Segregation and stabilization of thalamocortical afferents to eye-specific patches, so-called "ocular dominance (OD) columns," in visual cortex are hypothesized to be based on activity-dependent competition for trophic factors such as brain-derived neurotrophic factor (BDNF) between afferents representing the two eyes during the critical period of postnatal development. To test this hypothesis we observed effects of an intracortical infusion of BDNF on OD columns in monocularly deprived kittens and also compared effects between normal kittens and adult cats. BDNF had a hypertrophic action on afferents irrespective of visual inputs so that it desegregated OD columns in the visual cortex of deprived and normal kittens, but this action was not seen in the adults, substantiating its hypothesized trophic role in plasticity of OD columns in the developing visual cortex.
Brain-derived neurotrophic factor (BDNF) rapidly enhances excitatory synaptic transmission in cortical slices. To date, however, a question of how long such an action persists remains unanswered as it is hard to record synaptic responses longer than several hours in slice preparations. To address this question and to investigate possible age-dependency of the action, we analysed effects of a brief application of BDNF and nerve growth factor (NGF) on field potentials of visual cortex in rats of postnatal days 13-17 and 19-24 and in the adulthood for 10-24 h. Evoked potentials to stimulation of the lateral geniculate nucleus were recorded simultaneously from two cortical sites into which the neurotrophin and control solution were injected. An application of BDNF induced a slowly developing increase in the field potential amplitude in young rats. The amplitude attained a plateau level 3-4 h after the infusion; 139 +/- 26% (mean +/- SD) and 132 +/- 21% of the baseline in the rats at P13-17 and P19-24, respectively. This potentiation remained stable from 4 to 8 h, then gradually decreased to the baseline 15-16 h after the infusion. NGF applied in the same way did not induce potentiation. An inhibitor of BDNF receptors blocked the potentiation when it was applied immediately after the BDNF application, but was not effective about 2 h later. In the adults, BDNF did not potentiate field potentials. These results indicate that BDNF induces synaptic potentiation lasting for several hours only in the developing cortex through processes downstream of receptor activation.
Circadian variation in the expression of brain‐derived neurotrophic factor (BDNF) indicates that BDNF is involved in the regulation of diurnal rhythms in a variety of biological processes. However, it is still unclear which brain regions alter their BDNF levels in response to external light input. Therefore, in selected brain regions of adult male rats, we investigated diurnal variation, as well as the effects of a single eight‐hour phase advance of the light‐dark cycle, on the levels of BDNF and of other neurotrophins. The cerebellum, hippocampus and cerebral cortex containing visual cortex (VCX) showed diurnal variation in BDNF protein levels and the VCX also in NT‐3 levels. In the VCX and the region containing the entorhinal cortex and amygdala (ECX), BDNF protein levels were increased 12 h after the phase advance, while BDNF mRNA levels were increased significantly in the VCX and slightly in the ECX after 4 h. After one week, however, BDNF protein levels were reduced in eight brain regions out of 13 examined. BDNF levels in the ECX and VCX were significantly different between light rearing and dark rearing, while a hypothyroid status did not produce an effect. Cyclic AMP responsive element‐binding protein (CREB), a transcription factor for BDNF, was greatly activated by the phase advance in the ECX and VCX, suggesting the existence of CREB‐mediated pathways of BDNF synthesis that are responsive to external light input.
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