RTK class VII

Trk receptors are a family of tyrosine kinases that regulate the intensity and synaptic plasticity in the nervous system of a mammal. TRK receptor affects the survival and differentiation of neurons in the cascade several signals. However, activation of these receptors, a major impact on the functional properties of neurons. Ligand receptor common is a growth factor family is important TRK neurotrophin, the function of the nervous system. Binding of these molecules are very specific. Each type, I have an affinity neurotrophin different related to the Trk receptor of that. May lead to activation of the signaling cascade leading to promotion of functional regulation in other cell survival and activation of Trk receptors by neurotrophin binding.

TRK abbreviation, which means tropomyosin receptor kinase (pronounced case, “clue” of many). Trk receptor family is named after the carcinogenesis TRK, that led to the discovery members, of some of the TrkA identifical first. TRK identified in colon cancer first activated (25%) papillary thyroid cancer often. After chromosome 1 was through, oncogenes can be generated by mutations in the result of the merge of exon seven first tropomyosin the cytoplasmic domain of the receptor TrkA unknown. TRK receptors, does not contain a DNA sequence associated with tropomyosin normal or amino acid.

It is of TrkA TrkC there are three types of most common TRK receptor, and the TrkB. Each of these types of receptors, has a binding affinity for different neurotrophic factor specific. The difference of the signals derived from the different types of receptors These are important for the generation of biological various reactions. After processing the ligands meaning that they are synthesized in the immature form, neurotrophin ligands Trk receptors are converted by protease cleavage. Immature neurotrophins, is specific for the receptor p75NTR common. However, protease cleavage site generates neurotrophin having a high affinity receptors, respectively, of Trk. To bind to p75NTR still neurotrophin that has been treated of these, affinity much lower can.

The neurotrophin to be the effect of the proliferation and differentiation of their precursors or on nerve cells in the CNS neuroepithelial progenitor channels intestinal nervous system has been shown in many studies both in vitro and in vivo. Not only increase the survival of nociceptors neurons delta Class B, and as already mentioned, BDNF is functional properties neurons.4 these central nervous system, enhance the survival and function of cholinergic neurons, particularly not only affects the, and TrkA expression in the NGF, brain basal ganglia neurons, neurons in the cortex and hippocampus before.
BDNF neurotrophin, belongs to a family of growth factors that affect the survival and function of neurons in the central nervous system, particularly in brain regions susceptible to degeneration AD. As well as the nerve cells in the brain basal cholinergic before, BDNF, improve the survival rate of neurons in the cerebral cortex and hippocampus.
The expression of the TrkC NT3, that nerve cell culture channel, oligodendrocyte precursors, and to promote the growth and survival of hippocampal neurons differentiation of the precursor is shown.

In the development of the visual system of mammals, passes through lateral nucleus of the knee (LGN), axons from each eye, ending with a layer of separate striatal cortex. However, can be operated on one side of the eyes, but not both, axons each LGN are together. These axons that end in the layer IV of striate cortex result of ocular dominance columns. In one study, we show that it is possible density of control axons to exogenous BDNF increased IV layer from the LGN, since decreases with BDNF.Therefore endogenous pliers, may be involved in the sorting mechanism of these substances Rays that are not fully understood, yet. Previous studies with this cat model, the input of one of the mammalian eye shows that the absence when one eye deficiency occurs during the critical period (critical window). However, in one study, injection of NT-4 in the visual cortex, showed that preventing the influence of the lack of many eye showed during critical time. Surprisingly, it can recover the loss of response after the critical period of the injection of even-NT-4 is shown.

In the hippocampus of mammals, the axons to CA1 cells through the CA3 pyramidal cells project Shaffer side branch. Induction of long-term potentiation and (LTP), one of these pathways may be specific to those stimulated with tetanus. It does not affect the outflow beyond the time of axons [unknown] stimulus. Receptor TrkB was expressed in most of the hippocampal neurons, including inhibitory interneurons and CA1 pyramidal cell dentate gyrus granule cells, and in Ca3. Interestingly, it is possible to reduce the mutant BDNF significantly LTP. In similar studies of mutant mice decreased expression of the receptor TrkB, LTP in the CA1 cells was significantly decreased. That the loss of TrkB also interfere with memory acquisition and integration of life paradigm many are linked.

In the development of the visual system of mammals, passes through lateral nucleus of the knee (LGN), axons from each eye, ending with a layer of separate striatal cortex. However, can be operated on one side of the eyes, but not both, axons each LGN are together. These axons that end in the layer IV of striate cortex result of ocular dominance columns. In one study, it indicates that it is possible that the density of control axons to exogenous BDNF increase in layer IV from LGN, decreases with pliers endogenous BDNF. Thus, these agents could have been incorporated into some mechanism not fully understood yet increases. Previous studies with this cat model, the input of one of the mammalian eye shows that the absence when one eye deficiency occurs during the critical period (critical window). However, in one study, infusion of (Ligand TrkB) showed that preventing the influence of the lack of eye many showed NT-4 in the visual cortex during critical time. Surprisingly, it can recover the loss of response after the critical period of the injection of even-NT-4 is shown.

To affect the functional properties of neurons and (neurotrophic factor) and its ligands TRK receptor. [8] large single synapse excitement. Rise NT-3/trkC is important for the development and regulation of synapse that is formed between the motor neuron and afferent neurons as BDNF and NT-3 to connect the lead ” On the other hand. [8] to decrease polysynaptic component and (EPSPS) postsynaptic potential, binding of NT-3 increased to TrkB, the size of the monosynaptic excitatory postsynaptic potential [unknown] BDNF is a (EPSPS) to increase the multi-synaptic transmission If you have the opposite effect of decreasing.

Each of the neurotrophin to promote neurite outgrowth of above. Even if the signaling of NGF / TrkA is before sympathetic regulation of nerve growth cone, nerve cells have the support of (and maintenance feeding) adequate nutrition, experiment, not in the department it was related to the Zu NGF I showed that. To increase the innervation of the organization to receive the sense and sympathetic innervation, NGF causes abnormal innervation to the organization that has not been ruled correctly. Some TrkA signal-regulated BDNF is transported to the central terminals of peripheral and NGF / nocireceptive sensory nerves,. In the peripheral part and need, strongly TrkB/NT-4 sensitivity nocireceptive path combined with / BDNF binding to TrkB the presence of mast cells.

The neurotrophins, nerve cells that is the effect on proliferation and differentiation of CNS precursors on epithelial precursors thereof enteric nervous system or channel has been shown in many studies both in vitro and in vivo. Not only increase the survival of nociceptors neurons delta Class B, and as already mentioned, BDNF is functional properties neurons.4 these central nervous system, enhance the survival and function of cholinergic neurons, particularly not only affects the, and TrkA expression in the NGF, brain basal ganglia neurons, neurons in the cortex and hippocampus before.
BDNF neurotrophin, belongs to a family of growth factors that affect the survival and function of neurons in the central nervous system, particularly in brain regions susceptible to degeneration AD. As well as the nerve cells in the brain basal cholinergic before, BDNF, improve the survival rate of neurons in the cerebral cortex and hippocampus. The expression of the TrkC NT3, that nerve cell culture channel, oligodendrocyte precursors, and to promote the growth and survival of hippocampal neurons differentiation of the precursor is shown.