Early lesions of mouse vibrissal follicles: Their influence on dendrite orientation in the cortical barrelfield

Abstract

There is a statistically significant order in the tangential orientation of stellate cell dendrites, both spiny and smooth, in layer IV of the barrelfield of the mouse parietal cortex. Neurones situated in a barrel side have most of their dendrites oriented towards the barrel hollow; those situated in the hollow preferentially orient their dendrites parallel to the long axis of the barrel. A quantitative measure of the orientation of individual dendrites in barrelfields of 60-day old mice was obtained using a semi-automatic computer-microscope and a minicomputer. In the same manner, the dendrite orientation of layer IV stellate cells was determined in barrelfields, whose (cytoarchitectonic) pattern had been experimentally altered through lesions of the middle row of the mystacial vibrissal follicles at birth. The dendrites of these cells are oriented in harmony with the novel parcellation of the cortex. Consequently, for cells in the altered areas of the barrelfields, the dendrite orientation is different from that of cells with identical positions in a normal field (see Fig. 8). We tentatively interpret these findings as an adaptation of dendrite orientation to an altered pattern of thalamic input to layer IV that, in turn, is a consequence of the peripheral manipulation.

Activity-dependent maintenance and growth of dendrites in adult cortex

“…The control data of the present study confirm the tendency of pyramidal cells in the barrel field of rat primary somatosensory cortex to orient their dendritic arbors toward the center of their associated barrel (1,27). However, this orientation bias was not apparent weeks after permanent removal of the primary vibrissa of a barrel in adult rats.…”

“…One striking aspect of the anatomy of the barrel cortex is the tendency for upper-layer pyramidal cells to have dendritic arborization patterns with a centripetal bias toward the barrel center (1,27). In a search for structural changes that may contribute to the plasticity response in adult cortex, we investigated the directional bias of layer III and IV neuronal dendritic fields after loss of the primary vibrissal input to the barrels.…”

Columnar Organization of Dendrites and Axons of Single and Synaptically Coupled Excitatory Spiny Neurons in Layer 4 of the Rat Barrel Cortex

“…Earlier Golgi studies described the dendritic morphology of spiny neurons in rodent barrel cortex (Pasternak and Woolsey, 1975;Woolsey et al, 1975;Steffen, 1976;Steffen and van der Loos, 1980;Harris and Woolsey, 1981;Simons and Woolsey, 1984; for review, see Juliano and Jacobs, 1995) but lacked information about the axonal projections at the single-cell level and the target cells of these neurons. However, small extracellular biocytin deposits revealed that most of the projections are to supragranular layers, and relatively few direct connections exist between hollows of neighboring barrels (Kim and Ebner, 1999).…”

“…The dendritic arborization pattern of spiny neurons in layer 4 has been studied in detail previously (Pasternak and Woolsey, 1975;Woolsey et al, 1975;Steffen, 1976;Steffen and van der Loos, 1980;Figure 7. Electron microscopy of synaptic contacts established by spiny stellate neurons on different postsynaptic target structures in layers 4 (A-D) and 2/3 (E-H) as revealed from serial ultrathin sectioning through the entire axonal domain.…”

The representation of peripheral nerve inputs in the S-I hindpaw cortex of rats raised with incompletely innervated hindpaws

“…Cauterization of follicles or injury of the infraorbital nerve during the first several postnatal days results in (1) loss of primary sensory neurons and disruption of the cellular organization in the trigeminal ganglion (Bates and Killackey, 1984;Durham and Woolsey, 1984;Killackey, 1982, 1983;Jacquin and Rhoades, 1983;Math et al, 1984;Rhoades et al, 1983;Savy et al, 1981;Waite, 1984;Waite and Cragg, 1979); (2) disorganization and shrinkage of brain stem trigeminal nuclei due to transynaptic loss of neurons (Waite, 1984); (3) abnormal spatial patterns of cells and fiber terminals at synaptic relays in the brain stem (Bates and Killackey, 1984;Bates et al, 1982;Killackey, 1979a, b, 1980;Durham and Woolsey, 1984;Erzurumlu and Killackey, 1983;Jacquin and Rhoades, 1983;Killackey and Shinder, 1981;Rhoades ef. al., 1983); thalamus Killackey, 1979a, b, 1980;Durham and Woolsey, 1984;Killackey and Shindler, 1981;Woolsey et al, 1979) and S-I cortex Durham and Woolsey, 1984;Jeanmonod et al, 1977, 198 1;Jensen and Killackey, 1984;Belford, 1979, 1980;Killackey et al, 1976;Van der Loos and Woolsey, 1973;Waite and Cragg, 1979;Weller and Johnson, 1975;Woolsey and Wann, 1976); and (4) alterations in the dendritic organization of cortical cells (Harris and Woolsey, 1979, 198 1;Ryugo et al, 1975;Steffen and Van der Loos, 1980). These studies clearly indicate that the rodent somatosensory system is in a formative stage during the...…”