The GABAergic neurotransmission is a highly conserved system that has been attributed to various regulatory events. There has been a notable number of studies on the importance of GABAergic neurotrans

/pdf/epigenetic-regulations-of-gabaergic-neurotransmission-5aszwmn24m.pdf

Epigenetic Regulations of GABAergic Neurotransmission: Relevance for Neurological Disorders and Epigenetic Therapy

Background/Aims: Anxious responses are evolutionarily adaptive, but excessive fear can become disabling and lead to anxiety disorders. Translational models of anxiety might be useful sources for understanding the neurobiology of fear and anxiety and can contribute to future proposals of therapeutic intervention for the disorders studied. Brain-derived neurotrophic factor (BDNF), which is known for its importance on neuroplasticity and contextual memory, has emerged as a relevant element for emotional memory. Recent studies show that the Val 66 Met BDNF polymorphism

/pdf/translational-findings-on-brain-derived-neurotrophic-factor-3mrvoaflnv.pdf

Translational Findings on Brain-Derived Neurotrophic Factor and Anxiety: Contributions from Basic Research to Clinical Practice

Trk receptors are a family of three receptor tyrosine kinases, each of which can be activated by one or more of four neurotrophins-nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophins 3 and 4 (NT3 and NT4). Neurotrophin signaling through these receptors regulates cell survival, proliferation, the fate of neural precursors, axon and dendrite growth and patterning, and the expression and activity of functionally important proteins, such as ion channels and neurotransmitter receptors. In the adult nervous system, the Trk receptors regulate synaptic strength and plasticity. The cytoplasmic domains of Trk receptors contain several sites of tyrosine phosphorylation that recruit intermediates in intracellular signaling cascades. As a result, Trk receptor signaling activates several small G proteins, including Ras, Rap-1, and the Cdc-42-Rac-Rho family, as well as pathways regulated by MAP kinase, PI 3-kinase and phospholipase-C-gamma (PLC-gamma). Trk receptor activation has different consequences in different cells, and the specificity of downstream Trk receptor-mediated signaling is controlled through expression of intermediates in these signaling pathways and membrane trafficking that regulates localization of different signaling constituents. Perhaps the most fascinating aspect of Trk receptor-mediated signaling is its interplay with signaling promoted by the pan-neurotrophin receptor p75NTR. p75NTR activates a distinct set of signaling pathways within cells that are in some instances synergistic and in other instances antagonistic to those activated by Trk receptors. Several of these are proapoptotic but are suppressed by Trk receptor-initiated signaling. p75NTR also influences the conformations of Trk receptors; this modifies ligand-binding specificity and affinity with important developmental consequences.

Trk receptors: roles in neuronal signal transduction.

The neurotrophins are a family of proteins that are essential for the development of the vertebrate nervous system. Each neurotrophin can signal through two different types of cell surface receptor — the Trk receptor tyrosine kinases and the p75 neurotrophin receptor. Given the wide range of activities that are now associated with neurotrophins, it is probable that additional regulatory events and signalling systems are involved. Here, I review recent findings that neurotrophins, in addition to promoting survival and differentiation, exert various effects through surprising interactions with other receptors and ion channels.

/pdf/neurotrophins-and-their-receptors-a-convergence-point-for-3hfqpg5jyn.pdf

Neurotrophins and their receptors: a convergence point for many signalling pathways.

The corticosteroid receptor hypothesis of depression.

Neurotrophins are a family of structurally related proteins that regulate the survival, differentiation and maintenance of function of different populations of peripheral and central neurons. They are also essential for modulating activity-dependent neuronal plasticity. Here we show that neurotrophins elicit action potentials in central neurons. Even at low concentrations, brain-derived neurotrophic factor (BDNF) excited neurons in the hippocampus, cortex and cerebellum. We found that BDNF and neurotrophin-4/5 depolarized neurons just as rapidly as the neurotransmitter glutamate, even at a more than thousand-fold lower concentration. Neurotrophin-3 produced much smaller responses, and nerve growth factor was ineffective. The neurotrophin-induced depolarization resulted from the activation of a sodium ion conductance which was reversibly blocked by K-252a, a protein kinase blocker which prefers tyrosine kinase Trk receptors. Our results demonstrate a very rapid excitatory action of neurotrophins, placing them among the most potent endogenous neuro-excitants in the mammalian central nervous system described so far.

Neurotrophin-evoked rapid excitation through TrkB receptors

Brain-derived neurotrophic factor (BDNF) and other neurotrophins are critically involved in long-term potentiation (LTP). Previous reports point to a presynaptic site of neurotrophin action. By imaging dentate granule cells in mouse hippocampal slices, we identified BDNF-evoked Ca2+ transients in dendrites and spines, but not at presynaptic sites. Pairing a weak burst of synaptic stimulation with a brief dendritic BDNF application caused an immediate and robust induction of LTP. LTP induction required activation of postsynaptic Ca2+ channels andN-methyl-d-aspartate receptors and was prevented by the blockage of postsynaptic Ca2+ transients. Thus, our results suggest that BDNF-mediated LTP is induced postsynaptically. Our finding that dendritic spines are the exclusive synaptic sites for rapid BDNF-evoked Ca2+ signaling supports this conclusion.

https://science.sciencemag.org/content/sci/295/5560/1729.full.pdf

Postsynaptic Induction of BDNF-Mediated Long-Term Potentiation

Neurotrophine sind Proteine, die, ähnlich wie Nervenwachstumsfaktoren, die Entwicklung, das Überleben und Funktionieren von Neuronen gewährleisten bzw. fördern (Barde 1989). Dafür binden die Neurotrophine an Rezeptoren in der neuronalen Membran, die zu der Familie der Tyrosin-Rezeptor-Kinasen (Trk) gehören. Christine Rose und weitere Mitglieder der Arbeitsgruppe von Arthur Konnerth vom Physiologischen Institut der LM Universität München haben in ihrem Artikel jetzt eine neue Rolle dieser Proteine beschrieben, und zwar bei dem Dialog wenig von dem vollständigen TrkB-Rezeptor exprimieren, dafür aber um so mehr von dem verkürzten Rezeptor TrkB-T1. BDNF löst in Gliazellen über diesen verkürzten Rezeptor eine Signalkaskade aus, die nicht eine Tyrosinkinase aktiviert (die fehlt ja eben bei diesen Rezeptoren), sondern, wie viele Liganden metabotroper Rezeptoren, an ein G-Protein gekoppelt ist. So konnte erstmals gezeigt werden, dass auch die unvollständigen TrkB-T1-Rezeptoren funktionelle Rezeptoren darstellen, die, zumindest in Gliazellen, eine Signalkaskade in Gang setzen.

Truncated TrkB-T1 mediates neurotrophin-evoked calcium signalling in glia cells

http://cbr.meduniwien.ac.at/fileadmin/db_files/pub_art_195.pdf

Developmental profile and properties of sulforhodamine 101-Labeled glial cells in acute brain slices of rat hippocampus

Neurotrophins (NTs) are [?AUTHOR] a family of structurally related, secreted proteins that regulate the survival, differentiation and maintenance of function of different populations of peripheral and central neurons.1,2 Among these, BDNF (brain-derived neurotrophic factor) has drawn considerable interest because both its synthesis and secretion are increased by physiological levels of activity, indicating a unique role of this neurotrophin in coupling neuronal activity to structural and functional properties of neuronal circuits. In addition to its classical neurotrophic effects, which are evident within hours or days and which usually result from changes in cellular gene expression, BDNF exerts acute effects on synaptic transmission and is involved in the induction of long-term potentiation. Many of these rapid effects of BDNF are mediated by its modulation of ion channel properties following TrkB-mediated activation of intracellular second messenger cascades and protein phosphorylation. However, recent reports have shown that BDNF not only acts as a modulator of ion channels, but can also directly and rapidly gate a Na(+) channel, thereby assigning BDNF the properties of a classical excitatory transmitter. Thus, BDNF, in addition its role as a potent neuromodulator, emerges as an excitatory transmitter-like substance which acutely controls resting membrane potential, neuronal excitability, synaptic transmission and participates in the induction of synaptic plasticity.

From modulator to mediator: rapid effects of BDNF on ion channels

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