Sixth Postnatal Day Research Articles

Effects of Nicotine Administration in an Enriched Environment on the Behavior of Male MK-801-Exposed Rats.

Smoking is more common in patients with schizophrenia than in healthy populations. Some controversial hypotheses connect the disease with the high prevalence of smoking. Moreover, environmental factors affect the severity of the positive and negative symptoms of schizophrenia. The current study aimed to assess the effect of enriched environment (EE) and nicotine on the MK-801 animal model of schizophrenia. Male Wistar rat pups randomly received saline or MK-801 (dose:1 mg/kg) for five days from the sixth postnatal day (P) until the tenth. The pups were placed in EE or standard cages (SCs) after weaning (P21). Morris water maze (MWM) was used to assess spatial learning and memory. The rats received 0.6 mg/kg nicotine twice for three days at the end of the second month and were examined in an open-field box and three-chamber social interaction test. MK-801 rats' behaviors were the same as those of the saline rats when they were exposed to nicotine. No positive effects of EE were observed when the animals were exposed to nicotine. The results suggested that nicotine decreased schizophrenia-like symptoms and covered the positive effects of EE.

Low dose paracetamol for management of patent ductus arteriosus in very preterm infants: a randomised non-inferiority trial

ObjectiveTo compare the efficacy of low dose-short course intravenous paracetamol with a conventional dose regimen for early targeted closure of patent ductus arteriosus (PDA).DesignSingle-centre, double-blinded, active controlled, randomised non-inferiority trial.SettingLevel...

Propofol and Sevoflurane Anesthesia in Early Childhood Do Not Influence Seizure Threshold in Adult Rats.

Experimental studies have demonstrated that general anesthetics administered during the period of synaptogenesis may induce widespread neurodegeneration, which results in permanent cognitive and behavioral deficits. What remains to be elucidated is the extent of the potential influence of the commonly used hypnotics on comorbidities including epilepsy, which may have resulted from increased neurodegeneration during synaptogenesis. This study aimed to test the hypothesis that neuropathological changes induced by anesthetics during synaptogenesis may lead to changes in the seizure threshold during adulthood. Wistar rat pups were treated with propofol, sevoflurane, or saline on the sixth postnatal day. The long-term effects of prolonged propofol and sevoflurane anesthesia on epileptogenesis were assessed using corneal kindling, pilocarpine-, and pentylenetetrazole-induced seizure models in adult animals. Body weight gain was measured throughout the experiment. No changes in the seizure threshold were observed in the three models. A significant weight gain after exposure to anesthetics during synaptogenesis was observed in the propofol group but not in the sevoflurane group. The results suggest that single prolonged exposure to sevoflurane or propofol during synaptogenesis may have no undesirable effects on epileptogenesis in adulthood.

Excess of glucocorticoids during late gestation impairs the recovery of offspring's β-cell function after a postnatal injury.

Since prenatal glucocorticoids (GC) excess increases the risk of metabolic dysfunctions in the offspring and its effect on β-cell recovery capacity remains unknown we investigated these aspects in offspring from mice treated with dexamethasone (DEX) in the late pregnancy. Half of the pups were treated with streptozotocin (STZ) on the sixth postnatal day (PN). Functional and molecular analyses were performed in male offspring on PN25 and PN225. Prenatal DEX treatment resulted in low birth weight. At PN25, both the STZ-treated offspring developed hyperglycemia and had lower β-cell mass, in parallel with higher α-cell mass and glucose intolerance, with no impact of prenatal DEX on such parameters. At PN225, the β-cell mass was partially recovered in the STZ-treated mice, but they remained glucose-intolerant, irrespective of being insulin sensitive. Prenatal exposition to DEX predisposed adult offspring to sustained hyperglycemia and perturbed islet function (lower insulin and higher glucagon response to glucose) in parallel with exacerbated glucose intolerance. β-cell-specific knockdown of the Hnf4α in mice from the DS group resulted in exacerbated glucose intolerance. We conclude that high GC exposure during the prenatal period exacerbates the metabolic dysfunctions in adult life of mice exposed to STZ early in life, resulting in a lesser ability to recover the islets' function over time. This study alerts to the importance of proper management of exogenous GCs during pregnancy and a healthy postnatal lifestyle since the combination of adverse factors during the prenatal and postnatal period accentuates the predisposition to metabolic disorders in adult life.

The Effects of Hesperidin on Neuronal Apoptosis and Cognitive Impairment in the Sevoflurane Anesthetized Rat are Mediated Through the PI3/Akt/PTEN and Nuclear Factor-κB (NF-κB) Signaling Pathways.

BackgroundHesperidin (HPD) is a bioflavonoid found in citrus fruits. This study aimed to investigate the effects of HPD on cerebral morphology and cognitive behavior in sevoflurane anesthetized neonatal rats and the molecular mechanisms involved.Material/MethodsSixty neonatal Sprague–Dawley rats were divided into five groups, including the untreated control group, and the sevoflurane anesthesia groups untreated and treated with 25 mg/kg/day of HPD (HPD25), 50 mg/kg/day of HPD (HPD50), and 100 mg/kg/day of HPD (HPD100). The rat model was created by the administration of sevoflurane on the sixth postnatal day (P6) and for a further three days. Neonatal rats pre-treated with HPD for 19 days were given sevoflurane 30 minutes beforehand (P3 to P21). Rat hippocampal tissue specimens were investigated using the TUNEL assay for apoptosis. Hippocampal tissue homogenates underwent Western blot for the quantification of markers of neuroinflammation and oxidative stress. The neonatal rats were also investigated for behavior, learning, and memory.ResultsHPD significantly reduced sevoflurane-induced neuronal apoptosis and protein expression of cleaved caspase-3, BAD, BAX, NF-κB, TNF-α, IL-6, and IL-1β (p<0.05). HPD significantly increased the expression of Bcl-xL and Bcl-2 (p<0.05), and activated the PI3/Akt pathway. Learning and memory were significantly improved following HPD treatment (p<0.05). HPD treatment modulated the PI3/Akt/PTEN and NF-κB signaling pathways, and reduced oxidative stress (p<0.05).ConclusionsIn the sevoflurane anesthetized neonatal rat model, treatment with HPD reduced neuronal degeneration, hippocampal inflammation, and improvised memory, learning, and cognitive responses by modulating the PI3/Akt/PTEN and NF-κB signaling pathways.

Increased risk of refeeding syndrome-like hypophosphatemia with high initial amino acid intake in small-for-gestational-age, extremely-low-birthweight infants.

BackgroundRecent nutrition guidelines for extremely-low-birth-weight infants (ELBWIs) recommend implementation of high initial amino acid (AA) supplementation in parenteral nutrition.ObjectiveWe sought to evaluate the influence of AA intake on refeeding syndrome–like electrolyte disturbances including hypophosphatemia in ELBWIs.Study designMedical records of 142 ELBWIs were reviewed. Demographic, nutritional, outcome, and electrolyte data were compared between ELBWIs with initial low (1.5 g/kg/day) and high (3 g/kg/day) AA intake. Multivariate analysis was conducted to determine the odds ratio of hypophosphatemia with high AA intake and small-for-gestational-age (SGA) ELBWIs.ResultsThe incidence of hypophosphatemia and severe hypophosphatemia increased from 51% and 8% in period I to 59% and 20% in period II, respectively (p = 0.36 and < 0.01). Specifically, SGA ELBWIs showed higher incidence of hypophosphatemia than appropriate-for-gestational age (AGA) ELBWIs in period II, whereas there was no difference in period I. For severe hypophosphatemia, SGA ELBWIs presented a 27% incidence versus a 2% incidence in AGA ELBWIs, even with low initial AA intake. Despite no difference in phosphate intake between infants with and without hypophosphatemia, serum phosphate level reached a nadir at the sixth postnatal day and gradually recovered over the second week in infants with hypophosphatemia. In multivariate analyses, the odds ratios for severe hypophosphatemia were 3.6 and 6.6 with high AA intake and SGA status, respectively, with the highest being 18.0 with combined high AA intake and SGA status.ConclusionsIn summary, high initial AA intake significantly increased the risk of refeeding syndrome–like electrolyte dysregulations including severe hypophosphatemia in ELBWIs. In SGA ELBWIs, the risk of electrolyte disturbance was significantly higher, even with low initial AA intake. Therefore, new tailored parenteral nutrition protocols starting with lower energy intake and a gradual increase over the first week may be warranted for application in high-risk SGA ELBWIs.

Case 1: A Well-Growing Neonate with Features of Intestinal Obstruction

A 1,555-g, first of twin female infants is born at 38 4/7 weeks to a 24-year-old primigravida in a vaginal delivery through clear amniotic fluid. The infant is small for gestational age (<10th percentile on the Fenton intrauterine growth chart) with features of intrauterine malnutrition, such as triangular facies and loose skinfolds. The antenatal period is uneventful. The infant needs only basic steps at birth, with Apgar scores of 9, 9, and 9 at 1, 5, and 10 minutes, respectively. In view of the low birthweight, the neonate is transferred to the NICU and placed under the warmer with servo skin mode. Full tube feeding is initiated under observation. The infant passes meconium on the first postnatal day at 18 hours of age and has a normal stool transition. She tolerates feeds well until day 6 after birth, with an expected weight loss of 1.2% per day. On the sixth postnatal day, she has abdominal distention (an increase in girth of 3 cm) with multiple episodes of vomiting. On evaluation, she is found to be euthermic (temperature of 98.9°F [37.2°C]), euglycemic (glucose concentration of 64 mg/dL [3.5 mmol/L]), normocalcemic (calcium concentration of 4.04 mg/dL [1.01 mmol/L]), with no evidence of any systemic illness. Hence, surgical causes like volvulus, Hirschsprung disease, meconium ileus, and acute/subacute intestinal obstruction are the …

Incomplete pentalogy of Cantrell: a case report

Pentalogy of Cantrell is a rare congenital syndrome with an estimated incidence of 5.5 per 1 million live births. It is characterized by defects involving the supra-umbilical abdominal wall, lower sternum, anterior diaphragm, pericardium, and the intracardiac anomalies. The condition is believed to be caused by a failure in development of the lateral mesoderm, which occurs when the embryo is about 14–18 days old. The full spectrum of the syndrome is rare while incomplete expression of the syndrome and its variants are well-recognized. We described a neonate with a normal karyotype, diagnosed before birth as an incomplete pentalogy of Cantrell with complex intracardiac defects. The infant died on the sixth postnatal day, two days after surgical intervention to repair the abdominal wall, and diaphragm defects. The distinct findings relevant to pentad including the congenital heart anomalies, TOF type double outlet right ventricle, are highlighted.

Klebsiella pneumoniae Brain Abscess in Neonates: A Report of 2 Cases

Brain abscesses are uncommon in neonates. Klebsiella pneumoniae is a very uncommon microbial agent to cause brain abscess. We report 2 infants with Klebsiella pneumoniae sepsis who developed brain abscesses. One infant was a premature neonate who required mechanical ventilation for respiratory distress syndrome and subsequently developed nosocomial sepsis and brain abscess without evidence of preceding meningitis. Another infant was a full-term neonate without risk factors for sepsis who developed seizures on the sixth postnatal day and was found to have meningitis and brain abscess. Both infants had Klebsiella pneumoniae septicemia with multiple relatively large brain abscesses that responded poorly to antimicrobial agents. These infants were managed with transfontanel drainage and prolonged courses of antimicrobial agents. Key message of this report is that Klebsiella pneumoniae brain abscess may occur in the absence of meningitis and even in the absence of any identifiable risk factors.

Congenital Adrenal Hyperplasia: Diagnosis, Evaluation, and Management

1. Zoltan Antal, MD* 2. Ping Zhou, MD† 1. *Fellow 2. †Assistant Professor, Division of Pediatric Endocrinology, Department of Pediatrics, Albert Einstein College of Medicine, Bronx, NY After completing this article, readers should be able to: 1. Describe the pathophysiology of congenital adrenal hyperplasia (CAH). 2. Characterize the signs and symptoms of CAH. 3. Describe the appropriate laboratory evaluation of CAH. 4. Know that CAH can be diagnosed prenatally. 5. Recognize adrenal insufficiency by laboratory and clinical evaluation. 6. Anticipate and plan treatment for both acute adrenal crisis and long-term therapy for a patient who has CAH. 7. Discuss the value of newborn screening for salt-losing CAH in male infants. Congenital adrenal hyperplasia (CAH) refers to a family of inherited disorders of adrenal steroidogenesis. The common functional defect in each disorder is impaired cortisol secretion, resulting in hypersecretion of corticotropin-releasing hormone (CRH) and adrenocorticotropic hormone (ACTH) and consequent hyperplasia of the adrenal glands. More than 90% of cases of CAH are caused by a defect in the enzyme 21-hydroxylase (21-hydroxylase deficiency [21OHD]). Four other enzyme deficiencies in the steroid biosynthesis pathway, along with one cholesterol transport protein defect, account for the remaining cases. Depending on the severity of the enzyme deficiency, 21OHD is defined as classic (severe form) or nonclassic (mild form). Approximately 75% of patients who have the classic form also have salt wasting due to inadequate aldosterone production, further subdividing the classification into classic simple virilizing and classic salt-wasting forms. This review highlights the diagnosis and treatment of 21OHD, with a brief discussion of the other forms of CAH. A Hispanic baby girl is born at term, has a birthweight of 3.1 kg, and has ambiguous genitalia (Fig. 1). During the first week after birth, the baby is clinically stable but demands frequent feeding. On the sixth postnatal day, serum electrolyte measurements are normal. Additional evaluation reveals female internal organs on pelvic ultrasonography and female karyotype. Newborn screening results show 17-hydroxyprogesterone (17-OHP) values of 180 and 679 ng/mL 2 and 5 days …

Behavioral impairments related to lead-induced developmental neurotoxicity in chicks

Lead intoxication affects the central nervous system and produces structural disorders and behavioral deficits in several animal species. Although lead neurotoxicity is a well-reported phenomenon, studies on the developmental neurotoxicity induced by this metal in avian are scarce. The aim of this study was to evaluate how a single dose of 28 mug lead acetate administered into the yolk sac on the fifth incubation day of Gallus domesticus can affect the behavior and the brain tissue in the first postnatal week. Several behavioral tests, mainly those related to the motor and exploratory functions were evaluated at fifth and sixth postnatal days (PN). The lead deposition into mesencephalon and cerebellum was investigated by autometallography (AMG) method. Congenital anomalies, as failure on closure of body's ventral midline and leg dysfunction, were observed in treated chicks. During the first postnatal week, inactivity and anomalous movements were significantly high in lead treated chicks in comparison to control animals. Lead impregnation was observed in both mesencephalon and cerebellum and the cerebellar molecular layer presented higher lead deposition in comparison to granular layer and Purkinje cells. Our results indicate that the in ovo exposure to lead induces important deficits on motor behavior of chicks during the first postnatal week and such phenomena are related to lead deposition in the cerebellar tissue during embryonic development. The proposed exposure schedule represents an interesting experimental approach for studding behavioral and cellular mechanisms related to lead-induced developmental neurotoxicity.

Index of Suspicion in the Nursery

A 10-day old male infant in the neonatal intensive care unit (NICU) has a small amount of purulent drainage from his right eye, but no other signs of infection. His respiratory rate is 40 to 64 breaths/min, with oxygen saturations of more than 90% in room air and no significant episodes of apnea. His pulse is 140 to 164 beats/min, with no significant episodes of bradycardia, and his temperatures are recorded at 97.7° to 98.1°F (36.5° to 36.7°C) in a heated bed. He is tolerating feedings of expressed human milk through a feeding tube and has gained weight consistently since the sixth postnatal day, although he is still approximately 100 g below birthweight. His only medication is caffeine for apnea of prematurity, which was started on the second postnatal day. The patient was born at 29 4/7 weeks’ gestation to a 35-year-old, G2P1→2 woman who developed preterm labor that was resistant to tocolysis with magnesium and nifedipine. The infant was delivered vaginally and resuscitated in the delivery room with supplemental oxygen via facemask. Apgar scores were 7 at 1 minute and 8 at 5 minutes. His birthweight was 1,660 g. He was admitted to the NICU because of preterm birth and mild respiratory distress syndrome. Laboratory tests upon admission included a complete blood count (CBC) and blood cultures, and ampicillin and gentamicin administration was initiated. His initial CBC revealed a white blood cell count of 14.3×103/mcL (14.3×109/L), with 58% neutrophils, 3% bands, 25% monocytes, and 14% lymphocytes. He received a total of four doses of ampicillin and two doses of gentamicin over the first two postnatal days; antibiotics were discontinued when initial blood cultures showed no growth at 48 hours. He did not require intubation; he was maintained initially on continuous positive airway pressure and then …

Influence of prenatal nicotine exposure on postnatal development of breathing pattern.

To determine if prenatal nicotine exposure alters the postnatal development of the ventilatory pattern and the frequency and duration of apneas, we recorded respiratory airflow with head-out body plethysmography in awake neonates on postnatal days 1, 2, 6, 10, 14, and 18. Data from 12 nicotine-exposed animals were compared with data from 12 saline-exposed animals. Nicotine (6 mg/kg of nicotine tartrate per day) or saline exposure was induced by osmotic minipumps that were implanted subdermally on the fifth day of gestation in Sprague-Dawley Dams. Although both saline- and nicotine-exposed pups gained weight at the same rate throughout the studies, there were subtle differences in ventilatory indices between the two groups. Nicotine-exposed animals had a significantly higher breathing frequency on day 10, and a lower tidal volume on days 14 and 18. Although ventilation tended to be lower in the nicotine-exposed animals, the difference was not significant. There was a significantly higher frequency of apneas in the nicotine-exposed compared with the saline-exposed animals on postnatal days 1 and 2, but the apnea duration did not differ between the groups. No apneas were observed in any of the animals after the sixth postnatal day. Prenatal nicotine exposure is associated with a greater incidence of apneas on the first two postnatal days, and then an altered breathing pattern that manifests at a later stage of development.

Management of the Umbilical Cord

After completing this article, readers should be able to: 1. Describe the most serious infection that may result from inappropriate management of the umbilical cord and potential sources. 2. Describe the relationship between infant bacterial colonization and postpartum infection. 3. List the most common neonatal staphylococcal infections. 4. List the factors that affect the timing of cord separation. 5. Delineate the probable causes of drainage from the umbilical stump. This review addresses several aspects of the care of the umbilical cord: how to ligate and cut it, what (if anything) to apply to it, the problems that may be associated with ligation and cutting, and the natural history of cord separation. The traditional method of ligating the umbilical cord was to use string or twine to tie the cord before cutting it. In Southern Sudan, fine stringlike roots are used to tie the cord. More recently in the United States, special cotton tape (umbilical tape) was used and still is found on most trays used for insertion of catheters into umbilical blood vessels. Because the umbilical cord tends to shrink after birth, these types of ligature proved somewhat unreliable in preventing hemorrhage. Although the umbilical arteries tend to constrict rapidly after birth because of the muscular walls, this does not occur with the umbilical vein. Consequently, more efficient and effective methods of ligation were sought in the middle of the 20th century. The first method was to use constricting rubber bands, which were effective, but somewhat difficult to apply. This method recently found favor in a developing country (Ethiopia). However, the more usual method in developed countries currently is plastic or metal clamps, which produce safe, reliable constriction. In particular, the plastic Hollister® clamp (Double-Grip Umbilical Cord Clamp, Hollister, Libertyville, IL) has been very successful in preventing bleeding from the cord. These devices are removed …

Formation of projection pathways from the arcuate nucleus of the hypothalamus to hypothalamic regions implicated in the neural control of feeding behavior in mice.

The arcuate nucleus of the hypothalamus (ARH) is a critical component of forebrain pathways that regulate a variety of neuroendocrine functions, including an important role in relaying leptin signals to other parts of the hypothalamus. However, neonatal rodents do not lose weight in response to leptin treatment in the same way as do adults, suggesting that certain aspects of leptin signaling pathways in the hypothalamus may not be mature. We tested this possibility by using DiI axonal labeling to examine the development of projections from the ARH to other parts of the hypothalamus in neonatal mice, paying particular attention to the innervation of the paraventricular nucleus (PVH), the dorsomedial nucleus (DMH), and the lateral hypothalamic area (LHA), each of which have been implicated in the regulation of feeding. The results indicate that ARH projections are quite immature at birth and appear to innervate the DMH, PVH, and LHA in succession, within distinct temporal domains. The projections from the ARH to the DMH develop rapidly and are established by the sixth postnatal day (P6), whereas those to the PVH develop significantly later, with the mature pattern of innervation first apparent between postnatal day 8 (P8)-P10. Furthermore, the ability of leptin to activate Fos in the PVH, DMH, and LHA appears to be age-dependent and correlates with the arrival of ARH projections to each nucleus. Taken together, these findings provide new insight into development of hypothalamic circuits and suggest an anatomical basis for the delayed postnatal regulation of food intake and body weight by leptin.

Angiotensin II type 1 receptor A1166C polymorphism and prophylactic indomethacin treatment induced ductus arteriosus closure in very low birth weight neonates.

Altered pulmonary vascular resistance might be a factor for delayed closure of the ductus arteriosus (DA) in preterm infants. Angiotensin II plays a central role in the elevation of pulmonary vascular resistance. Angiotensin II exerts its vasoconstrictor effect on the angiotensin II type 1 receptor (AT1R). Homozygous carriers of the AT1R A1166C genetic variant present an exaggerated vasoconstrictor response to angiotensin II. We have investigated whether the presence of AT1R CC1166 influences the effect of prophylactic indomethacin treatment on the closure of DA until the fifth postnatal day in preterm infants. In this retrospective study detailed medical history of the first postnatal week was obtained in 159 infants born before the 33rd gestational week. All were treated by prophylactic indomethacin to induce permanent closure of the DA. On the sixth postnatal day the DA was still open in 56, whereas it was permanently closed in 103. The AT1R A1166C genotype of the infants was determined from Guthrie spots. Stepwise binary logistic regression analysis was used to assess the effect of medical conditions and genotype on the risk of patent DA (PDA). Birth weight, infantile respiratory distress, and severe hypotension were independent risk factors for PDA (p < 0.01, p < 0.05, p < 0.05, respectively). The carrier state of AT1R CC1166 was protective against PDA (p < 0.05; odds ratio, 0.067). AT1R AC1166 genotype was not associated with PDA. Our results indicate that the risk of PDA might be lower in infants of AT1R CC1166 than in those with AC or AA genotypes.

Transcutaneous bilirubinometry in preterm infants

The aim of this study was to evaluate the accuracy and safety of transcutaneous bilirubinometry in preterm infants using the new bilirubin analyser BiliCheck. The study included 145 preterm children (23-36 wk gestation). Capillary blood sampling for determination of serum bilirubin (BS) was combined with transcutaneous bilirubin measurement (BTc) every morning until the sixth postnatal day and related to several clinical data (phototherapy (PT), infection signs, breathing disturbances, skin bleeding, etc.). Overall bilirubin concentration ranged from 17 to 371 micromol/l, and from 21 to 325 micromol/l for BS and BTc, respectively. Mean values obtained by BTc were significantly higher than BS values. The correlation coefficient between BS and BTc was r= 0.64 for the whole group, and r = 0.73 in infants without PT. As demonstrated by multiple regression analysis, BS-BTc correlations were related only to gestational age (beta -0.32) and breathing disturbances (beta 0.29), indicating that the lower the gestational age and the more seriously ill the baby, the higher the incoherence between BS and BTc. BiliCheck provides a convenient, non-invasive possibility for bilirubin estimation in preterm infants. However, there are limitations: the method gives reliable results only in newborns older than 30 wk gestation, without PT and artificial ventilation.

Congenital diaphragmatic hernia associated with a gastroesophageal duplication cyst: A case report

Severe left congenital diaphragmatic hernia was diagnosed in a baby prenatally, and she underwent hernia repair on the sixth postnatal day of life. She was found to have a huge symptomatic gastroesophageal duplication cyst on day 24 of life. A thoracoabdominal dissection allowed successful cyst excision. J Pediatr Surg 36:626-628. Copyright © 2001 by W.B. Saunders Company.

Chiasmatic specificity in the regenerating mammalian optic nerve.

The mammalian central nervous system is capable of regenerating; however, there is no evidence that the regenerating axons can navigate along their normal pathways and reestablish topographically organized projections: essential for functional return of vision. Here retinal ganglion cells in the opossum Monodelphis were birthdated with tritiated thymidine on the sixth postnatal day (P6), before being lesioned in the temporal retina at P8. Retrograde tracing with horseradish peroxidase injected into the ipsilateral optic tract at P24 showed that the temporal crescent had reformed behind the retinal lesion. By comparisons of cell and thymidine counts from lesioned and control regions of retina, it was estimated that about 40% of the normal number of ganglion cells are able to regenerate into the ipsilateral optic tract following a lesion in the temporal retina at P8. A clear line of decussation (separation of ipsilateral and contralateral projections) reformed in the lesioned temporal retina and regenerating ganglion cells labeled with DiI were turned at appropriate points on passing through the optic chiasm. This is evidence of chiasmatic specificity with regard to lesioned retinal ganglion cells regenerating into the ipsilateral optic tract.

Postnatal Development of Binocular Disparity Sensitivity in Neurons of the Primate Visual Cortex

In macaque monkeys, the age at which neurons in the primary visual cortex (V1) become sensitive to interocular image disparities, a prerequisite for stereopsis, is a matter of conjecture. To resolve this fundamental issue in binocular vision development, we measured the responsiveness of individual V1 neurons in anesthetized and paralyzed infant monkeys as a function of the relative, interocular, spatial phase of dichoptic sine-wave gratings. We found that an adult-like proportion of units were sensitive to interocular image disparity as early as the sixth postnatal day, several weeks before the onset age for stereopsis in monkeys. The ocular dominance distributions of cells in infant monkeys were also indistinguishable from those of adults. Thus, at or only a few days after birth, V1 neurons are capable of combining neural signals from the two eyes as in adults and are sensitive to interocular image disparities. However, the monocular spatial-frequency response properties of these disparity-sensitive units were immature, and their overall responsiveness was far lower than that in adults. During the first 4 postnatal weeks, both the spatial frequency response properties and the peak response amplitude rapidly improved, which resulted in a corresponding increase in the absolute sensitivity of individual units to interocular disparity. The results demonstrate that early binocular vision development in monkeys is not constrained by a paucity of disparity-sensitive V1 neurons but, instead, by the relative immaturity of the spatial response properties and the overall unresponsiveness of existing disparity-sensitive neurons.