BFCS. In addition, by selectively lesioning the BFCS cortical fibers with the immunotoxin 192 IgG-saporin, we show that NGF-induced WFR-cortical plasticity is eliminated. These results, taken together with our previously reported imaging results that demonstrated that agonists of the cholinergic system (particularly nicotine) showed transient NGF-like augmentations of a WFR, implicate the BFCS cortical projections as necessary for NGF's rapid plasticity in the adult rat somatosensory cortex.

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