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Sickle cell disorder (SCD) is a chronic illness that in England disproportionately affects marginalized ethnic groups, but has yet to feature extensively within educational or disability research. This review of existing literature makes the case for a sustained developmental research programme around SCD, disability and education. There are potentially life-saving decisions that could be made by teachers in caring for a child with SCD. The place of the school as a venue for health screening with respect to vision, hearing and dental care is also complicated by SCD. The lack of a formal school policy to address the combined episodic and longer term school absences correlated with SCD clearly disadvantages a group of pupils whose academic potential may already have been curtailed by teacher expectations based on their ethnicity. Both the physical and social milieu of the school could be adapted so that the environmental triggers of severe painful episodes associated with SCD are greatly reduced. Systems of pastoral care and health education elements of the school curriculum need to be attuned to the challenges and opportunities for learning that SCD raises. SCD may be considered as a resource for education across a range of national curriculum subjects, could bring an anti-racist dimension to subjects such as mathematics, biology, history and geography and could challenge a number of prevailing disabling and racist discourses in wider society. In short, SCD could be one bridge to more inclusive education for pupils of marginalized ethnic groups. [ABSTRACT FROM AUTHOR]

This study explores attitudes and motivations towards volunteering in nursing students in Ghana compared with nursing students in the United Kingdom (UK). Ghana traditionally follows a western model of nurse education, with students studying programmes commensurate in theory and practice, making Ghana a suitable location for a comparative study. We explored similarities and differences in attitudes and motivation towards volunteering to challenge and inform our common place practice towards nursing pedagogy. Ghanaian students displayed positive attitudes towards volunteering, although these did not translate into increased motivation to volunteer while at university. Students reported financial constraints as reasons for not volunteering as did UK students, although Ghanaian students used available resources for daily living expenses, whereas UK students prioritised available resources to pay down student debt. Structured volunteering was absent from both Ghanaian and UK nursing programmes, despite its potential to increase the variety of social groups or situations to which students are exposed, to increase self-confidence and to encourage greater reflection on practice through doing. Structural challenges within countries may provide a better explanation of variation in student motivation towards volunteering, than cross-cultural variation in attitudes towards volunteering between countries., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

In the aftermath of the Francis Report nurses are being called to account for an apparent lack of care and compassion, leading to debate around pedagogy in nurse education. Absent from this debate is a consideration of student volunteering within undergraduate nursing programmes and its potential to promote student nurses self-esteem and to enhance the development of critical thinking skills. The aim of this study was therefore to understand the extent of and attitudes towards volunteering among nursing students. A mixed methods approach using a specifically developed questionnaire, followed by in-depth interviews to ascertain extent, variability, and attitudes towards volunteering revealed low levels of volunteering among nursing students. Limited time, limited access, and lack of academic support were cited as reasons. Nevertheless, students displayed positive attitudes towards volunteering. While volunteering has been shown to impact upon students abilities to think critically, to develop personal values and respond to the needs of others, volunteering within the UK undergraduate nursing programme considered here is neither structured nor formalized. Nurse educators should pay attention to the positive benefits of volunteering for nursing students and consider ways in which volunteering might be incorporated into the curriculum., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

The experiences of young people living with a sickle cell disorder in schools in England are reported through a thematic analysis of forty interviews, using Bourdieu's notions of field, capital and habitus. Young people with sickle cell are found to be habitually dys-positioned between the demands of the clinic for health maintenance through self-care and the field of the school, with its emphases on routines, consistent attendance and contextual demands for active and passive pupil behaviour. The tactics or dispositions that young people living with sickle cell can then employ, during strategy and struggle at school, are therefore fragile: they work only contingently, transiently or have the unintended consequences of displacing other valued social relations. The dispositions of the young people with sickle cell are framed by other social struggles: innovations in school procedures merely address aspects of sickle cell in isolation and are not consolidated into comprehensive policies; mothers inform, liaise, negotiate and advocate in support of a child with sickle cell but with limited success. Reactions of teachers and peers to sickle cell have the enduring potential to drain the somatic, cultural and social capital of young people living with sickle cell., (© 2011 The Authors. Sociology of Health & Illness © 2011 Foundation for the Sociology of Health & Illness/Blackwell Publishing Ltd.)

Sickle cell is a leading genetic condition, both globally and in England. Little research has been conducted into the experiences of young people with sickle cell at school. A mixed methods study (May 2007-September 2008) based on 569 questionnaires and 40 taped interviews with young people living with sickle cell disorder (SCD) in England found that students with SCD are faced with a dilemma as to whether or not to disclose their sickle cell to teachers and pupils: the latent and hidden characteristics of their symptoms make it possible, in Goffmanesque terms, to "pass". However the variable and unpredictable course of sickle cell is a reminder of Goffman's notion of being "discreditable". We found that teacher or pupil knowledge that a young person has sickle cell is not statistically associated with reported better treatment of young people with SCD at school. Analysis of interviews suggests most young people favour disclosing their sickle cell status (on the basis that teachers will then know what actions to take in the face of bouts of illness and in terms of making allowances for illness or school absences). A minority disagreed because disclosure was felt to attract unwarranted attention or disabling attitudes. Attitudes to disclosing to peers were more varied: either for or against disclosure to peers, or ambivalent in that they felt a tension between acknowledging the reality of their sickle cell, and not wanting it to be a central part of their identity. Some health promotion advice appears to assume that teacher and/or peer awareness is the key to improving school experience for young people with SCD, but this is not borne out by this study. Rather a change in wider school environments is required such that young people with SCD are supported irrespective of whether they themselves foreground or play down their disabled identity., (Copyright 2010 Elsevier Ltd. All rights reserved.)

Detection of aspiration by bedside examination has frequently been found to be clinically inadequate when compared with videofluoroscopy (VF) as the gold standard. In Doncaster, UK, a new multidisciplinary approach to bedside assessment was devised using physiotherapists (PT) performing bronchial auscultation (BA) in combination with the speech and language therapists' (SLT) clinical examination of dysphagia. In this study 105 patients referred for VF examination of dysphagia were first tested by the BA team. Comparison was made between the results of the VF team and the results of the BA team in classifying the patients as "aspirating" or at "risk of aspirating." A high degree of agreement was found for risk of aspiration (sensitivity 87%), although specificity was low (37%). BA was highly specific (88%) when confirming the absence of aspiration, but sensitivity to the presence of aspiration was 45%. From the 105 patients tested, the BA team would have failed to modify the diet in only one subject who was aspirating and would have unnecessarily modified the diet of 17 subjects. In conclusion, in the sample population of individuals with complex dysphagia, the BA team approach reliably detected patients identified by VF as at risk of aspiration. In the group of patients identified by VF as aspirating, the BA team proved unreliable in detecting the presence of aspiration, although it did reliably identify patients who were not aspirating. BA is a potentially useful clinical tool which requires further research.

Epaulette sharks inhabiting reef platforms are exposed to hypoxic and hyperoxic cycles. The adaptive mechanisms used to prevent neurological damage during these cycles have not been examined. Nitric oxide has a neuroprotective role in some hypoxia-tolerant species. We examined epaulette brains following a severe experimental hypoxic regimen (0.39 mgO2/l for 2 h) and compared nitric oxide synthase (NOS) expression with that in normoxic controls using NADPH-diaphorase staining. Intense NOS activity occurred in microvasculature following exposure to a severely hypoxic environment in contrast to the low levels seen in controls. We established for the first time that the epaulette shark was hypoxia-tolerant because there was no delayed phase of neuronal apoptosis. Enhanced NOS production in response to hypoxia may cause vasodilation, which would maintain the appropriate metabolic environment for continued neuronal survival during exposure to hypoxia.

Changes in the metabolic activity of embryonic chick spinal cords were examined following alpha-bungarotoxin (alpha-BTX) administration, in order to investigate a potential mechanism by which this toxin arrests motoneurone apoptosis during neurogenesis. Chick embryos were injected i.p. with alpha-BTX and after 25 h the metabolic markers 2-deoxyglucose and cytochrome oxidase were examined in alternate serial sections of the brachial and lumbar spinal cord. Glucose uptake and cytochrome oxidase activity were reduced throughout the spinal cord and pronounced in the lateral motor columns. Iodinated alpha-BTX reaches and binds to neuronal alpha-BTX-sensitive nicotinic cholinoceptors. Binding of alpha-BTX to these neuronal receptors and to those at the neuromuscular junction has now been shown to have a demonstrable effect on neuronal metabolism. The decreased metabolic activity in spinal cord neurones as a result of toxin treatment may have an important role in the prevention of motoneurone apoptosis at a critical developmental phase.

The efficacy of Schwann cell-filled polycarbonate tubes as a bridging substrate for regrowing axons following lesions of the rat optic tract or cerebral cortex has been assessed after short (11-31 days) or long (82-119 days) survival times. Tubes were impregnated with Iaminin and poly-L-lysine, soaked in basic FGF and filled with Schwann cells. They were implanted into optic tract lesions in 34 rats aged 15-21 days and into cortical lesion cavities in 3 adult rats. Gelfoam soaked in basic FGF and Schwann cell conditioned medium was placed over the tubes. In one group of rats, axon regrowth into implants was assessed using neurofilament antibody RT97; antibodies to proteolipid protein, Po, Iaminin, the low-affinity nerve growth factor receptor (NGFr), S-100 and EDI were also used to study myelination and the cellular content of the tubes. In a second group of rats, anterograde tracing techniques were used to specifically identify host retinal axons within the implanted polymers. After long survival times, the relationships between regrown axons and cells inside the tubes were also examined ultrastructurally. In all implants examined immunohistochemically at short survival times, large numbers of RT97+ axons were found throughout the tubes, usually in association with Iaminin+, NGFr+ Schwann cells. At longer survival times, viable Schwann cells were still present, but tubes contained fewer axons and less cellular material. This material often formed a cord (200-250 μm thick) which extended the length of the implant. In the second group of rats, labelled retinal axons were found in 11 of the 16 implants that were attached to the dLGN. Axons regrew up to 1 mm but did not reach the distal (tectal) end of the implants. Interestingly, there was no evidence of myelinogenesis by either implanted Schwann cells or by host-derived oligodendroglia which had migrated into the tubes. Oligodendroglia were usually encircled by processes, many of which originated from Schwann cells, suggesting that the grafted cells may have been involved in isolating the central glia. The data show that Schwann cell-filled polycarbonate tubes provided a favourable milieu for axonal regeneration in the short term; however over time there was a decrease in the cellular and fibre content of the tubes. After intracranial implantation, an additional supporting matrix inside the polycarbonate tubes may aid in providing an environment conducive to the long term maintenance of regenerated retinal and other axons.

The cochlear nucleus of 90 day-old rats was studied to determine whether bilateral visual deafferentation at birth induced compensatory structural changes in the auditory system. Computer-assisted reconstructions of the cochlear nucleus were used to demonstrate the three-dimensional organization of the nucleus and for calculating volumes of the subdivisions. In enucleated rats the volume of the granular region of the nucleus (GCD) increased 22.6% relative to controls, and the volume of the anterior ventral nucleus (AVCN) also increased by 10.0%. The posterior ventral nucleus (PVCN) and dorsal nucleus (DCN) were not affected. Since the volume change in GCD was substantial, this region was subjected to further analysis. Two types of granular cells were identified in the GCD of both control and enucleated rats with Kluver-Barrera staining. Type 1 cells contained an ovoid dark nucleus with clumpy chromatin and possessed only a very thin rim of cytoplasm. Type 2 cells were larger with pale spheroidal nuclei and with a more prominent cytoplasmic rim. There was an obvious stratification of these two cell types in the superficial layers over the lateral aspect of the AVCN in both groups. In contrast to this, the subpeduncular corner was not distinctively laminated and contained predominantly Type 2 cells. In enucleated animals the nuclear size of Type 1 cells increased by 3.8% while the size of Type 2 nuclei was not affected. Granule cell numbers increased by 28% in the visually deafferented rats. The GCD seems to be more highly developed in species which are dependent on non-visual modalities for spatial location. The regional hypertrophy of the GCD and AVCN seen in the present study may indicate that intermodal sensory compensation is taking place in the auditory system of visually deafferented rats.

Attempts were made to enhance the regrowth of retinal axons which had been lesioned in the brachial region of the rat optic tract. Pieces of nitrocellulose paper (Millipore) were placed into the lesioned area between the dorsal lateral geniculate nucleus (dLGN) and superior colliculus (SC) in 13- to 18-day-old Wistar rats. Five types of implant were used: (1) uncoated implants, (2) coated with Poly-l-lysine (PLL), (3) coated on one side with cortical astrocytes, (4) coated with tectal astrocytes and (5) coated with Schwann cells. About half the Schwann cell-covered implants were precoated with PLL. Schwann cell-coated implants (16-40 × 103 cells per implant) were placed with the cells lying on either the dorsal or ventral (inverted) surface of the paper. 5-7 weeks after surgery, eyes were injected with WGA-HRP, the animals were perfused and frozen or vibratome sections (40-50 μm) processed for TMB histochemistry. Selected sections containing retinal axons were osmicated and prepared for electron microscopic examination. 45 out of 86 implants were found attached to the caudal dLGN. A small number of retinal axons were found growing onto the rostral end of one uncoated implant, two PLL-coated implants and over the surface of 4 of the astrocyte-coated implants. The densest and most extensive growth was seen on the Schwann cell-coated implants. In 15 of the 30 animals with such implants attached to the dLGN, retinal axons were found regrowing for 50-1120 μm (mean 530 μum). In about half of these rats (8 out of 15), the regrowth involved relatively large numbers of optic axons which were sometimes densely packed together. In the subgroup of Schwann cell-coated implants where the cells were placed upwards, retinal axons regrew on the dorsal surface of the paper for more than 500 μm in 7 animals. Almost no growth was seen on the uncoated (ventral) surface of the implants. In the subgroup of inverted implants, where the Schwann cells were placed downwards, in 4 animals retinal axon regrowth was densest on the ventral surface and extended for 300-550 μm. In 3 cases, occasional axons were also seen on the dorsal implant surface. Myelin sheaths surrounding some of the regenerating axons had PNS characteristics, suggesting that they were formed by the implanted Schwann cells, but most of the myelin appeared to be of central origin. The data suggest that Schwann cells placed just caudal to the dLGN and adjacent to lesioned retinal axons can enhance and direct the regrowth of these axons in the rat optic tract.

The development of synaptic junctions in rat occipital cortex has been studied at 7 and 20 days postnatal in control and undernourished animals. In addition, adult control cortex has been compared with cortex derived from animals undernourished until 35 days postnatal and then nutritionally rehabilitated. Emphasis has been placed on material stained with phosphotungstic acid (E-PTA technique) although osmicated material has been examined. The body weights of the undernourished animals were lower than those of their age-matched controls, the deficit at 20 days being 55%. The number of synaptic junctions per unit area of the molecular layer was lower in the undernourished animals at 7 and 20 days, the most prominent deficit being at 20 days. In an attempt to detect ultrastructural correlates of undernutrition, E-PTA stained synaptic junctions were divided into 5 types (A-E), based upon their presynaptic characteristics are reflecting varying degrees of maturity. During normal development the immature synaptic types, particularly type E, are predominant, giving way to the more mature types (A-C) as development proceeds. Undernutrition however, appears to disrupt this developmental sequence, with a higher than normal percentage of immature synaptic types present at the age studied. Nutritional rehabilitation rectifies the imbalance to a degree, the adult rehabilitated pattern resembling the 20-day control pattern. Preliminary examination of the 20-day osmicated material confirmed the deficit of synapses per area of tissue in the undernourished cortex. It also revealed decreases in the number of vesicles per terminal unit area and in the internal area of the synaptic vesicles in the undernourished tissue.

Morphological variation of the synaptic active zone during later development and maturation (15-224 days) has been studied in the molecular layer of the rat occipital cortex. Both E-PTA stained and osmicated tissue have been used. In the E-PTA stained material the degree of specialization of the presynaptic thickening is directly related to junction length. Junctions with well-developed dense projections (Types A and B) are longest and continue to increase in length with maturation, suggesting that active remodelling of the synaptic apposition is an ongoing process. The presence of perforated junctions, possessing two or more regions with specializations of different maturity and different curvature, raises the possibility that these junctions may arise by the addition and differentiation of new paramembranous material at an existing junction. In osmicated tissue, presynaptic terminals possessing multiple active zones have been quantitated. The maturational increase in number of simple perforated junctions (Type 1), is paralleled by a smaller increase in the number of multiple perforated junctions (Type 2). A spine apparatus is frequently observed in these perforated terminals, suggesting that it is intimately involved in the reorganization. The direction of curvature of the closely apposed junctions is predominantly negative (indenting the postsynaptic process). Other types of arrangement, with separate postsynaptic processes, are described (Types 3-5), and micrographs suggestive of sequential stages in pre- and postsynaptic terminal splitting are presented. The total length of the postsynaptic thickening of perforated terminals is twice the mean synaptic length of non-perforated terminals, again suggestive that duplication of the active zone may have occurred. Division of existing synaptic terminals by duplication and subsequent splitting would readily account for the increased dendritic spinal numbers seen in Golgi preparations of animals raised under enriched conditions. This would be a straight-forward mechanism by which reinforcement of neuronal connections could occur in response to use.

Quantitative ultrastructural technique were employed to compare the development and maturation of cortical synapses in rats subjected to protein deprivation, control diet, nutritional rehabilitation and a normal-low crossover diet. Osmicated preparations of the molecular layer of occipital cortex were prepared at 15, 20, 28, 75 and 224 days postnatal in male rats. At 15 and 30 days the values for mitochondrial and synaptic densities, vesicle number and packing per terminal, synaptic length, terminal area and brain weight were lower in the protein-deprived than in the control animals. These initial deficits were progressively transformed to excesses, with the most marked crossover period occurring between 20 and 28 days. By 224 days only brain weight and presynaptic terminal area were lower in the protein-deprived material. A further parameter, synaptic curvature, showed a decrease in negativity in protein-deficient junctions between 15 days (64%) and 224 days (41%). Well-nourished tissue had fewer negatively-curved synapses during early development. These data suggest that the morphological development of the presynaptic terminals is not simply delayed, but is ultimately different in the protein-deprived animals. The nature of these changes may facilitate an adaptation to provide more efficient functioning in the adverse condition. Nutritionally rehabilitated tissue ultimately approaches the control, although significant differences occur in synaptic and mitochondrial densities and in brain weight. The normal--low crossover procedure intensities the differences noted in animals subjected to continuous deprivation.

Glial-connective tissue membranes which form bridges over lesion cavities in the brachial and pretectal region of the rat visual system contain regenerated myelinated and unmyelinated axons. The lesions were made between 10 and 16 days postnatal--a time at which neonatal regeneration would not be expected. A detailed ultrastructural study of these membrane bridges has been undertaken in order to describe the cellular and extracellular conditions that are associated with the regeneration, myelination and continued survival of identified retinal and other axons. The lesion-induced membrane bridges possessed a limiting surface of fibroblasts and were composed of glial cells, macrophages, endothelial cells, pericytes and collagen. There was some variability in the ultrastructural appearance of the glial cells; the majority of criteria indicate that they were astrocytes. These astrocytes formed 'glia limitans'-like surfaces beneath the fibroblasts. They contained numerous filaments and extended fine, electron-dense cytoplasmic processes, often arranged into lamellated stacks. Basal lamina was present on the outer surfaces of the astrocytes. Astrocytic processes isolated clusters of myelinated and unmyelinated axons in lacunae which may have served as conduits for axonal elongation. This suggests a role for these astrocytes in the regeneration and maintenance process which appears to recapitulate events which occur during normal development. Interestingly, regrowing retinal axons were never found adjacent to astrocytic surfaces possessing a basal lamina. We did not detect evidence of Schwann cell invasion into the lesion. By ultrastructural criteria the myelin ensheathment which occurred on the larger axons in the membrane bridge was of central rather than peripheral type. The cytoplasmic domain external to the sheath was limited to a small tongue; no basal lamina invested the fibre; and the periodicity of the myelin was equivalent to that of other CNS structures. Similarly, the CNS character of the myelin was demonstrated by intense immunostaining of myelin sheaths for myelin basic protein and proteolipid [corrected] protein and lack of staining for the PNS component PO. The oligodendrocytes responsible for this myelination may either have extended cytoplasmic processes from the adjacent neuropil, or may have differentiated from precursor cells within the membrane bridge.

The molecular layer of rat occipital cortex was studied at a number of ages throughout postnatal development in an attempt to a formulate a quantitative morphogenetic scheme of synaptic development. As previous work had pointed to the potential usefulness of E-PTA stained material in synaptogenic studies, this technique was employed. Synaptic junctions were assigned to five categories, A-E, on the basis of variations in the organization of their presynaptic densities. Of these categories, Type A represented a mature junctional form with well-defined and discrete dense projections. Type E, by contrast, represented the immature end of the spectrum, its presynaptic apposition generally lacking recognizable densities. Types B-D represented intermediate forms. As development proceeded, the percentage of A type junctions increased from 0.3% at 7 days to 25% in the adult. Type E junctions showed the opposite trend falling from 42% at 7 days to 5% in the adult. On the basis of these results, and those relating to types B-D, possible morphogenetic schemes involving the five synaptic categories are put forward. These schemes incorporate and extend those previously suggested by other workers. By placing observations on a quantitative footing, the schemes proposed here lend themselves to use in experimental investigations.

Developing blood vessels in rat cerebral cortex were studied at a number of stages between 3 and 28 days postnatal, in an attempt to obtain data on the mechanisms by which the lumen is established within cords of mesodermal cells. A combination of techniques was utilized in an attempt to elucidate these mechanisms. These were: (a) aldehyde fixation and block staining with phosphotungstic acid; (b) aldehyde perfusion followed by perfusion of a lead solution and post-fixation in osmium tetroxide; (c) conventional preparation of tissue with aldehyde and osmium fixation. Support for interendothelial lumen formation was readily forthcoming, including vessels with junctions between two or more endothelial cells cut transversely. There was some support for intraendothelial lumen formation, in the form of "seamless" endothelial cells. Other features noted included the presence of free ribosomes and vacuoles in the endothelial cells, endothelial flaps, sprouts and tendrils, intraluminal debris, endothelial degeneration and a junction with a nonendothelial cell. Large numbers of endothelial vacuoles were noted, many of them occurring at the abluminal edge of the cells. These vacuoles may be involved in the formation of intraendothelial lumina and also in the enlargement of both types of lumina. This study provides evidence that besides the well-established interendothelial lumen formation, intraendothelial mechanisms may also be operative in rat cerebral cortex. The techniques employed in this study offer the potential for clarifying these and related issues.

The development and maturation of synapses in the molecular layer of the occipital cortex of rats at 15, 20, 28, 75 and 224 days postnatal were examined and quantitative ultrastructural techniques were employed. The parameters evaluated display a diverse set of trends. A steady increase in mean terminal area is noted, the proportions of the smallest terminals declining progressively over this period. The mean length of the postsynaptic thickening fluctuates throughout the developmental series. A close association is found between terminal area and junction lengthlarger junction lengths being consistently associated with larger areas. Synaptic vesicle numbers within each terminal increase markedly between 15 and 28 days. There is an increase in the frequency of flat and positively curved junctions with increasing age, the bimodal distribution of negative and positive curvatures at 15 days being replaced by a normal distribution in the adult. When synaptic length is compared with curvature, flat junctions emerge as the longest and the most highly curved junctions as the shortest. The terminal areas of positive junctions are greater than those of negative ones. The consequences of these results for the flat disc model of synapses are discussed, and it is postulated that negatively curved synaptic junctions may be non-functional.

Suction lesions of the left rostral superior colliculus (SC) and pretectal area were made in young rats. One to 50 days later, the right eye of each animal was injected with horseradish peroxidase (HRP). Animals were subsequently perfused and the brains processed with tetramethylbenzidine. In many older animals, lesioned areas were covered with thin membranes composed of glial and connective tissue cells. HRP-labelled optic axons were traced running through these membranes for up to 3 mm. On occasion, regrowing retinal fibres reached the rostral border of the remaining SC but did not grow into the tectal neuropil.

Visual thalamocortical projections of neonatally enucleated and control rats were studied after tracer injections into the striate and peristriate areas of adult pigmented rats. The distribution of retrogradely labeled neurons in the visual thalamic nuclei was mapped after (a) small localized injections of horseradish peroxidase into either area 17, 18, or 18a and (b) simultaneous injections of three different retrograde tracers (fast blue, HRP, and diamidino yellow) into the anterior, medial, and posterior regions of area 17. It was shown in both normal and neonatally enucleated rats, that the dorsal lateral geniculate nucleus projects to the striate cortex (area 17), whereas the laterodorsal thalamic nucleus of the lateral thalamus projects to the medial peristriate area 18, and the lateral posterior thalamic nucleus has a projection to the lateral peristriate area 18a. Additionally, both extrageniculate visual thalamic nuclei project to area 17. Neurons in the dorsoanterior region of the dorsal lateral geniculate nucleus project to the posterior part of area 17, while neurons in the ventroposterior region of the nucleus send their axons to the anterior part of area 17. A similarly inverted projection of anterior and posterior divisions of the lateral posterior thalamic nucleus to visual area 18a was detected. In enucleated rats, the general topography of the projections from the thalamic neurons to the striate and peristriate cortices was indistinguishable from that in the controls. Nonetheless, there was noticeable shrinkage of the dorsal lateral geniculate nucleus and lateral thalamus and a significant decrease in the size of the somata of projecting neurons. Mean somal area of the HRP-labeled neurons in the dorsal lateral geniculate nucleus of enucleated rats was reduced by 19.0% and the mean maximum cell diameter by 14.3% compared with controls.