Changes In Soma Size Research Articles

Age-Related Changes in Soma Size of Y Neurons in the Cat Dorsal Lateral Geniculate Nucleus: Dorsoventral and Centroperipheral Gradients

Age-Related Changes in Soma Size of Y Neurons in the Cat Dorsal Lateral Geniculate Nucleus: Dorsoventral and Centroperipheral Gradients

The vulnerability of spinal motoneurons and soma size plasticity in a mouse model of amyotrophic lateral sclerosis.

Motoneuron soma size is a largely plastic property that is altered during amyotrophic lateral sclerosis (ALS) progression. We report evidence of systematic spinal motoneuron soma size plasticity in mutant SOD1-G93A mice at various disease stages and across sexes, spinal regions and motoneuron types. We show that disease-vulnerable motoneurons exhibit early increased soma sizes. We show via computer simulations that the measured changes in soma size have a profound impact on the excitability of disease-vulnerable motoneurons. This study reveals a novel form of plasticity in ALS and suggests a potential target for altering motoneuron function and survival. α-Motoneuron soma size is correlated with the cell's excitability and function, and has been posited as a plastic property that changes during cellular maturation, injury and disease. This study examined whether α-motoneuron somas change in size over disease progression in the G93A mouse model of amyotrophic lateral sclerosis (ALS), a disease characterized by progressive motoneuron death. We used 2D- and 3D-morphometric analysis of motoneuron size and measures of cell density at four key disease stages: neonatal (P10 - with earliest known disease changes); young adult (P30 - presymptomatic with early motoneuron death); symptom onset (P90 - with death of 70-80% of motoneurons); and end-stage (P120+ - with full paralysis of hindlimbs). We additionally examined differences in lumbar vs. sacral vs. cervical motoneurons; in motoneurons from male vs. female mice; and in fast vs. slow motoneurons. We present the first evidence of plastic changes in the soma size of spinal α-motoneurons occurring throughout different stages of ALS with profound effects on motoneuron excitability. Somatic changes are time dependent and are characterized by early-stage enlargement (P10 and P30); no change around symptom onset; and shrinkage at end-stage. A key finding in the study indicates that disease-vulnerable motoneurons exhibit increased soma sizes (P10 and P30). This pattern was confirmed across spinal cord regions, genders and motoneuron types. This extends the theory of motoneuron size-based vulnerability in ALS: not only are larger motoneurons more vulnerable to death in ALS, but are also enlarged further in the disease. Such information is valuable for identifying ALS pathogenesis mechanisms.

Characterizing microglia activation: a spatial statistics approach to maximize information extraction

SummaryMicroglia play an important role in the pathology of CNS disorders, however, there remains significant uncertainty about the neuroprotective/degenerative role of these cells due to a lack of techniques to adequately assess their complex behaviour in response to injury. This talk briefly describes a novel technique for microglia analysis, combining improved immunohistological image analysis with spatial statistical techniques (Ripley‐K function and Dixon's χ2‐test). Using this approach, a comprehensive set of morphological parameters describing microglia activation status was developed to characterise microgliosis in a murine optic nerve injury model. In addition to monitoring global changes in microglia density, nearest neighbour distance, and regularity index, cluster analyses based on changes in soma size and roundness were used to yield novel insights into the behaviour of different microglia phenotypes. These methods should be considered a generic tool to quantitatively assess microglia activation status, to profile these phenotypic changes into microglia subpopulations, and to map their spatial distributions in virtually every CNS region and disease state.

Characterizing microglia activation: a spatial statistics approach to maximize information extraction

Microglia play an important role in the pathology of CNS disorders, however, there remains significant uncertainty about the neuroprotective/degenerative role of these cells due to a lack of techniques to adequately assess their complex behaviour in response to injury. Advancing microscopy techniques, transgenic lines and well-characterized molecular markers, have made histological assessment of microglia populations more accessible. However, there is a distinct lack of tools to adequately extract information from these images to fully characterise microglia behaviour. This, combined with growing economic pressures and the ethical need to minimise the use of laboratory animals, led us to develop tools to maximise the amount of information obtained. This study describes a novel approach, combining image analysis with spatial statistical techniques. In addition to monitoring morphological parameters and global changes in microglia density, nearest neighbour distance, and regularity index, we used cluster analyses based on changes in soma size and roundness to yield novel insights into the behaviour of different microglia phenotypes in a murine optic nerve injury model. These methods should be considered a generic tool to quantitatively assess microglia activation, to profile phenotypic changes into microglia subpopulations, and to map spatial distributions in virtually every CNS region and disease state.

Maintenance of neuronal size gradient in MNTB requires sound-evoked activity

The medial nucleus of the trapezoid body (MNTB) is an important source of inhibition during the computation of sound location. It transmits fast and precisely timed action potentials at high frequencies; this requires an efficient calcium clearance mechanism, in which plasma membrane calcium ATPase 2 (PMCA2) is a key component. Deafwaddler (dfw2J ) mutant mice have a null mutation in PMCA2 causing deafness in homozygotes (dfw2J /dfw2J ) and high-frequency hearing loss in heterozygotes (+/dfw2J ). Despite the deafness phenotype, no significant differences in MNTB volume or cell number were observed in dfw2J homozygous mutants, suggesting that PMCA2 is not required for MNTB neuron survival. The MNTB tonotopic axis encodes high to low sound frequencies across the medial to lateral dimension. We discovered a cell size gradient along this axis: lateral neuronal somata are significantly larger than medially located somata. This size gradient is decreased in +/dfw2J and absent in dfw2J /dfw2J The lack of acoustically driven input suggests that sound-evoked activity is required for maintenance of the cell size gradient. This hypothesis was corroborated by selective elimination of auditory hair cell activity with either hair cell elimination in Pou4f3 DTR mice or inner ear tetrodotoxin (TTX) treatment. The change in soma size was reversible and recovered within 7 days of TTX treatment, suggesting that regulation of the gradient is dependent on synaptic activity and that these changes are plastic rather than permanent.NEW & NOTEWORTHY Neurons of the medial nucleus of the trapezoid body (MNTB) act as fast-spiking inhibitory interneurons within the auditory brain stem. The MNTB is topographically organized, with low sound frequencies encoded laterally and high frequencies medially. We discovered a cell size gradient along this axis: lateral neurons are larger than medial neurons. The absence of this gradient in deaf mice lacking plasma membrane calcium ATPase 2 suggests an activity-dependent, calcium-mediated mechanism that controls neuronal soma size.

Dissecting mechanisms of brain aging by studying the intrinsic excitability of neurons.

Several studies using vertebrate and invertebrate animal models have shown aging associated changes in brain function. Importantly, changes in soma size, loss or regression of dendrites and dendritic spines and alterations in the expression of neurotransmitter receptors in specific neurons were described. Despite this understanding, how aging impacts intrinsic properties of individual neurons or circuits that govern a defined behavior is yet to be determined. Here we discuss current understanding of specific electrophysiological changes in individual neurons and circuits during aging.

Treadmill training induces plasticity in spinal motoneurons and sciatic nerve after sensorimotor restriction during early postnatal period: New insights into the clinical approach for children with cerebral palsy

The aim of the present study was to investigate whether locomotor stimulation training could have beneficial effects on the morphometric alterations of spinal cord and sciatic nerve consequent to sensorimotor restriction (SR). Male Wistar rats were exposed to SR from postnatal day 2 (P2) to P28. Control and experimental rats underwent locomotor stimulation training in a treadmill for three weeks (from P31 to P52). The cross-sectional area (CSA) of spinal motoneurons innervating hind limb muscles was determined. Both fiber and axonal CSA of myelinated fibers were also assessed. The growth-related increase in CSA of motoneurons in the SR group was less than controls. After SR, the mean motoneuron soma size was reduced with an increase in the proportion of motoneurons with a soma size of between 0 and 800 μm 2. The changes in soma size of motoneurons were accompanied by a reduction in the mean fiber and axon CSA of sciatic nerve. The soma size of motoneurons was reestablished at the end of the training period reaching controls level. Our results suggest that SR during early postnatal life retards the growth-related increase in the cell body size of motoneurons in spinal cord and the development of sciatic nerve. Additionally, three weeks of locomotor stimulation using a treadmill seems to have a beneficial effect on motoneurons’ soma size.

Experience-Dependent Plasticity and Vision Restoration in Rats after Optic Nerve Crush

Within the first weeks after brain damage the visual system can spontaneously recover, but it is not known if visual experience plays a role in this process. Therefore, we studied the role of visual experience during recovery by exposing rats to normal, enriched, and impoverished visual conditions. Adult rats, which had learned a six-choice brightness discrimination task, received bilateral partial optic nerve crush (ONC), and were then exposed daily for 34 days to either (1) total darkness, (2) a standard 12-h light:12-h dark cycle, or (3) a 2-h selective visual enrichment. The percentage of correct choices and the maximal performance levels reached were used as recovery end-points. Retinal ganglion cell (RGC) morphology was evaluated following retrograde transport of fluorescent tracer with in vivo confocal neuroimaging (ICON) before and after ONC. Whereas rats kept under normal daylight conditions after ONC recovered their visual functions rather well, rats housed in complete darkness did not recover at all. However, only 2 h of daily exposure to visual enrichment induced significantly enhanced recovery, which was even faster than that seen in rats housed under normal daylight conditions. RGC soma size changes were observed after ONC, but they did not correlate with any measures of behavioral recovery. We conclude that visual experience, even if provided for short daily periods, is a critical factor determining the dynamics of early phases of recovery.

Time course of adult castration-induced changes in soma size of motoneurons in the rat spinal nucleus of the bulbocavernosus

The spinal nucleus of the bulbocavernosus (SNB) innervates striated muscles, the bulbocavernosus and levator ani (BC/LA), which control penile reflexes. Castration results in shrinkage in the size of SNB somata and dendrites, as well as BC/LA muscle mass. However, there is no information about how quickly these regressive changes occur compared to the rapid effects of castration upon penile reflexes, which are greatly diminished a few days after surgery. Therefore we examined the time course of change in the size of SNB somata after castration of adult male rats. Males were sacrificed 2, 14, or 28 days after either castration or sham surgery and somata were measured in the SNB and in a control population of motoneurons, the retrodorsolateral nucleus (RDLN). BC/LA weight was reduced in castrates compared to intact males 14 and 28 days post surgery, but SNB somata were significantly smaller in castrates only at 28 days after surgery. As has been previously observed, castration did not affect soma size in the RDLN. These data indicate that SNB somata respond more slowly after castration than BC/LA mass or penile reflexes, suggesting that the size of SNB somata cannot account for the loss of penile reflexes. Androgenic effects on SNB somata may contribute to aspects of reproductive behavior that are not apparent in penile reflexes tested ex copula.

Brain-derived neurotrophic factor inhibits changes in soma-size of retinal ganglion cells following optic nerve axotomy in rats.

To determine if optic nerve axotomy affects the cell soma size of retinal ganglion cells and to establish whether such quantitative analysis is useful as a new way of evaluating retinal ganglion cell damage, we measured the changes in both the number and soma size of retinal ganglion cells after optic nerve axotomy in rats. Retinal ganglion cells were retrogradely labeled by fluoro-gold injection into the superior colliculus, and the soma size was measured using image-analysis software. We detected a decrease in the proportion of large-sized retinal ganglion cells that was significant at 3, 5 and 7 days after the axotomy, and an increased proportion of small-sized ones that was significant at 5 and 7 days after the axotomy, indicating that retinal ganglion cells shrank following axotomy, that there was a shift away from the largest category of retinal ganglion cells towards the smallest category. On days 3 and 5 post-axotomy, there was no significant change in the proportion of medium-sized retinal ganglion cells. Intravitreal injection of brain-derived neurotrophic factor one hour before the axotomy significant inhibited the increase in the proportion of small-sized retinal ganglion cells otherwise seen at 3 days after the axotomy. These results may suggest that larger retinal ganglion cells are more sensitive to optic nerve axotomy than small- and medium-sized ones, and that a quantitative analysis of soma size is a useful way of detecting retinal ganglion cell damage in the early phase after axotomy.

Age-related changes in soma size of neurons in the spinal cord motor column of the cat

The present study was undertaken to examine the effect of the aging process on the soma size and number of motoneurons and interneurons in the motor column of the spinal cord of old cats. Neurons in the motor column were divided into small and large populations based on a bimodal distribution of their soma cross-sectional areas. A 17% decrease in the cross-sectional area of small neurons was observed, this decrease was statistically significant ( P < 0.0001). The cross-sectional area of large neurons decreased by only 6%, which was statistically significant ( P < 0.05). On the other hand, there was no significant difference in the number of large, small or of these combined population of ventral horn neurons in the aged cats compared with the control animals. This data suggest that neurons in the motor column are not uniformly affected by the aging process because morphological changes are proportionally greater in small neurons than in large neurons.

Three gonadotropin-releasing hormone genes in one organism suggest novel roles for an ancient peptide.

Gonadotropin-releasing hormone (GnRH) is known and named for its essential role in vertebrate reproduction. Release of this decapeptide from neurons in the hypothalamus controls pituitary gonadotropin levels which, in turn, regulate gonadal state. The importance of GnRH is underscored by its widespread expression and conservation across vertebrate taxa: five amino acids are invariant in all nine known forms, whereas two others show only conservative changes. In most eutherian mammals, only one form, expressed in the hypothalamus, is thought to exist, although in a recent report, antibody staining in developing primates suggests an additional form. In contrast, multiple GnRH forms and expression loci have been reported in many non-mammalian vertebrates. However, evidence based on immunological discrimination does not always agree with analysis of gene expression, since GnRH forms encoded by different genes may not be reliably distinguished by antibodies. Here we report the expression of three distinct GnRH genes in a teleost fish brain, including the sequence encoding a novel GnRH preprohormone. Using in situ hybridization, we show that this form is found only in neurons that project to the pituitary and exhibit changes in soma size depending on social and reproductive state. The other two GnRH genes are expressed in other, distinct cell populations. All three genes share the motif of encoding a polypeptide consisting of GnRH and a GnRH-associated peptide. Whereas the GnRH moiety is highly conserved, the GnRH-associated peptides are not, reflecting differential selective pressure on different parts of the gene. GnRH forms expressed in nonhypothalamic regions may serve to coordinate reproductive activities of the animal.

Evidence for Target Regulations of the Development of Androgen Sensitivity in Rat Spinal Motoneurons

Specific neuronal circuits within the vertebrate nervous system express high levels of steroid receptors and are sensitive to the effects of steroid hormones. The mechanisms by which these neuronal circuits develop their unique steroid sensitivity are unknown. One intriguing hypothesis is that retrograde influences during early postnatal life play a role in determining which central nervous system (CNS) neurons become sensitive to steroids. We now present evidence that during a critical period in early postnatal development, axonal injury disrupts the normal development of steroid sensitivity. The spinal nucleus of the bulbocavernosus (SNB) is a neuromuscular system that is highly androgen-sensitive at the level of both the motoneurons and their target muscles. Testosterone levels regulate the size of SNB motoneurons and their muscles in adult rats. Cutting the axons of SNB motoneurons on postnatal day 14 (P14) caused permanent decreases in SNB motoneuronal soma size, as well as in SNB target muscle weight. Interestingly, SNB motoneurons that survived axotomy on P14 failed to develop their normal ability to respond to testosterone in adulthood. That is, they did not respond to changes in testosterone levels with changes in soma size. The same effect was not seen after axotomy 1 week later in development, suggesting a critical period for this effect. Thus, separation from the target muscles during an early critical period in development blocked the differentiation of androgen sensitivity by SNB motoneurons, consistent with a role for the target in the normal development of steroid sensitivity by CNS neurons.

Social regulation of the brain-pituitary-gonadal axis.

Reproduction in vertebrates is regulated by the hypothalamic-pituitary-gonadal axis via neural and hormonal feedback. This axis is also subject to exogenous influences, particularly social signals. In the African cichlid fish Haplochromis burtoni, gonadal development in males is socially regulated. A small fraction of the males, which are brightly colored, maintain territories and aggressively dominate inconspicuously colored nonterritorial males. Here we show through manipulation of the social and endocrine environment that changes in social status and gonadal state are accompanied by soma size changes in a population of gonadotropin-releasing hormone-containing neurons in the ventral forebrain. In territorial males, these cells are significantly larger than in nonterritorial males. When an animal switches from being territorial to nonterritorial through a change in social situation, these cells shrink; in animals that change from nonterritorial to territorial status, the cells enlarge. These gonadotropin-releasing hormone-containing cells project to the pituitary and are ultimately responsible for regulating gonadal growth. This mechanism of socially induced cell size change provides the potential for relatively quick adaptive changes in the neuron-endocrine system without nerve cell addition or death. Since the structure of this regulatory axis is conserved among all vertebrates, other species with socially modulated reproductive physiology may exhibit a similar form of physiological regulation.

Regeneration and soma size changes following axotomy of the trochlear nerve

The effects of CNS and PNS axotomy of the IVth nerve on cell death, soma size, axon size, and axon number were investigated. In adult cats, the IVth nerve was axotomised by using four surgical paradigms: (1) peripheral IVth nerve crush, (2) peripheral IVth nerve cut, (3) peripheral IVth nerve resection, and (4) a CNS IVth nerve cut in the velum. The extent of cell death resulting from each surgical paradigm was determined. Following axotomy distal to the decussation of the IVth nerves, cell death was least after nerve crush, intermediate after nerve cut, and maximal after resection of 5-7 mm of the nerve. Following axotomy at the decussation--a CNS lesion--most cells died but some successful regeneration was observed. Soma size measurements following a short-term survival (3 days to 4 weeks) before the regenerating axons reached their target muscle revealed that somas of axotomised cells underwent hypotrophy within 1 week of axotomy and then gradually increased in size. They re-attained normal size by 4 weeks postoperative when regenerating axons first reach their target. Following a long-term survival (greater than 2 months), somas were significantly hypertrophied, and the degree of hypertrophy was inversely related to the extent of cell survival up to a limit of 40% soma size increase. Counts and measurements of axons revealed that mean axon diameter of regenerated axons was much smaller than normal 3 months after axotomy, increased during the third to sixth postoperative months, but then showed no subsequent increase and remained below normal. In animals with cell death varying from 10% to 70%, the number of axons in the nerve was maintained constant at approximately 1,000. These data indicate that there is a mechanism for the production and maintenance of the appropriate number of regenerative axonal branches following axotomy. In animals in which cell death exceeded 70%, the number of axons was controlled by a maximum ratio of 3 to 4 axon branches per surviving cell. The results suggest that axon number is strongly influenced by the target muscle and that hypertrophy of regenerated cells is related to the number of axonal sprouts each cell has to produce and support in order to re-establish the preoperative number of axons in the regenerated trochlear nerve.

Regeneration and soma size changes following axotomy of the trochlear nerve

AbstractThe effects of CNS and PNS axotomy of the IVth nerve on cell death, soma size, axon size, and axon number were investigated. In adult cats, the IVth nerve was axotomised by using four surgical paradigms: (1) peripheral IVth nerve crush, (2) peripheral IVth nerve cut, (3) peripheral IVth nerve resection, and (4) a CNS IVth nerve cut in the velum. The extent of cell death resulting from each surgical paradigm was determined. Following axotomy distal to the decussation of the IVth nerves, cell death was least after nerve crush, intermediate after nerve cut, and maximal after resection of 5–7 mm of the nerve. Following axotomy at the decussation—a CNS lesion—most cells died but some successful regeneration was observed.Soma size measurements following a short‐term survival (3 days to 4 weeks) before the regenerating axons reached their target muscle revealed that somas of axotomised cells underwent hypotrophy within 1 week of axotomy and then gradually increased in size. They re‐attained normal size by 4 weeks postoperative when regenerating axons first reach their target. Following a long‐term survival (&gt;2 months), somas were significantly hypertrophied, and the degree of hypertrophy was inversely related to the extent of cell survival up to a limit of 40% soma size increase.Counts and measurements of axons revealed that mean axon diameter of regenerated axons was much smaller than normal 3 months after axotomy, increased during the third to sixth postoperative months, but then showed no subsequent increase and remained below normal. In animals with cell death varying from 10% to 70%, the number of axons in the nerve was maintained constant at approximately 1,000. These data indicate that there is a mechanism for the production and maintenance of the appropriate number of regenerative axonal branches following axotomy. In animals in which cell death exceeded 70%, the number of axons was controlled by a maximum ratio of 3 to 4 axon branches per surviving cell.The results suggest that axon number is strongly influenced by the target muscle and that hypertrophy of regenerated cells is related to the number of axonal sprouts each cell has to produce and support in order to re‐establish the preoperative number of axons in the regenerated trochlear nerve.

The retinohypothalamic tract in the cat: retinal ganglion cell morphology and pattern of projection

The pattern of retinal projection to the hypothalamus and the morphological properties of the retinal ganglion cells that comprise the retinohypothalamic tract have been examined in the cat. Intraocular injections of horseradish peroxidase revealed a dense retinal projection to the ventral suprachiasmatic nucleus; however, lighter projections were seen in the dorsal suprachiasmatic nucleus, and in hypothalamic regions both dorsal and lateral to the suprachiasmatic nucleus. Intrasuprachiasmatic nucleus injections of horseradish peroxidase retrogradely labelled retinal ganglion cells that were small to medium in soma size. The labelled ganglion cells exhibited long thin dendrites that were sparsely branched. The labelled retinal ganglion cells exhibited a significant change in soma size associated with retinal eccentricity. The morphological characteristics of the ganglion cells that project to the suprachiasmatic nucleus are similar to those of gamma cells.

A morphometric study of the retinal ganglion cell response to optic nerve severance in the frogRana pipiens

This study examines the cell body response to axotomy of retinal ganglion cells in the frog Rana pipiens. Cell soma sizes were measured in carefully matched regions of Nissl-stained wholemounted retinae after either nerve crush, nerve cut with stump separation, nerve crush with intraocular nerve growth factor (NGF) or nerve cut with NGF applied to the proximal stump. The state of axonal regeneration was also assessed in each case by anterograde transport of HRP. Following nerve crush axons crossed the lesion by 7 days, reached the chiasma by 14 days and entered the tectum around 20-30 days. The normally evenly stained ganglion cells exhibited granular Nissl staining at 7 and 10 days but very little change in soma size. From 10 to 28 days the mean retinal ganglion cell area increased by 102% and maintained this size until at least 75 days. By 102 days soma size had nearly returned to normal. A population of displaced amacrine cells retained a normal appearance and soma size throughout regeneration. Following nerve cut and stump separation the retinal ganglion cells were slightly more reactive in appearance at 7 days after crush but otherwise the soma reaction developed in a similar manner. Axon tracing revealed no extension beyond the lesion site in these animals and therefore the state of axonal growth did not affect the early soma response. NGF applied at the time of the lesion had no detectable effect on the soma reaction. Although many retinal ganglion cells re-establish contact with visual centres after axotomy in the frog, a considerable proportion die. This contrasts with both the goldfish, where all cells regenerate successfully, and various mammals, where none do so and all retinal ganglion cells die. All retinal ganglion cells in the frog undergo reactive changes similar to those of goldfish and there is no sign of the cell shrinkage seen in mammals. Therefore the cell death in frog would appear to be different from that in mammalian retina but similar to that of mammalian peripheral nerve in which chromatolysis generally preceeds death.

The development of soma size changes in the C-laminae of the cat lateral geniculate nucleus following monocular deprivation

This study examined the pattern of soma size changes in the cat dorsal lateral geniculate nucleus (dLGN) from 4 weeks of age to adulthood following monocular lid suture at two weeks of age. Different patterns of soma size changes were found between the A-laminae and C-laminae. In layers A, A 1, and C significant soma size differences were found between the deprived and non-deprived laminae by 4 weeks of age. However, the magnocellular portion of layer C was affected more by deprivation than the parvocellular portion. Layer C 1 did not reveal significant soma size changes until 20 weeks of age. Layer C 2 did not exhibit any soma size changes at any age. These differential responses to monocular deprivation suggest different time courses of development among the dLGN laminae.

Bilateral changes in soma size of geniculate relay cells and corticogeniculate cells after neonatal monocular enucleation in rats

Some areas of relay cells of the lateral geniculate nucleus and of corticogeniculate cells of normal rats (n= 4) were compared with those of neonatally unilaterally eye-enucleated adult rats (n= 13). These cells were labeled by retrogradely transported HRP. Monocular enucleation was performed on postnatal days 1 (PND 1) (n= 4), 3 (PND 3), (n= 5) and 6 (PND 6)_(n= 4). The resulsts are summarized as follows. (1) In PND 1 rats soma areas of relay cells were 12–16% smaller than those of normal rats, but only for the geniculate nucleus ipsilateral to the remaining eye. In PND 3 and 6 rats the areal shrinkage of relay cells was 27–39% of the normal control for both hemispheres, though it was less marked in the hemisphere contralateral to the remaining eye. (2) The corticogeniculate cells were distributed in layers V and VI in eye-enucleated rats as well as in normal rats. Soma areas of both layer V and VI cells increased in PND 1 rats for both hemispheres by about 15–47% of the normal control. InPND 3 rats increase in soma size tended to occur for layer VI cells, although the data varied from animal to animal. In summary, it was established that unilateral eye-enucleation in rats at birth induced soma size changes of the geniculate relay cells and of the corticogeniculate cells in the non-deafferented as well as in the deafferented hemisphere. Possible mechanisms for the bilateral changes in soma area of central visual cells after neonatal monocular enucleation are discussed.