The inferotemporal (IT) cortex is responsible for object recognition, but it is unclear how the representation of visual objects is organized in this part of the brain. Areas that are selective for categories such as faces, bodies, and scenes have been found [1][2][3][4][5] , but large parts of IT cortex lack any known specialization, raising the question of what general principle governs IT organization.Here we used functional MRI, microstimulation, electrophysiology, and deep networks to investigate the organization of macaque IT cortex. We built a low-dimensional object space to describe general objects using a feed forward deep neural network trained on object classification 6 . Responses of IT cells to a large set of objects revealed that single IT cells project incoming objects onto specific axes of this space. Anatomically, cells were clustered into four networks according to the first two components of their preferred axes, forming a map of object space. This map was repeated across three hierarchical stages of increasing view invariance, and cells that comprised these maps collectively harboured sufficient coding capacity to approximately reconstruct objects. These results provide a unified picture of IT organization in which categoryselective regions are part of a coarse map of object space whose dimensions can be extracted from a deep network.

How developing axons in the corpus callosum (CC) achieve their homotopic projection to the contralateral cortex remains unclear. We found that axonal position within the CC plays a critical role in this projection. Labeling of nearby callosal axons in mice showed that callosal axons were segregated in an orderly fashion, with those from more medial cerebral cortex located more dorsally and subsequently projecting to more medial contralateral cortical regions. The normal axonal order within the CC was grossly disturbed when semaphorin3A/neuropilin-1 signaling was disrupted. However, the order in which axons were positioned within the CC still determined their contralateral projection, causing a severe disruption of the homotopic contralateral projection that persisted at postnatal day 30, when the normal developmental refinement of contralateral projections is completed in wild-type (WT) mice. Thus, the orderly positioning of axons within the CC is a primary determinant of how homotopic interhemispheric projections form in the contralateral cortex.axon development | axon fiber order | cortical axon guidance | cortical development T he largest commissural tract in the human brain is the corpus callosum (CC), with more than 200 million axons connecting the two cerebral hemispheres. Callosal axons originate primarily from neurons of layer II/III and layer V of the neocortex (1) and project homotopically to the contralateral cortex. For example, callosal axons of the primary motor cortex (M1) and primary somatosensory cortex (S1) project to topographically equivalent locations in the contralateral M1 and S1, respectively. This pattern of homotopic projection is essential for coordinated motor and somatosensory functions as well as for higher associative and cognitive processes (2-4). Abnormal CC development has been noted in psychiatric and developmental disorders (5, 6), and deviant asymmetry of cortical areas found in patients with developmental dyslexia also may be attributed to callosal abnormalities (7,8). However, the mechanism by which normal homotopic projection pattern is achieved during development remains largely unknown.The majority of axonal projections in the nervous system are organized topographically. To facilitate the formation of orderly projections over long distances, axons originating from adjacent areas may preserve their topographic order within the nerve tract along their entire path toward the target region (9, 10). This preservation of topographic order has been shown in the thalamocortical tract (11)(12)(13)(14) and in the optic and olfactory nerves (15-17). By performing a series of random microinjections of biotinylated dextran amine in the dorsal thalamus and reconstructing the labeled fibers, Powell et al. (14) showed that labeled axons within the thalamocortical tract preserve a topography similar to that in the ventral telencephalon before they reach the cortex. In the developing olfactory system, axons within the olfactory nerve from three different regions of the olfactory epitheli...

Dendrite development of newborn granule cells (GCs) in the dentate gyrus of adult hippocampus is critical for their incorporation into existing hippocampal circuits, but the cellular mechanisms regulating their dendrite development remains largely unclear. In this study, we examined the function of brain-derived neurotrophic factor (BDNF), which is expressed in adult-born GCs, in regulating their dendrite morphogenesis. Using retrovirus-mediated gene transfection, we found that deletion and overexpression of BDNF in adult-born GCs resulted in the reduction and elevation of dendrite growth, respectively. This effect was mainly due to the autocrine rather than paracrine action of BDNF, because deletion of BDNF only in the newborn GCs resulted in dendrite abnormality of these neurons to a similar extent as that observed in conditional knockout (cKO) mice with BDNF deleted in the entire forebrain. Furthermore, selective expression of BDNF in adult-born GCs in BDNF cKO mice fully restored normal dendrite development. The BDNF autocrine action was also required for the development of normal density of spines and normal percentage of spines containing the postsynaptic marker PSD-95, suggesting autocrine BDNF regulation of synaptogenesis. Furthermore, increased dendrite growth of adult-born GCs caused by voluntary exercise was abolished by BDNF deletion specifically in these neurons and elevated dendrite growth due to BDNF overexpression in these neurons was prevented by reducing neuronal activity with coexpression of inward rectifier potassium channels, consistent with activitydependent autocrine BDNF secretion. Therefore, BDNF expressed in adult-born GCs plays a critical role in dendrite development by acting as an autocrine factor.