TRKB

TrkB Receptor ligands promote activity-dependent inhibitory synaptogenesis.

Caffeine prevents age-associated recognition memory decline and changes brain-derived neurotrophic factor and tirosine kinase receptor (TrkB) content in mice.

BDNF stimulates TrkB receptors of lamina I secondary sensory neurons in dorsal horn to cause down-regulation of the potassium-chloride transporter KCC2, resulting in an increase in intracellular [[Cl.sup.-]] and a depolarizing shift in the anion reversal potential ([E.sub.anion]).

Pb also inhibits the vesicular release of BDNF (brain-derived neurotrophic factor) and subsequent TrkB (tropomyosinrelated kinase B) activation in the presynaptic neuron (Neal et al.

BDNF is the most widely distributed neurotrophin in the CNS and plays a central role in the regulation of neuronal survival mainly by activating through the neurotrophic tyrosine kinase receptor B (TrkB).

[5] FDP decreases, the expression of brain-derived neurotrophic factor (BDNF) and its receptor tropomyosin-related kinase (TrkB) which are found to be essential for seizure activity.

Leung et al., "Cerebrovascular degradation of TRKB by MMP9 in the diabetic brain," The Journal of Clinical Investigation, vol.

In a rat model of experimental glaucoma, artificial elevation of IOP cripples the optic nerve head at the level of the lamina cribrosa, swelling nerve fibers and blocking the axonal flow of BDNF, while expression of the cognate receptor TrkB is increased at the optic nerve head [42].