Messenger RNAs for trk and the low-affinity NGF receptor in rat basal forebrain

Vazquez, Marcelo E.; Ebendal, Ted

doi:10.1097/00001756-199110000-00010

Cited by 97 publications

(34 citation statements)

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“…These results are in agreement with the observation that the CBF neurons constitute the major population of cells expressing receptors for NGF (Vazquez and Ebendal, 1991;Urschel and Hulsebosch, 1992;Holtzman et al, 1995;). Further evidence that these neurons are able to respond to exogenously added NGF has come from studies of fimbria fornix transection in rats and from nonlesioned, aged animals (Hefti, 1986;Ogawa et al, 1993;Fisher, 1994;Lindsay et al, 1994).…”

Section: Discussionsupporting

confidence: 92%

“…The role of NGF as a target-derived neurotrophic agent for certain cell populations in the peripheral nervous system has been well documented (Levi-Montalccini, 1987). This trophic concept has been extended to the CNS, and recent evidence suggests that NGF may be essential for supporting the cholinergic neurons of the basal forebrain (Araujo et al, 1990;Vazquez and Ebendal, 1991). The CBF neurons have also been demonstrated to be the major population of cells in the CNS expressing receptors for NGF (Vazquez and Ebendal, 1991;Urschel and Hulsebosch, 1992;Holtzman et al, 1995;).…”

Section: Abstract: Inhibitory Avoidance; Conditioned Taste Aversion;mentioning

confidence: 99%

“…This trophic concept has been extended to the CNS, and recent evidence suggests that NGF may be essential for supporting the cholinergic neurons of the basal forebrain (Araujo et al, 1990;Vazquez and Ebendal, 1991). The CBF neurons have also been demonstrated to be the major population of cells in the CNS expressing receptors for NGF (Vazquez and Ebendal, 1991;Urschel and Hulsebosch, 1992;Holtzman et al, 1995;). However, no direct evidence has shown an active, physiological dependency of the brain cholinergic neurons on a target-derived trophic factor (Mannes et al, 1994).…”

Section: Abstract: Inhibitory Avoidance; Conditioned Taste Aversion;mentioning

confidence: 99%

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Learning Impairment and Cholinergic Deafferentation after Cortical Nerve Growth Factor Deprivation

1997

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Cholinergic basal forebrain (CBF ) neurons have been shown to respond in vivo to exogenous administration of NGF. Although neurotrophins and their receptors are widely expressed in the CNS, little data exist for the physiological significance of endogenous neurotrophin signaling in CNS neurons. To test directly whether cortically derived NGF is functionally required for the cholinergic functions mediated by the cerebral cortex, repeated injections of anti-NGF mAbs were locally applied into the insular cortex (IC) of rats. The biochemical results, using an in vivo microdialysis technique, showed a dramatic lack of extracellular release of acetylcholine after high potassium stimulation compared with controls. Furthermore, by using small injections of the neurotracer fluorogold, we found a corresponding disruption in the connectivity between the IC and the CBF. Behavioral experiments showed that the NGF antibodies applied into the IC produced a significant disruption on the acquisition of conditioned taste aversion and inhibitory avoidance learning. However, the same animals were able to recall the taste aversion when the conditioning trial was established before injections of NGF antibodies. Given these results, it seems that cortical cholinergic functions are actively dependent on locally derived NGF in the adult normal brain, and that the cholinergic activity from the CBF is not necessary for recalling aversive stimuli, but is necessary for the acquisition of aversively motivated conditionings.

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Section: Discussionsupporting

confidence: 92%

Section: Abstract: Inhibitory Avoidance; Conditioned Taste Aversion;mentioning

confidence: 99%

Section: Abstract: Inhibitory Avoidance; Conditioned Taste Aversion;mentioning

confidence: 99%

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Learning Impairment and Cholinergic Deafferentation after Cortical Nerve Growth Factor Deprivation

1997

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“…NGF, when injected in relatively large quantities directly into the visual cortex, has recently been reported to interfere with formation of the ocular dominance columns in the cat primary visual cortex (37). The physiological role of NGF in the formation of ocular dominance columns is, however, complicated by the fact that the expression of trk, the signal-transducing receptor unit for NGF (38, 39), has not been reported to be expressed by cortical neurons but seems to be confined to the septum (40). Our data indicate that, at least in rats, the expression of NGF in the visual cortex is quite low and it seems to be independent of visual input.…”

Section: Resultsmentioning

confidence: 99%

“…There is evidence to suggest that high concentrations of NGF may act as an agonist at the functional BDNF high-affinity receptor (41). As the BDNF receptor trkB is widespread in neocortex (40,42), and BDNF mRNA is regulated by visual input both during development and in adulthood, it seems reasonable to suggest that BDNF, rather than NGF, would be the neurotrophin that plays a role in formation of the ocular dominance columns.…”

Section: Resultsmentioning

confidence: 99%

Light regulates expression of brain-derived neurotrophic factor mRNA in rat visual cortex.

Ċastrén¹,

Zafra²,

Thoenen³

et al. 1992

Proc. Natl. Acad. Sci. U.S.A.

458

260

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Specific sensory input has profound transient and long-lasting effects on the function of corresponding sensory cortical areas both during development and in adulthood. To study whether neurotrophic factors might play a role in such processes, we investigated the effects of light on the nerve growth factor and brain-derived neurotrophic factor (BDNF) mRNA levels in rat visual cortex. Keeping adult rats in the dark or preventing normal activity of retinal ganglion cells by intraocular injection of tetrodotoxin significantly decreased the levels of BDNF mRNA in the visual cortex but not in other cortical areas. Exposure to light after a period in darkness rapidly restored the mRNA to control levels. These alterations in visual input had no effect on nerve growth factor mRNA. The mRNA of trkB, the putative signal-transducing receptor unit for BDNF, was also decreased in darkness, although less than BDNF mRNA. BDNF mRNA levels increased in the visual cortex of newborn rats after eye-opening. This increase is retarded, although not completely abolished, by rearing the pups in darkness. Thus, the levels of BDNF mRNA are rapidly regulated by sensory input during development and in adulthood. BDNF may therefore play an important role in formation and in activity-dependent modulation of specific connections in the visual cortex.Visual input has profound influences on neuronal connectivity in the visual cortex. During a critical period of development, receptive fields in the visual cortex are determined in a use-dependent competition between the two eyes (1, 2). Although the neuronal connections in adult visual cortex were previously thought to be fairly stable, recent experiments indicate that alterations in sensory input have rapid and marked effects on functional and structural connectivity in the adult sensory cortex (3, 4). The activation of N-methyl-D-aspartate (NMDA)-type glutamate receptors is thought to play an essential role in these use-dependent changes (5). However, the mechanisms through which NMDA receptor activation leads to alterations in the neuronal connectivity are poorly understood.Nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF), two members of the neurotrophin gene family, are predominantly synthesized by neurons in the central nervous system (6-17). Neuronal activity has been shown to regulate the mRNAs for NGF and BDNF in the hippocampus (18)(19)(20). The basal expression of these two neurotrophins in hippocampal neurons seems to be predominantly determined by the balance between glutamatergic and GABAergic transmitter systems (19). The rapid and subtle activity-dependent regulation of synthesis of these two neurotrophins suggests that, in addition to supporting the survival and regulation of specific neuronal properties, these neurotrophins may also act as mediators of functional and structural changes in neuronal connectivity. We have investigated here whether changes in visual input regulate the expression of NGF and BDNF mRNA in the visual cortex during developmen...

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TRK and p75 neurotrophin receptor systems in the developing human brain

1996

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The prenatal development of the neurons immunoreactive for high-affinity tropomycin-related kinase (trk) receptor (pan trk which recognizes trkA, trkB, and trkC) and low-affinity p75 neurotrophin receptor (p75NTR) was examined in the human brain from embryonic weeks 10 to 34 of gestation. In the embryonic week 10 specimen in which only brainstem regions were available for evaluation, trk immunoreactivity (trk-ir) was observed in the ventral cochlear, solitary, raphe, spinal trigeminal, and hypoglossal nuclei, as well as the vestibular complex and medullary reticular formation. At this time point of gestation, p75ntr-immunoreactive (p75NTR-ir) staining was observed within these same regions plus the inferior olivary and ambiguus nuclei. At embryonic week 14, trk-ir neurons were seen within the subplate zone of the entorhinal cortex, basal forebrain, caudate nucleus, putamen, external segment of the globus pallidus, specific thalamic nuclei, lateral mammillary nucleus, habenula nucleus, select brainstem nuclei, and the dentate nucleus of cerebellum. At this gestational time point, p75NTR-ir neurons were observed in each of these structures, with the exception of the caudate nucleus, specific thalamic nuclei, lateral mammillary nucleus, and habenula nucleus. Additionally, p75NTR-ir neurons were observed within the corpus callosum. The staining pattern for both trk and p75NTR remained unchanged at embryonic weeks 15 to 16 except for the addition of trk-ir and p75NTR-ir within the cortical subplate zone, hippocampus, and subthalamic nucleus. By embryonic week 18, trk-ir neurons were widely expressed within mostly all thalamic nuclei. In contrast, trk-ir was no longer seen within the hypoglossal, cuneate, and gracile nuclei at this time point. This staining pattern for trk and p75NTR remained virtually unchanged from embryonic weeks 19 to 20 and embryonic weeks 16 to 20, respectively. From embryonic weeks 22 to 34, the distribution of both trk-ir and p75NTR-ir neurons changed gradually. During this period, neurons in most thalamic and some brainstem nuclei became progressively immunonegative for trk, whereas neurons in the neocortical subplate zone, corpus callosum, and hilar region of dentate gyrus gradually lost immunoreactivity for p75NTR. These data demonstrate an important and complex role for both the high-(trk) and low- (p75) affinity neurotrophin receptors during the development of multiple neuronal systems in the human brain.

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Messenger RNAs for trk and the low-affinity NGF receptor in rat basal forebrain

Cited by 97 publications

References 0 publications

Learning Impairment and Cholinergic Deafferentation after Cortical Nerve Growth Factor Deprivation

Learning Impairment and Cholinergic Deafferentation after Cortical Nerve Growth Factor Deprivation

Light regulates expression of brain-derived neurotrophic factor mRNA in rat visual cortex.

TRK and p75 neurotrophin receptor systems in the developing human brain

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