Areal changes in mouse cortical barrels following vibrissal damage at different postnatal ages

Abstract

The normal cytoarchitectonic pattern of barrels in layer IV of mouse SmI face cortex is altered by early damage to the mystacial vibrissae (Van der Loos and Woolsey, '73). In the present study, the middle row of vibrissae (row-C) on one side of the face in groups of Swiss mice was cauterized on the day of birth (postnatal day [PND] -1)or on PND's - 2, 3, 4, 5, 7, 10, 12, 15, 20 and 30; littermates in each group served as controls. All animals were perfused on PND-60 and the brains sectioned parallel to SmI layer IV. For each specimen, the posteromedial barrel subfields (PMBSF) of the two hemispheres were reconstructed with a camera lucida and the cross-sectional areas of individual barrels measured using a small computer. The findings are: (1) The hemispheres ipsilateral to the vibrissal damage are quantitatively indistinguishable from the littermate controls indicating that the ipsilateral hemispheres in lesioned animals can serve as controls for observations of the type reported in this paper. (2) There are no consistent differences in the cross-sectional areas of the PMBSF's as a whole in the hemispheres ipsi- and contralateral to the peripheral damage, suggesting that there is no net loss of cortex as a result of the lesions. (3) The contralateral row-C barrels are reduced in size. Expressed as a percentage of normal values; row-C is reduced to 17% for animals lesioned on PND-1, 16% on PND-2, 38% on PND-3, 52% on PND-4 and 79% on PND-5; on PND-7 and later the cross-sectional areas of row-C barrels are normal. This implies that the barrel field of the SmI face cortex becomes progressively refractory to the effects of peripheral damage during the first postnatal week and in the period prior to PND-6, an intact periphery is necessary for normal cortical development. (4) In every case, the decreased cross-sectional area of row-C is accompanied by precisely increased cross-sectional areas of the barrels in adjacent rows-B and D. in the case of the restricted peripheral damage which we produced, there is a "compensation" in the contralateral hemisphere, which can be correlated with patterns of the specific thalamocortical projections.

An Early Critical Period for Long-Term Plasticity and Structural Modification of Sensory Synapses in Olfactory Cortex

“…Our results are consistent with reports of critical periods for anatomical and synaptic plasticity in the visual (Wiesel and Hubel, 1963), somatosensory (Woolsey and Wann, 1976), and auditory (Zhang et al, 2001) cortices. The plasticity of developing olfactory sensory inputs could provide a substrate for enhancing the cortical representation of odors experienced during an early postnatal time window.…”

Postnatal development of A-type and Kv1- and Kv2-mediated potassium channel currents in neocortical pyramidal neurons

“…Active whisker exploration begins during postnatal week 2 (P11-P13; Landers and Ziegler 2006;Woolsey and Wann 1976) and is mature at the end of the third week. Synaptogenesis also peaks in the second postnatal week (Micheva and Beaulieu 1996), although the number of excitatory and inhibitory synapses increases until P32 (after which it declines; De Felipe et al 1997).…”

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...…”