Initiation of lipogenic enzyme activities in rat mammary glands.

The activities of acetyl-CoA carboxylase, ATP citrate-lyase and fatty acid synthetase remained low until parturition at 22 days of gestation and increased significantly within 1 day post partum. Administration of progesterone on days 20 and 21 and at parturition abolished the increases for at least 48 h after parturition. Removal of the pups of normal rats prevented the increases in activities of acetyl-CoA carboxylase and ATP citrate-lyase, but not of fatty acid synthetase, and administration of prolactin corticosterone or insulin did not stimulate activity. Tissue from suckled glands in which the ducts had been ligated at parturition showed no increase in the activities of acetyl-CoA carboxylase and ATP citrate-lyase within 24 h, whereas fatty acid synthetase activity was similar to that in the sham-operated contralateral glands. Foetoplacentectomy on day 18 increased the activity of fatty acid synthetase but not of acetyl-CoA carboxylase and ATP citrate-lyase; suckling of these dams by foster pups increased both acetyl-CoA carboxylase and ATP citrate-lyase.     

The effect of progesterone on prolactin stimulation of fatty acid synthesis, glycerolipid synthesis and lipogenic-enzyme activities in mammary glands of pseudopregnant rabbits, after explant culture or intraductal injection.

The activities of lipogenic enzymes, such as acetyl-CoA carboxylase, fatty acid synthetase and glucose-6-phosphate dehydrogenase, and glycerolipid synthesis increased significantly in mammary explants of 11-day-pseudopregnant rabbits in response to prolactin, in the presence of near-physiological concentrations of insulin and corticosterone in culture. Increasing the concentration of progesterone in culture resulted in suppression of glycerolipid synthesis and activities of acetyl-CoA carboxylase and fatty acid synthetase, but not the pentose phosphate dehydrogenases. However, at near-physiological concentration of progesterone, only acetyl-CoA carboxylase activity was decreased. Injection of prolactin intraductally into 11-day-pseudopregnant rabbits stimulated glycerolipid synthesis, fatty acid synthesis and enzymes involved in fatty acid synthesis, after 3 days. Intraductal injection of progesterone separately or together with prolactin had no significant effect on basal or stimulated lipogenesis in mammary glands. Intramuscular injection of progesterone at 10 mg/day did not suppress fatty acid synthesis stimulated when prolactin was injected intraductally, but a significant inhibition was observed at a higher dose (80 mg/day).     

Development of fatty acid-synthetic capacity in interscapular brown adipose tissue during suckling in genetically obese Zucker rats.

The development of the lipogenic capacity in brown adipose tissue was studied in suckling lean (Fa/fa) and obese (fa/fa) Zucker pups aged from 7 to 22 days. In both lean and obese pups, activities of the two key lipogenic enzymes, fatty acid synthetase and acetyl-CoA carboxylase, and of citrate cleavage enzyme rose from the early to the late suckling period. Compared with lean pups, 7-day-old fa/fa pups showed a 35% increase in fat accumulation in interscapular brown adipose tissue and a 25% increase in fatty acid synthetase activity. By 10 days of age, fat deposition, lipogenesis in vivo (assessed by the incorporation of 3H from 3H2O into fatty acids) and fatty acid synthetase activity were 1.5-2-fold higher in pre-obese than in lean pups. Compared with lean pups, the increased lipogenesis in vivo observed in brown adipose tissue of 10-day-old pre-obese pups could not entirely account for the difference in fat deposition observed in this tissue, suggesting that additional mechanisms are at play to explain the increased fat content of this tissue.     

Lipid metabolism and production of progesterone and prostaglandin F during induced regression of porcine corpora lutea

Patterns of luteal lipid and arachidonic acid accumulation were examined in relation to luteal progesterone and prostaglandin F synthesis in 30 sows and gilts between days 8 and 18 of the estrous cycle. Net release of progesterone from luteal tissue declined from 722 ng/100 mg tissue at day 8 to 81 ng/100 mg tissue at day 18. Although statistical significance was not present, net prostaglandin F release increased slightly from 8.6 to 13.9 ng/100 mg tissue. Luteal free cholesterol, esterified cholesterol, and free fatty acid contents did not change between days 8 and 18 whereas triglycerides accumulated rapidly between days 14 and 18 of the estrous cycle. Phospholipids increased between days 8 and 12, plateaued at 20.2 mg/g between days 14 and 16, and decreased to 15.4 mg/g on day 18. Between days 12 and 18, arachidonic acid increased from 19.4 to 34.8% in cholesterol esters, from 10.1 to 22.5% in triglycerides, and from 12.3 to 27.2% in luteal free fatty acids. Arachidonic acid in luteal phospholipids increased from 21.3 to 25.1% between days 14 and 16 of the estrous cycle. Luteal regression was associated with conservation of arachidonic acid. Based on blood plasma lipid fatty acid compositions, the corpus luteum elongated and desaturated essential fatty acids. Within porcine corpora lutea, calculated free arachidonic acid content was adequate for maintenance of prostaglandin synthesis.     

Breeding biology of weddell seals (Leptonychotes weddellii) at Drescher Inlet,riiser larsen ice shelf,Antarctica

Summary The breeding biology of Weddell seals (Leptonychotes weddellii) was studied at Drescher Inlet (Antarctica) during the austral late winter and spring 1986. The whelping season was estimated to last about 40 days, with a peak in pupping at late October. No post natal mortality was observed during the whole study. The attachment between parous females and their pups was strong during the first five weeks after parturition. From the third week on mothers spent more time in the water than the pups. Data on daily peak haul-out time of pups, post natal presence of pups on the ice and distribution of births during the whelping season, indicate that censuses should be carried out between 12.00 hours and 16.00 hours local time and during three weeks after the peak of the pupping season. Pups weaned between 6 and 7 weeks of age. Hormone concentrations (oestradiol-17 and progesterone) indicated that females did not come into oestrus during lactation. Throughout the whole lactation period the mother dominates the relationship with her pup. Growth of the pups was linear during the first 5 weeks post partum, during which period birth weight (x=29.1kg) increased more than 3 1/2 times. Until the 6th week of age the pups gained on average 2.6 kg/day, the respective weight loss in cows was 5.8 kg/day. The latter represents an average loss of nearly 38% of the initial weight at parturition. During the course of lactation, suckling frequency decreased, whereas the length of each bout increased resulting in an approximately constant total suckling duration per week. Of the energy used by females during the first 5 weeks, 52% was consumed by pups. Pups only took milk and the cows did not feed at all during the whole period of observation. Therefore the realized growth in pups, 10 g/min of suckling, was totally derived from energy stored by the cows.     

Lipid and arachidonic acid accumulation in naturally regressing porcine corpora lutea

Patterns of luteal lipid and arachidonic acid accumulation were examined in relation to luteal progesterone and prostaglandin F synthesis in 30 sows and gilts between days 8 and 18 of the estrous cycle. Net $\text{in vitro}$ release of progesterone from luteal tissue declined from 722 ng/100 mg tissue at day 8 to 81 ng/100 mg tissue at day 18. Although statistical significance was not present, net prostaglandin F release increased slightly from 8.6 to 13.9 ng/100 mg tissue. Luteal free cholesterol, esterified cholesterol, and free fatty acid contents did not change between days 8 and 18 whereas triglycerides accumulated rapidly between days 14 and 18 of the estrous cycle. Phospholipids increased between days 8 and 12, plateaued at 20.2 mg/g between days 14 and 16, and decreased to 15.4 mg/g on day 18. Between days 12 and 18, arachidonic acid increased from 19.4 to 34.8% in cholesterol esters, from 10.1 to 22.5% in triglycerides, and from 12.3 to 27.2% in luteal free fatty acids. Arachidonic acid in luteal phospholipids increased from 21.3 to 25.1% between days 14 and 16 of the estrous cycle. Luteal regression was associated with conservation of arachidonic acid. Based on blood plasma lipid fatty acid compositions, the corpus luteum elongated and desaturated essential fatty acids. Within porcine corpora lutea, calculated free arachidonic acid content was adequate for maintenance of prostaglandin synthesis.     

Fatty acid biosynthesis in rabbit mammary gland during pregnancy and early lactation

The pattern of fatty acids synthesized by mammary-gland explants from rabbits during pregnancy and early lactation has been studied. From day 12 to day 18 of pregnancy, long-chain (C(14:0)-C(18:1)) fatty acids were the major products. From day 18 to day 21 of pregnancy there was an increase of up to 12-fold in the rate of fatty acid synthesis per unit wet weight of tissue that was almost exclusively caused by the synthesis of octanoic fatty acid and decanoic fatty acid, which are characteristic of rabbit milk. These medium-chain fatty acids were mainly incorporated into triglycerides. From day 22 to day 27 of pregnancy there was little change in the rate of fatty acid synthesis and the proportions of fatty acids synthesized were essentially the same as those synthesized by the lactating gland, i.e. 80-90% octanoic acid plus decanoic acid. About 2-4 days before parturition a second lipogenic stimulus occurred, although the pattern of fatty acids synthesized did not change.     

Fatty acid oxidation in isolated rat liver mitochondria. Developmental changes and their relation to hepatic levels of carnitine and glycogen and to carnitine acyltransferase activity

Prompted by an apparent relationship between ketosis and fatty acid utilization, we studied the capacities for fatty acid oxidation through β-oxidation and Krebs cycle in liver mitochondria isolated from fetal and suckling rats. Rates of state 3 oxidation, as measured by oxygen consumption, were low for both palmitylcarnitine and palmityl CoA plus carnitine at 2 days before term and at birth, but increased at least ninefold during the first 8 days of life and at least sixfold during the remaining suckling period. Despite these sharp increases, oxygen consumption in suckling rats did not exceed the value for fed adult rats. Also, the rates of state 3 oxidation of succinate were low in suckling rats. Respiratory control indices, determined with each of the three substrates, were lower in suckling rats than fed adults. By contrast, ratios of fatty acyl ester to succinate oxidation, a relative measure of the oxidation of palmitylcarnitine and palmityl CoA, were 21–66% and 27–77% higher in suckling than in fed adult rats. The increased ratios indicate that the capacity for fatty acid oxidation is higher during postnatal development than in the fetal stage or adulthood. The oxidation capacity was inversely related to glycogen content in the liver. Although hepatic carnitine concentration and carnitine palmityltransferase activity increased during suckling period, they are not rate limiting for fatty acid oxidation. Studies of the partitioning of fatty acids showed that about two-thirds of the fatty acid oxidized through β-oxidation did not enter Krebs cycle for further oxidation. These results support our working hypothesis that ketosis of suckling rats stems from rapid oxidation of fatty acids and increased partitioning of acetyl CoA into ketogenesis.     

Development of hepatic and adipose tissue lipogenic enzymes and insulinemia during suckling and weaning on to a high-fat diet in Zucker rats

This study was designed to monitor the developmental changes in insulinemia and lipogenic enzyme activities in both inguinal adipose tissue and liver during suckling (7, 9, 14, and 17 days of age) and weaning (22 and 30 days of age) on to either a low-fat or a high-fat diet in lean (Fa/fa) and obese (fa/fa) rats. Tissues were removed through surgery and genotypes were retrospectively determined. During suckling, there was no difference in liver enzyme activities between the two groups. In contrast, adipose tissue fatty acid synthetase was increased by 50% and citrate cleavage enzyme and malic enzyme by 30% by 9 days of age. By 17 days of age, there was a threefold elevation in these enzyme activities and 6-phosphogluconic dehydrogenase and a twofold increase in glucose-6-phosphate dehydrogenase per inguinal fat pad in fa/fa versus Fa/fa. Consistent with these results, fat pad weight was increased by 20%, 50%, and 100% at 9, 14, and 17 days of age, respectively, in obese as compared to lean pups. However only by 17 days of age could a slight but significant increase in insulin level be detected in obese pups. Enlargement of inguinal fat pad accelerated after weaning on to a low-fat diet and still more after weaning on to a high-fat diet. Weaning on to a low-fat diet elicited an induction of hepatic lipogenic enzymes two or three times greater in fa/fa than in lean pups, while weaning on to a high-fat diet blunted the differences between genotypes. The lipogenic enzyme activities displayed per total inguinal fat were three to ten times greater in obese than in lean pups, regardless of the diet. However, adipose tissue lipogenic enzyme activities were much lower after weaning on to a high-fat than on to a low-fat diet in obese pups. The high-fat diet was as effective as the low-fat diet in triggering hyperinsulinemia in obese pups. The increased adipose tissue capacity for lipogenesis, starting during the suckling period, could play an important etiologic role in the development and maintenance of obesity in the Zucker rat.-Bazin, R., and M. Lavau. Development of hepatic and adipose tissue lipogenic enzymes and insulinemia during suckling and weaning on to a high-fat diet in Zucker rats.     

Lipid metabolism and in vitro production of progesterone and prostaglandin F during induced regression of porcine corpora lutea

The effects of Cloprostenol administration on porcine luteal lipid and arachidonic acid accumulation were examined in relation to luteal $\text{in vitro}$ progesterone and prostaglandin F synthesis in 18 mature gilts at day 12 of the estrous cycle. Basal and net $\text{in vitro}$ release of progesterone from luteal tissue was depressed at 8 hr after treatment whereas net $\text{in vitro}$ release of prostaglandin F was elevated at 8 hr. Inclusion of copper dithiothreitol or reduced glutathione in the incubation media resulted in minor alterations of $\text{in vitro}$ release of progesterone and prostaglandin F and no changes in composition of luteal lipids or fatty acids. Luteal contents of triglyceride had increased by 8 hr after treatment whereas contents of free and esterified cholesterols had increased by 32 hr after Cloprostenol administration. Luteal contents of phospholipid and free fatty acids were not affected by Cloprostenol administration. At 32 hr after treatment, percentages and content of arachidonic acid had increased in luteal cholesterol esters and triglycerides. Although arachidonic acid percentages increased in luteal free fatty acids and phospholipids, calculated arachidonic acid contents did not change following Cloprostenol administration. Induced luteal regression was associated with decreased $\text{in vitro}$ progesterone release, increased $\text{in vitro}$ prostaglandin F release, and accelerated lipid and arachidonic acid accumulation within the corpus luteum. The effects of altered lipid metabolism on release of prostaglandin F could not be defined. However, availability of arachidonic acid did not appear to be rate-limiting in relation to luteal $\text{in vitro}$ prostaglandin F synthesis.     

Adaptations of adipose tissue metabolism and number of insulin receptors in pregnant sheep

The endocrine control of adipose tissue metabolism during pregnancy in sheep has been investigated. The number of insulin receptors of sheep adipocytes was increased during pregnancy. There was no apparent change in the concentration of serum insulin during pregnancy in sheep while the rise in serum progesterone concentration was smaller and more gradual than in rats. Net lipid deposition in adipocytes occurred during the first 55 days of pregnancy, probably due primarily to increased lipoprotein lipase activity. Net deposition of lipid had ceased by mid-pregnancy while by 125 days of pregnancy, the rate of fatty acid synthesis in adipose tissue was decreased and the serum fatty acid concentration had risen, suggesting the onset of net lipid mobilization in the tissue. Results are compared with those from other studies with rats; it would appear that different mechanisms regulate lipid deposition during pregnancy in sheep and rats.     

Reduced anxiety in postpartum rats requires recent physical interactions with pups, but is independent of suckling and peripheral sources of hormones

Changes in emotional behavior occur across the reproductive cycle in female rodents, with reduced anxiety found during the postpartum period, but relatively little is known about factors contributing to this decreased anxiety. Using increased duration of time spent in the open arms of an elevated plus-maze as an indicator of reduced anxiety, it was found in a series of experiments that (1) anxiety is significantly reduced in Long-Evans females during the first week of lactation, but not thereafter, (2) relatively recent contact with pups before testing (within 4 h) is necessary for their reduced anxiety, (3) dams that receive only distal sensory cues from pups for the 4 h prior to testing do not show reduced anxiety, (4) the absence of nipples, and therefore a lack of suckling by pups, has no effect on dams' anxiety, (5) cesarean delivery of pups 2 days prior to expected parturition did not alter later anxiety in dams, (6) hypophysectomy during mid-pregnancy or ovariectomy within 24 h after parturition also did not prevent reduced anxiety in dams, and (7) differences in anxiety between lactating and virgin females are greatest 4-8 min after being placed in the plus-maze. Therefore, exposure to their own peripheral hormones through mid-pregnancy is sufficient to prime female rats to show reduced anxiety, but only if they later have recent physical interaction with pups. Furthermore, because suckling and the peripheral hormones released during suckling appear to be unnecessary, decreased anxiety in maternal rats may instead be regulated by the transient intracerebral release of neuropeptides or neurotransmitters while dams receive other types of tactile inputs from their infants.     

Lack of stimulation of relaxin secretion in lactating sows by suckling in vivo or by oxytocin in vitro.

After parturition, eight sows were zero weaned by removing all piglets 6 h after birth; a further 18 sows suckled at least ten piglets each. Blood samples were collected on Day 4 after zero weaning or on Days 4, 14 and 21 of lactation and the sampling frequency increased during suckling bouts. Ovaries were recovered from sows on these days and corpora lutea were either extracted for estimation of relaxin and progesterone concentration, fixed for immunohistochemical analysis or incubated in vitro in the presence or absence of luteinizing hormone (LH) or oxytocin. Luteal weight and progesterone were higher in the zero-weaned sows than in lactating sows (P less than 0.05 and less than 0.001, respectively); relaxin content was below detection by Day 14. This was supported by immunohistochemical staining for relaxin, which showed limited immunostaining in zero-weaned and Day 4 sows, but none in the tissue recovered on Days 14 and 21, which showed typical signs of regression. Secretion of progesterone and relaxin by luteal tissue in vitro was highest in zero-weaned sows (P less than 0.05), decreased as lactation progressed and neither LH nor oxytocin had any significant effect. Concentrations of plasma relaxin were all less than 0.2 ng/ml in three of the four zero-weaned and Day-4-suckled sows assayed; there was no detectable increase during suckling bouts. It was concluded that during lactation the old corpus luteum of pregnancy is not able to release relaxin in response to suckling in vivo or to oxytocin treatment in vitro.     

Prolactin does not mediate the suppressive effect of the suckling stimulus on luteinizing hormone secretion in ovariectomized lactating rats

The plasma LH concentration in ovariectomized lactating rats is low for 14 days postpartum, while the prolactin concentration is high during this period. We examined the effect of the inhibition of increased prolactin secretion with bromocriptine (CB-154) on the LH secretion in lactating rats ovariectomized on day 2 (day 0 = day of parturition). Blood samples were collected through an indwelling atrial cannula every day. LH levels were kept low until day 9 in lactating rats injected daily with CB-154 (0.6 mg/day, s.c.). The duration of the period during which LH secretion was suppressed was shorter in lactating rats treated with CB-154 than in saline-injected controls. The replacement with ovine prolactin by means of a mini-osmotic pump (0.3 mg/day, s.c.) in CB-154-treated lactating rats restored the duration of LH suppression. In rats deprived of their pups on day 2, the LH concentration rose immediately after removal of the pups and the LH level was not significantly different between rats treated with CB-154, ovine prolactin and saline, indicating that neither the CB-154 treatment nor the high level of prolactin alone has any effect on LH secretion in rats deprived of their pups. The present results clearly demonstrate that prolactin does not mediate the suppressing effect of the suckling stimulus on LH secretion in early lactation and support our theory that the suckling stimulus controls the LH and prolactin secretion independently at the hypothalamic level.     

Litter Size Determines Circadian Periodicity of Nursing in Rabbits

Nursing in rabbits occurs inside the nest with circadian periodicity. To determine the contribution of suckling stimulation in regulating such periodicity, we varied the size of the litters provided (1, 2, 4, or 6–8 pups). Nursing does, kept under a 14:10 (L:D) photoperiod, were continuously videotaped from parturition into lactation day 15. Although parturitions occurred throughout the day, a significant negative linear correlation (p?<?0.0001; r?=??0.68) was evident between time of delivery and time of nursing on lactation day 1, regardless of newborn number: longer intervals between these two events were seen in does delivering in the early morning than in those that gave birth late in the day. In rabbits suckling 6–8 pups, a Rayleigh analysis revealed that the population vector best describing their nursing pattern (across lactation days 1–15) had a phase angle?=?58° (corresponding to solar time 0352?h and rho?=?0.78; p?<?0.001). In contrast, the nursing pattern of does nursing litters smaller than 6 pups did not show circadian periodicity; rather, mothers showed multiple entrances into the nest box throughout the day. Cluster analysis revealed that the main equilibrium point of intervals between suckling bouts shifted from 24?h (6–8 pups) to 6?h (4 and 2 pups) and to as low as 4?h with 1 pup. In the groups nursing 2, 4, or 6–8 pups, most nursing episodes were followed by food and water intake. Those mothers also showed self-grooming of the ventrum and nipples after nursing. The incidence of these behaviors was lower in does nursing 1 pup. In conclusion, nursing in rabbits spontaneously occurs with circadian periodicity, but it is largely modulated by a threshold of suckling stimulation. (Author correspondence: gabygmm@gmail.com)     

Demonstration of a quiescent period for feeding controls in the developing rat

Feeding behaviour of rats during development was assessed by weighing pups before and after a 4 h feeding session. During the first postnatal week, fasted pups gained significantly more weight than fed pups. This difference disappeared during the second week, but reappeared during the third week and persisted through the fourth week. In another series, pups were weighed at 2 and 4 h after beginning feeding. This showed that fasted pups aged 6 days compensate by suckling longer than fed pups. At 10 and 14 days of age there were no differences between fed and fasted pups at either 2 or 4 h, but from 16 days onward, fasted pups had eaten significantly more than fed pups at both times. A control experiment showed that the lack of compensation by fasted pups aged 10-14 days did not reflect lack of availability of milk. Video-analysis of suckling behaviour at ages 6, 10 and 15 days provided further evidence for lack of feeding controls during the second postnatal week: at 6 and 15 days fasted pups spent more time actively sucking than did fed pups. Whereas at 10 days, there were no differences between fed and fasted pups. It is concluded that feeding controls are present during the first postnatal week, become quiescent during the second week and reappear during the third week.     

Neonatal hypoxic hyperlipidemia in the rat: effects on aldosterone and corticosterone synthesis in vitro

Neonatal hypoxia increases aldosterone production and plasma lipids. Because fatty acids can inhibit aldosterone synthesis, we hypothesized that increases in plasma lipids restrain aldosteronogenesis in the hypoxic neonate. We exposed rats to 7 days of hypoxia from birth to 7 days of age (suckling) or from 28 to 35 days of age (weaned at day 21). Plasma was analyzed for lipid content, and steroidogenesis was studied in dispersed whole adrenal glands untreated and treated to wash away lipids. Hypoxia increased plasma cholesterol, triglycerides, and nonesterified fatty acids in the suckling neonatal rat only. Washing away lipids increased aldosterone production in cells from 7-day-old rats exposed to hypoxia, but not in cells from normoxic 7-day-old rats or from normoxic or hypoxic 35-day-old rats. Addition of oleic or linolenic acid to washed cells inhibited both aldosterone and corticosterone production, although cells from hypoxic 7-day-old rats were less sensitive. We conclude that hypoxia induces hyperlipidemia in the suckling neonate and that elevated nonesterified fatty acids inhibit aldosteronogenesis.     

Maternal essential fatty acid deficiency depresses serum leptin levels in suckling rat pups

Dietary lipid quantity and quality have recently been shown to affect serum leptin levels in adult rats. Moreover, suckling pups from dams fed a high fat diet had increased serum leptin levels. The aim of the present study was to analyze the influence of essential fatty acid (EFA) deficiency on serum leptin levels in dams and their pups during the suckling period. For the last 10 days of gestation and throughout lactation, pregnant rats were fed a control or an EFA-deficient (EFAD) diet. The levels of leptin and EFA in the serum of the dams and pups were analyzed 1, 2, and 3 weeks after delivery. In parallel, serum levels of glucose and corticosterone were analyzed in the pups. Low serum leptin levels were found in the control lactating dams during the entire lactation period compared with the age-matched nonlactating animals. The leptin concentrations in the lactating dams fed the EFAD diet were lower compared with those fed the control diet. The serum leptin levels of suckling pups from dams on the EFAD diet were markedly decreased compared with controls (P < 0.05). The reduced serum leptin levels could not be explained by nutritional restriction as evaluated by serum levels of glucose and corticosterone. These results indicate the importance of the EFA composition of the maternal diet for serum leptin levels in both dams and pups. EFA deficiency in lactating dams may cause long-term effects on the pups through dysregulation of leptin and leptin-dependent functions. -- Korotkova, M., B. Gabrielsson, L. A. Hanson, and B. Strandvik. Maternal essential fatty acid deficiency depresses serum leptin levels in suckling rat pups. J. Lipid Res. 2001. 42: 359--365.     

The effect of late prenatal and/or early postnatal zinc deficiency on the development and some biochemical aspects of the cerebellum and hippocampus in rats

In rats, late prenatal and/or early postnatal zinc deficiency results in behavioural anomalies in adult animals, but not in overt dysmorphogenesis of the central nervous system. Cerebellar and hippocampal development occurs mainly in the first three weeks postnatally and zinc accumulates specifically in the mossy fibres of the hippocampus during this period.In the present investigation, rat pups were suckled by dams fed a zinc-deficient (<0.5 mg/kg) diet either from day 19 of pregnancy or from parturition. Control animals were restricted-fed the same diet supplemented with 100 mg zinc/kg. Studies were performed on pups either on day 18 postpartum in the case of animals fed the experimental diets from parturition, or on day 20 for pups which received treatment from day 19 of gestation.Cerebellar and hippocampal weights were lower in pups suckling from zinc-deficient dams but zinc levels were not affected in either organ, although histological evidence suggested less zinc in the hippocampal mossy fibres. Incorporation of H-thymidine into cerebellar and hippocampal DNA was not affected by maternal zinc status, nor was the activity of the zinc metalloenzyme alkaline phosphatase.The activity of the myelin-marker enzyme 2′, 3′-cyclic nucleotide 3′-phosphohydrolase was substantially lower in both regions of the brain in zinc deprived pups, especially in the hippocampus. Activity of the zinc metalloenzyme L-glutamic acid dehydrogenase was also diminished in both tissues from 20-day-old pups and in the hippocampi of 18-day-old animals.The data suggest that cerebellar and hippocampal DNA synthesis is not seriously affected by late prenatal and/or early postnatal zinc depletion, but that the activities of two enzymes associated with neural function are. The possibility is raised that these defects may be associated with the behavioural changes observed in rats subjected to zinc impoverishment during the period of maximal cerebellar and the hippocampal development.