Neuronal colocalization of mRNAs for neurotrophins and their receptors in the developing central nervous system suggests a potential for autocrine interactions.

Miranda, Rajesh C.; Sohrabji, Farida; Toran-Allerand, C. Dominique

doi:10.1073/pnas.90.14.6439

Cited by 230 publications

(157 citation statements)

References 43 publications

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“…Additionally, both BDNF and its TrkB receptor are often coexpressed in the same neuron (Kokaia et al 1993;Miranda et al 1993). These findings support the notion that BDNF exerts its actions by activating TrkB receptors, which trigger signal transduction pathways in both preand postsynaptic compartments, acting in both autocrine and paracrine fashions.…”

Section: Bdnf and Memory Consolidationsupporting

confidence: 76%

From Acquisition to Consolidation: On the Role of Brain-Derived Neurotrophic Factor Signaling in Hippocampal-Dependent Learning

Tyler¹,

Alonso²,

Bramham³

et al. 2002

Learn. Mem.

627

398

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One of the most rigorously investigated problems in modern neuroscience is to decipher the mechanisms by which experience-induced changes in the central nervous system are translated into behavioral acquisition, consolidation, retention, and subsequent recall of information. Brain-derived neurotrophic factor (BDNF) has recently emerged as one of the most potent molecular mediators of not only central synaptic plasticity, but also behavioral interactions between an organism and its environment. Recent experimental evidence indicates that BDNF modulates synaptic transmission and plasticity by acting across different spatial and temporal domains. BDNF signaling evokes both short-and long-term periods of enhanced synaptic physiology in both pre-and postsynaptic compartments of central synapses. Specifically, BDNF/TrkB signaling converges on the MAP kinase pathway to enhance excitatory synaptic transmission in vivo, as well as hippocampal-dependent learning in behaving animals. Emerging concepts of the intracellular signaling cascades involved in synaptic plasticity induced through environmental interactions resulting in behavioral learning further support the contention that BDNF/TrkB signaling plays a fundamental role in mediating enduring changes in central synaptic structure and function. Here we review recent literature showing the involvement of BDNF/TrkB signaling in hippocampal-dependent learning paradigms, as well as in the types of cellular plasticity proposed to underlie learning and memory.

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Section: Bdnf and Memory Consolidationsupporting

confidence: 76%

From Acquisition to Consolidation: On the Role of Brain-Derived Neurotrophic Factor Signaling in Hippocampal-Dependent Learning

Tyler¹,

Alonso²,

Bramham³

et al. 2002

Learn. Mem.

627

398

View full text Add to dashboard Cite

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“…Acheson et al, 1995). Previous authors have reported transcripts for neurotrophins and Trk receptors in patterns that seem to indicate auto/paracrine or anterograde neurotrophin signaling (Schecterson and Bothwell, 1992;Miranda et al, 1993). However, limited information is available on the mechanisms of action of neurotrophins in the CNS in vivo.…”

Section: Discussionmentioning

confidence: 99%

Neurotrophins Suppress Apoptosis Induced by Deafferentation of an Avian Motor-Cortical Region

et al. 1997

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Studies of the developing nervous system led to the general view that growth factors promote neuronal survival in a "retrograde" manner. For example, release of NGF from postsynaptic peripheral targets followed by uptake and retrograde transport by presynaptic neurons provided a widely accepted conceptual framework for the action of neurotrophins. In contrast, although presynaptic or "anterograde" influences on the survival of developing neurons have been recognized for some time, the mechanisms by which afferent input regulates the survival of postsynaptic cells have received considerably less attention. In the forebrain network for learned vocal behavior in zebra finches, lesions of a cortical region for song control, the lateral magnocellular nucleus of the anterior neostriatum (lMAN), remove presynaptic input to a motor-cortical song region, the robust nucleus of the archistriatum (RA), and cause massive RA neuron death in young birds that are entering the sensitive period for song learning. Here we report that lesions of lMAN followed by infusions of neurotrophins directly into RA completely suppress neuronal apoptosis in RA. Moreover, we show that lMAN neurons are able to transport neurotrophins in the anterograde direction to RA, that neurotrophin-like immunoreactivity is present in cells in lMAN and RA, and that neurotrophin receptor-like immunoreactivity is present in RA. Expression of neurotrophins in lMAN and RA suggests that lMAN presynaptic input could regulate RA neuron survival by synthesizing, transporting, and releasing neurotrophins anterogradely or by regulating the auto/paracrine release of neurotrophins within RA, or perhaps by both. These data provide the first in vivo demonstration that neurotrophins can prevent the death of deafferented cortical neurons, and they raise the possibility that nonretrograde signaling by neurotrophins may be a common means of promoting neuronal survival in the vertebrate telencephalon. Anterograde and auto/ paracrine neurotrophin signaling, along with the more established view that neurotrophins regulate neuron survival via retrograde mechanisms, suggests multidirectional neurotrophin signaling in the vertebrate telencephalon.

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“…Infusion of NGF into neonatal rat pups increases ChAT activity within the striatum (Mobley et al, 1985). Striatal neurons during development express the low-affinity NGF receptor in rodents (Yan and Johnson, 1988;Lu et al, 1989) and humans (Kordower and Mufson, 1993), and striatal neurons express the high-affinity trkA receptor during rodent development (Miranda et al, 1993;Ringstedt et al, 1993) and in adulthood (Steininger et al, 1993). In the case of the striatum, it is likely that NGF acts within the striatum through interactions with the trkA receptor.…”

Section: Discussionmentioning

confidence: 99%

TrkA‐immunoreactive profiles in the central nervous system: Colocalization with neurons containing p75 nerve growth factor receptor, choline acetyltransferase, and serotonin

Sobreviela

Clary

Reichardt

et al. 1994

J of Comparative Neurology

308

197

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The present investigation used an antibody directed against the extracellular domain of the signal transducing nerve growth factor receptor, trkA, to reveal immunoreactive perikarya or fibers within the olfactory bulb and tubercle, cingulate cortex, nucleus accumbens, striatum, endopiriform nucleus, septal/diagonal band complex, nucleus basalis, hippocampal complex, thalamic paraventricular and reunions nuclei, periventricular hypothalamus, interpeduncular nucleus, mesencephalic nucleus of the fifth nerve, dorsal nucleus of the lateral lemniscus, prepositus hypoglossal nucleus, ventral cochlear nucleus, ventral lateral tegmentum, medial vestibular nucleus, spinal trigeminal nucleus oralis, nucleus of the solitary tract, raphe nuclei, and spinal cord. Colocalization experiments revealed that virtually all striatal trkA-immunoreactive neurons (> 99%) coexpressed choline acetyltransferase (ChAT) but not p75 nerve growth factor receptor (NGFR). Within the septal/diagonal band complex virtually all trkA neurons (>95%) coexpressed both ChAT and p75 NGFR. More caudally, dual stained sections revealed numerous trkA/ChAT (> 80%) and trkA/p75 NGFR (> 95%) immunoreactive neurons within the nucleus basalis. In the brainstem, raphe serotonergic neurons (45%) coexpressed trkA. Sections stained with a pan-trk antibody that recognizes primarily trkA, as well as trkB and trkC, labeled neurons within all of these regions as well as within the hypothalamic arcuate, supramammilary, and supraoptic nuclei, hippocampus, inferior and superior colliculus, substantia nigra, ventral tegmental area of T'sai, and cerebellar Purkinje cells. Virtually all of these other regions with the exception of the cerebellum also expressed pan-trk immunoreactivity in the monkey. The widespread expression of trkA throughout the central neural axis suggests that this receptor may play a role in signal transduction mechanisms linked to NGF-related substances in cholinergic basal forebrain and non-cholinergic systems. These findings suggest that pharmacological use of ligands for trkA could have beneficial effects on the multiple neuronal systems that are affected in such disorders as Alzheimer's disease. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptThe classic research of Levi-Montalcini and coworkers (for review, see Levi-Montalcini and Angeletti 1968;Thoenen and Barde, 1980) first demonstrated that nerve growth factor (NGF) was an important trophic substance for the development and maintenance of noradrenergic peripheral sympathetic neurons. A potential role for NFG within the central nervous system (CNS) was first identified in the adult rat brain following injection of radiolabeled NGF into the cortex and hippocampus. These investigations did not reveal retrogradely labeled perikarya within the noradrenergic locus coeruleus as expected, but instead exclusively labeled neurons within the septal/diagonal band complex and the nucleus basalis magnocellularis (Schwab et al., 1979; Seiler and Schwab, 1984). These transpor...

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Neuronal colocalization of mRNAs for neurotrophins and their receptors in the developing central nervous system suggests a potential for autocrine interactions.

Cited by 230 publications

References 43 publications

From Acquisition to Consolidation: On the Role of Brain-Derived Neurotrophic Factor Signaling in Hippocampal-Dependent Learning

From Acquisition to Consolidation: On the Role of Brain-Derived Neurotrophic Factor Signaling in Hippocampal-Dependent Learning

Neurotrophins Suppress Apoptosis Induced by Deafferentation of an Avian Motor-Cortical Region

TrkA‐immunoreactive profiles in the central nervous system: Colocalization with neurons containing p75 nerve growth factor receptor, choline acetyltransferase, and serotonin

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