Six commercial hatcheries were visited in the United Kingdom, three of which processed laying hen chicks and three of which processed broiler chicks. The accelerations experienced by the chicks passing through the handling systems were evaluated using miniature data logging accelerometers, which were sent through the systems. The lengths, speeds, and heights of drops of the pathways within each system were also measured. The response of the chicks to the handling was measured in terms of mortality, orientation, righting time (as a measure of disorientation) and tonic immobility. The study showed there to be a range in the physical severity of handling across the hatcheries that could also be seen in terms of differences in the measurements made on the chicks. Nonetheless, the welfare of the chicks passing through the automated systems appeared to be generally acceptable. However, given the velocities and accelerations within these handling systems, there is scope for considerable damage to the chicks, and for poor welfare, if systems are not properly set up or maintained.

Studies into the mechanisms underlying the active emmetropization process by which neonatal refractive errors are corrected, have described rapid, compensatory changes in the thickness of the choroidal layer in response to imposed optical defocus. While high frequency A-scan ultrasonography, as traditionally used to characterize such changes, offers good resolution of central (on-axis) changes, evidence of local retinal control mechanisms make it imperative that more peripheral, off-axis changes also be tracked. In this study, we used in vivo high resolution spectral domain-optical coherence tomography (SD-OCT) imaging in combination with the Iowa Reference Algorithms for 3-dimensional segmentation, to more fully characterize these changes, both spatially and temporally, in young, 7-day old chicks (n = 15), which were fitted with monocular +15 D defocusing lenses to induce choroidal thickening. With these tools, we were also able to localize the retinal area centralis, which was used as a landmark along with the ocular pectin in standardizing the location of scans and aligning them for subsequent analyses of choroidal thickness (CT) changes across time and between eyes. Values were derived for each of four quadrants, centered on the area centralis, and global CT values were also derived for all eyes. Data were compared with on-axis changes measured using ultrasonography. There were significant on-axis choroidal thickening that was detected after just one day of lens wear (∼190 µm), and regional (quadrant-related) differences in choroidal responses were also found, as well as global thickness changes 1 day after treatment. The ratio of global to on-axis choroidal thicknesses, used as an index of regional variability in responses, was also found to change significantly, reflecting the significant central changes. In summary, we demonstrated in vivo high resolution SD-OCT imaging, used in combination with segmentation algorithms, to be a viable and informative approach for characterizing regional (spatial), time-sensitive changes in CT in small animals such as the chick.

During chick embryo development, there exists an antioxidant-oxidant balance in the tissues, which supports normal embryonic development and post-hatch chick viability. This balance is maintained by natural antioxidants including vitamins A, E, C and carotenoids, glutathione peroxidase (GSH-PX), catalase (CAT) and superoxide dismutase (SOD). Chick viability is an important factor in determining post-hatch health and profitability. Factors that interrupt growth and development during the embryonic period affect the overall performance and health during the post-hatch period. During the 21-day incubation period for chickens, antioxidant defence systems protect the embryo against the lipid peroxidation (LPO) derived from undesirable conditions. The purpose of this review is to explain the antioxidant mechanisms that contribute to chick embryo development resulting in a healthy hatchling.

Glutamate, which is one of the most important contributors to oxidative metabolism in the intestinal mucosa, is mainly transported by the excitatory amino acids transporters (EAATs) that are expressed in enterocytes. The objective of this study was to evaluate the effects of in ovo administration of l-trans pyrrolidine-2,4-dicarboxylic acid (l-trans-PDC), a potent competitive inhibitor of glutamate uptake by EAATs, on the growth of the small intestine in chicks. Two series of experiments were conducted with hatching eggs; 100 μl of various l-trans-PDC solutions (0, 0.075 or 0.225 mg/egg for the Control group, low-dose l-trans pyrrolidine 2,4-dicarboxylic acid group (L-PDC) or high-dose l-trans pyrrolidine 2,4-dicarboxylic acid group (H-PDC), respectively) was injected into the albumen sac of these hatching eggs before incubation. Hatchlings were sacrificed by cervical dislocation to determine the embryonic development in Experiment I, whereas the birds in Experiment II were raised or sampled at hatching, days 7 and 14 (D7 and D14) for further study. Gene expression in the small intestines was determined by real-time RT-PCR; and serum concentration of free amino acids was determined by an amino acid analyzer. The results showed that the hatchability was decreased by in ovo administration of l-trans-PDC. The small intestinal weights of the H-PDC group were decreased (P<0.05) at hatching and increased (P<0.05) on D7 and D14 compared with those in the Control group. In addition, the gene expression of EAAT2 in the completed or segmental small intestines was not changed (P>0.05); EAAT3 gene expression in the duodenum (P<0.05), jejunum (P=0.084) and ileum (P=0.060) on D14 was lower in the H-PDC group than in the Control group. Furthermore, the serum concentrations of free proline, threonine and phenylalanine but not glutamate or aspartate were increased (P<0.06) in H-PDC group. In conclusion, this paper is the first to report that in ovo administration of l-trans-PDC induces small intestinal growth retardation during the embryonic period and catch-up growth after hatching.

The embryonic and immediate post-hatch developmental period represents a significant phase in attaining quality broiler performance at marketing. An efficient transition period from late term embryo to a viable independent chick is necessary to achieve such results. Immediately, post-hatch birds must undergo a shift from egg and embryonic nutrients to exogenous feed. Under practical conditions, many birds have access to feed only 36 to 48 hours after hatching, and during this time body weight decreases, and intestine and muscle development are retarded. In order to overcome these limitations, a continuous feeding process can be established which would supply nutrients to the developing embryo, feed and water to the newly hatched chick within the hatchery, and a highly digestible pre-starter diet at placement. In ovo feeding stimulates intestinal development by enhancing villi, increasing intestinal capacity to digest and absorb nutrients and provides a basis for muscle growth. Immediate access to feed (1 hour after clearing the shell) initiates uptake and growth processes some 24 hours post-ingestion compared to poultry with delayed feed intake. The enhanced growth caused by early feeding improves nutritional maturity of the bird, stimulates yolk utilisation, increases intestinal development, and has long term metabolic effects. Providing highly digestible ingredients in the pre-starter diet increases body weight performance at day seven, and through to marketing. Together, these processes provide appropriate nutrition pre- and post-hatch which can accelerate gastrointestinal development, muscle growth and therefore result in increased performance. This paper will summarise studies dealing with the different approaches to early nutritional strategies in our modern, fast growing broiler.

In this study, the possible role of the retinal enkephalin system in form-deprivation myopia (FDM) in the chick eye was investigated. Daily intravitreal injection of the nonspecific opiate antagonist naloxone blocked development of FDM in a dose-dependent manner, while injection of the opiate agonist morphine had no effect at any dose tested. The ED50 for naloxone (calculated maximum concentration in the vitreous) was found to be in the low picomolar range. The results using receptor-subtype-specific drugs were contradictory. Drugs specific for μ and δ receptors had no effect on FDM. The κ-specific antagonist nor-binaltorphimine (nor-BNI) reduced FDM by about 50% at maximum daily retinal doses ranging between 4 X 10-10 and 4 X 10 -7 M, while the κ-specific agonist U50488 blocked FDM in a dose-dependent manner with an ED50 between 5 X 10-8 and 5 X 10-7 M. Met-enkephalin immunoreactivity (ME-IR) was localized immunocytochemically to a subset of amacrine cells (ENSLI cells) and their neurites in the inner plexiform layer (IPL). As reported previously, ENSLI cells from untreated chick retinas showed a cyclical pattern of immunoreactivity, with increased immunoreactivity in the light compared to the dark. Form-deprivation did not appear to change this pattern. Amounts of preproenkephalin mRNA from normal or form-deprived eyes were approximately the same under all conditions. Daily injection of naloxone, however, did increase ME-IR in the dark. These results suggest that naloxone may affect release of enkephalin from the ENSLI cells. The results as presented are inconclusive with regards to the role of the enkephalin system in FDM. While the κ receptor may participate, there is no conclusive evidence here for a direct effect of opiate receptors. The effect of naloxone on form-deprived eyes may be due to its effect on release of peptides from the ENSLI cells.

The neurotrophins are trophic and mitogenic factors critical for the development of specific classes of neurons in the central and peripheral nervous systems. In the retina, BDNF and NT-3 have been shown to promote the survival of differentiated ganglion cells (Rodriguez-Tebar et al., 1989; De La Rosa et al., 1994). NT-3 has also been demonstrated to support the survival of amacrine cells and facilitates the differentiation of retinal neurons in culture (De La Rosa et al., 1994). Here, we examine immunohistochemically the expression of BDNF and NT-3 proteins, their cognate receptors, trk B and trk C, respectively, and the p75 neurotrophin receptor in the developing chick retina. At E8, the earliest stage of retinal development examined, all of these proteins exhibit diffuse expression throughout the width of the retina, with the strongest reactivity in the innermost layers. A gradual restriction in expression to ganglion cells and amacrine cells, the staining of which is most prominent at E15, is followed by a downregulation of expression with the strongest immunoreactivity persisting in the ganglion cell layer. Overlapping patterns of expression throughout embryonic development indicate a colocalization of the neurotrophins and their receptors, although NT-3 and p75 alone are present in the inner plexiform layer and only p75 is observed in the outer plexiform layer. Although some of the immunoreactivity for BDNF, NT-3, and their receptors in retina may reflect trophic mechanisms operating in association with the optic tectum and isthmo-optic nucleus, the colocalization of ligands and receptors in retina strengthens the assertion that these neurotrophins function locally during development.

In birds, neurons of the isthmo-optic nucleus (ION), as well as “ectopic” neurons, send axons to the retina, where they synapse on cells in the inner nuclear layer (INL). Previous work has shown that centrifugal axons can be divided into two anatomically distinct types depending on their mode of termination: either “convergent” or “divergent” (Ramon y Cajal, 1889; Maturana & Frenk, 1965). We show that cytochrome-oxidase histochemistry specifically labels “convergent” centrifugal axons and target neurons which appear to be amacrine cells, as well as three “types” of ganglion cells: two types found in the INL (displaced ganglion cells) and one in the ganglion cell layer. Labeled target amacrine cells have distinct darkly labeled “nests” of boutons enveloping the somas, are associated with labeled centrifugal fibers, and are confined to central retina. Lesions of the isthmo-optic tract abolish the cytochrome-oxidase labeling in the centrifugal axons and in the target amacrine cells but not in the ganglion cells. Cytochrome-oxidase-labeled ganglion cells in the INL are large; one type is oval and similar to the classical displaced ganglion cells of Dogiel, which have been reported to receive centrifugal input; the other type is rounder. Rhodamine beads injected into the accessory optic system results in retrograde label in both types of cells, showing that two distinct types of displaced ganglion cells project to the accessory optic system in chickens. The ganglion cells in the ganglion cell layer that label for cytochrome oxidase also project to the accessory optic system. These have proximal dendrites that ramify in the outer inner plexiform layer. Neither the target amacrine cells nor either of the displaced ganglion cells are immunoreactive for the inhibitory transmitter gamma aminobutyric acid. At least some of the target amacrine cells may, however, be cholinoceptive: we found that the antibody to the alpha-7 subunit of the nicotinic ACh receptor labels a population of cells in the INL that are similar in location, size, and the presence of labeled bouton-like structures to those we find labeled with cytochrome oxidase. This antibody also labels neurons in the ION proper but not ectopic cells. In conclusion, it appears that cytochrome oxidase may be a marker for “convergent” centrifugal axons and at least one of their target cells in the INL.

We have developed two brain slice preparations for studying tectofugal visual pathways in the chick: conventional, 400-μm slices (“thin slices”), and “thick slices” which encompass the rostral pole of the optic tectum and the contralateral optic nerve. Stimulation was delivered with a bipolar electrode positioned in stratum opticum in thin slices and in the contralateral optic nerve in thick slices. While the latter preparation provided a means of exclusively and unambiguously activating retinal afferents, several lines of evidence also indicated that the evoked field potentials in thin slices were chiefly consequent to retinal afferent excitation: (1) the similarity of evoked field potentials in thin slices to those in thick slice preparations; (2) their precise localization in retinorecipient layers as shown by prelabeling from retina with FITC-coupled cholera toxin; (3) transmission delays appropriate for retinal afferents as established with the thick slice preparation; (4) patterns of labeled afferents resulting from applications of Dil crystals to slices fixed after recording; and (5) the similarity in transmitter pharmacology between thin and thick slice preparations. Pharmacological manipulations carried out with bath-applied antagonists indicated that glutamate is the principal retinotectal transmitter. The broadly active glutamate receptor blocker, kynurenic acid, reversibly eliminated the postsynaptic component of the field potential as confirmed with 0 Ca2+ saline. A complete block was also effected by the non-NMDA antagonists CNQX and DNQX. The specific NMDA antagonist, APS, caused a smaller and variable reduction in response amplitude. The GABA antagonist, bicuculline, caused a prolongation of the monosynaptic field epsp in retinorecipient layers and an enhancement of the long-latency, negative wave in cellular layers below, supporting a late, excitation-limiting role for this inhibitory transmitter.

Although excitotoxins derived from acidic amino acids are known to damage neurons in the inner nuclear and ganglion cell layers of the retina, little is known about their effects on photoreceptors. This study examines the acute and long-term effects of excitotoxins on photoreceptors of the chick retina. The zinc-iodide-osmium (ZIO) technique, which darkly labels a substantial subpopulation of synaptic vesicles in normal photoreceptor terminals, was used to supplement routine electron microscopy. Two-day-old chicks received a single intraocular injection of either 10, 50, or 200 nmoles kainic acid (KA), 200 nmoles N-methyl-D-aspartic acid (NMDA), or 200 nmoles quisqualic acid (QUIS), and were allowed to survive for either 6 h, 7 d, or 21 d. At 6 h, following exposure to 10, 50, and 200 nmoles KA, there was swelling and disruption of photoreceptor lamellae of the outer segments. At 7- and 21-d survival, 50 and 200 nmoles KA resulted in rounded, condensed synaptic terminals, which contained a high density of synaptic vesicles. However, there was complete loss of ZIO-positive vesicles within these photoreceptors. Outer segments were still disrupted, although small patches of lamellae were evident, suggestive of regeneration. Following exposure to QUIS, there was extensive swelling of outer segment lamellae at 6 h survival. Synaptic ribbons in terminals were also swollen. At longer survival periods, QUIS exposure resulted in a reduction of ZIO-positive vesicles, as well as swollen lamellae in outer segments. NMDA exposure, at either short or long-term survival, did not alter photoreceptor morphology, including the pattern of ZIO stain. The prolonged effects of KA, and to a lesser extent QUIS, on photoreceptors suggests that these drugs have a long-term effect on photoreceptor function. The ZIO technique provides a novel and potentially useful approach for identification of damaged photoreceptors.

The impact of practically all the everyday stress factors occurring in the first days of the chick life on the rate of the utilisation of the yolk sac content, on the chicken immune status and on the growth of the animal's body and intestinal masses was investigated. The impact of the stress was investigated during the first five days of chick's life. The chicks were divided into five groups, each comprising 44 birds. The first chick group was exposed to moderate cold (2–3°C below the optimal temperature for the chick age). The second group was exposed to moderate heat (2–3°C above the optimal temperature for the age). The third and fourth group were deprived of feed and drinking water for 12 hours and 24 hour, respectively. The fifth chick group was the control group: the birds in this group had optimal environmental conditions and received feed and drinking water immediately upon entering the trial. Ten chicks were taken every day and weighed. Their blood samples were obtained for the assessment of infectious bursal disease virus antibody titres using ELISA method. After that, the birds were sacrificed, their intestinal masses weighed and the quantity of resorbed yolk measured.

The greatest body and intestinal masses were found in the control animals. The body and intestinal masses were the lowest in the group which was denied water and food for 24 hours. The resorption of the yolk sac content was approximately equal in all the chick groups, but the resorption rate varied by days. The highest resorption was observed in the chick groups on the day when feed was denied to them, so that this high resorption could be associated with the bird's body energy requirements. The resorption of the remaining yolk is associated with feed intake: in chicks to which feed is withheld the yolk is resorbed through the yolk sac wall directly into the blood, which increased its usability. When energy requirements are not satisfied, the chick's body probably utilises resorbed antibodies from the yolk remnants, as their glycoprotein composition is suitable for this purpose.

Myopia is increasing in prevalence world-wide, nearing epidemic proportions in some populations. This has led to expanded research efforts to understand how ocular growth and refractive errors are regulated. Eye growth is sensitive to visual experience, and is altered by both form deprivation and optical defocus. In these cases, the primary targets of growth regulation are the choroidal and scleral layers of the eye that demarcate the boundary of the posterior vitreous chamber. Of significance to this review are observations of local growth modulation that imply that the neural retina itself must be the source of growth-regulating signals. Thus the retinal pigment epithelium (RPE), interposed between the retina and the choroid, is likely to play a critical role in relaying retinal growth signals to the choroid and sclera. This review describes the ion transporters and signal receptors found in the chick RPE and their possible roles in visually driven changes in eye growth. We focus on the effects of four signaling molecules, otherwise implicated in eye growth changes (dopamine, acetylcholine, vasoactive intestinal peptide (VIP), and glucagon), on RPE physiology, including fluid transport. A model for RPE-mediated growth regulation is proposed.

Confocal microscopy allows for optical sectioning of tissues, thus obviating the need for physical sectioning and subsequent registration to obtain a three-dimensional representation of tissue architecture. However, practicalities such as tissue opacity, light penetration, and detector sensitivity have usually limited the available depth of imaging to 200 μm. With the emergence of newer, more powerful systems, we attempted to push these limits to those dictated by the working distance of the objective. We used whole-mount immunohistochemical staining followed by clearing with benzyl alcohol-benzyl benzoate (BABB) to visualize three-dimensional myocardial architecture. Confocal imaging of entire chick embryonic hearts up to a depth of 1.5 mm with voxel dimensions of 3 μm was achieved with a 10× dry objective. For the purpose of screening for congenital heart defects, we used endocardial painting with fluorescently labeled poly-L-lysine and imaged BABB-cleared hearts with a 5× objective up to a depth of 2 mm. Two-photon imaging of whole-mount specimens stained with Hoechst nuclear dye produced clear images all the way through stage 29 hearts without significant signal attenuation. Thus, currently available systems allow confocal imaging of fixed samples to previously unattainable depths, the current limiting factors being objective working distance, antibody penetration, specimen autofluorescence, and incomplete clearing.

Based on studies of the molecular and cellular cascades that occur during memory consolidation for a one-trial passive-avoidance learning task in the young chick, I review the evidence that memory is encoded in permanent changes in synaptic connectivity in a specific brain region, the Hebb hypothesis. I conclude that despite the fact that such a cascade occurs, culminating in the synthesis of cell-adhesion molecules that are involved in synaptic remodelling, synaptic events are not in themselves sufficient to account for the phenomena of memory. Both whole brain (neuromodulator) and whole body (hormonal) processes are engaged. Memories are labile, disarticulated and stored in a distributed manner; how the mind/brain recreates coherent memories from this pattern is a mystery.

To accommodate the rapid transition to external nutrients, the chick's gastrointestinal tract undergoes dramatic changes within the first few days of life. These include a rapid increase in mass, villi number and length, enterocyte number, crypt depth and proliferating cells. Concomitant with the development of digestive structures and functions a rapid development of the gut associated lymphoid tissue (GALT) occurs. This lymphoid system works within and in concert with digestive tract parenchyma, however, there is little information describing the normal development and immunological function of the avian GALT in the immediate post-hatch period. The purpose of this review is to summarize current knowledge on the structure and function of the avian GALT during the early post-hatch period. At hatch, the gut is poorly populated by both innate immune leukocytes and lymphocytes. The basal numbers of lymphocytes are the result of early waves migrating from the thymus and bursa of Fabricius. Further waves of lymphocyte migration occur after 4 days of life and continue intermittently with time. In concert with this pattern of lymphocyte population adaptive immunity develops. Hence, the gut of the hatchling is unprotected by adaptive immunity during the first few days of life. Protection during this critical period might be the result of maternal antibody activity or that of the innate immune system. This system appears to be functional at this time, though much work is needed to establish this possibility. Upon maturity of the immune system, most of the immunological activity within the chick GALT is concentrated in the hindgut, and specifically so in the caeca and bursa of Fabricius. Once immune responses have become established the relevant cells disseminate systemically and to other areas of the small intestines. Finally, observations on the beneficial effects of early feeding on development of gut and GALT are discussed with reference to management of hatchlings.

Ingestion of carbohydrates from the small intestine is the major route of energy supply in animals. In mammals these functions develop both pre- and postnatally and are coordinated for the sucking period. In birds, the physiological requirements are different and hatchlings ingest diets rich in complex carbohydrates soon after hatching. The present study examined the ontogeny of intestinal carbohydrate uptake in the chicken. The expression of mRNA for a brush border enzyme, sucrase–isomaltase (SI), which is critical in disaccharide digestion, was determined, together with that of the Na–glucose transporter (SGLT)-1, which is the major apical glucose transporter, In addition, the homeobox gene cdx, which is involved in inducing SI expression in mammals was examined. It was found that the expression of cdxA mRNA and cdxA protein increased from day 15 of incubation until hatch, after which further changes were small. CdxA protein was shown to bind to the promoter region of SI in the chick indicating that cdxA is similar to the mammalian cdx2. The mRNA of SI was observed at 15 d incubation, increased from 17 d of incubation to a peak on day 19, decreased at hatch and had a further peak of expression 2 d post-hatch. In contrast, the mRNA of SGLT-1 was not detected until 19 d of incubation when a major peak of expression was observed followed by a decrease to low levels at hatch and small increases post-hatch. It appears that both SI and SGLT-1 mRNA are expressed before hatch in the chick, but the ontogeny of expression is controlled by different mechanisms.

Hatching birds which have been dependent on the yolk for their energy supply during much of the embryonic period must undergo a rapid transition to utilising carbohydrate rich exogenous feed. This change is accompanied by the preferential growth of the small intestine and activation of digestive enzymes and absorption pathways. The ontogeny of these processes is described and includes the intense development immediately after hatching. The effect of delayed access to feed on intestinal development is also discussed.

The small intestines of hatching chicks undergo rapid developmental changes in the immediate post-hatch period when the birds are making the transition from endogenous nutrient supply from yolk to dependence on exogenous feed. This transition usually only begins 48 h or more after hatching, owing to logistical considerations of production. The effects of fasting for 48 h at different times during this critical period on small intestinal development and enterocyte dynamics were examined by morphometric determinations and use of staining for proliferative-cell nuclear antigen and 5-bromo-2-deoxyuridine. The effects of fasting were specific to both time of fasting and the intestinal segment examined. Decreased development was found in the duodenum and jejunum, but was less apparent in the ileum. Fasting between 0 and 48 h decreased crypt size in the duodenum and jejunum, the number of crypts per villus, crypt proliferation, villus area and the rate of enterocyte migration. Fasting at later times resulted in smaller effects, although the jejunum appeared to be the most sensitive of the intestinal segments. Growth was correlated with the number of cells in the crypts, the number of cells along the villus and the segment surface area. The common practice whereby feed is first available to chicks more than 48 h post-hatch may depress subsequent development.

The role of diet on the growth, survival and movement of red grouse Lagopus lagopus scoticus chicks was examined. We compared two areas of moorland in Scotland: a dry heath with a low density of red grouse and poor chick survival; and a wetter heath/bog with relatively higher red grouse numbers and higher rates of chick survival. There were no differences in clutch size or the proportion of eggs hatching between the two moors but brood survival was significantly lower on the dry heath. Radio-tagged hens with broods were monitored during the first 12 days following hatching; the chicks were captured, weighed and faecal samples collected. Invertebrate samples were collected within brood feeding ranges. Analysis of chick faeces was used to identify dietary components. Heather comprised the major dietary component on both moors. Invertebrates formed a higher component of diet on the wet moor, and this was positively correlated with growth rates, which in turn were positively correlated with chick survival. We present data from an experiment carried out in 1982, in which chicks showed higher growth rates with increasing insect availability. We also show that broods in which all the chicks survived (4–10 days) had smaller home-range areas than broods in which some of the chicks died during this period. We suggest that the differences in chick survival between the two populations were the result of variations in the abundance of invertebrates, particularly tipulids. The protein provided by a high invertebrate component in the diet is, therefore, an important determinant of the growth and survival of young red grouse chicks in some areas.

Ostrich chick production is highly management intensive. An artificial production system should be able to provide adequate protection to ostrich chicks up to four weeks of age. Factors influencing the successful growth of chicks include the provision of proper housing, adequate ventilation, exemplary hygiene and correct dietary requirements. Inadequate nutrition is commonly the cause of microbial infections. It is important for the producer to do an accurate on-farm cost management appraisal, the greatest variable production cost being feed. There is need to generate more finance for further research on ostrich chicks, and the development of an integrated system between producers, ostrich producer associations and industry in order to maximise productivity and economies of scale.