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PubMed1991

Influence of the presence of a mature female on puberty attainment in gilts.

At 90 days of age, 40 Large White gilts were assigned to one of two treatments. At 155 days, a mature female which was left intact (Treatment I) or ovariectomized (Treatment O) was placed in each pen of five experimental gilts. From 180 days, estrus was checked daily with the back pressure test, and the occurrence of ovulation was detected by measuring the concentration of plasma progesterone at weekly intervals. From 240 days, a mature boar was introduced, for 5 minutes daily, into each pen during estrus detection. Gilts were slaughtered within 12 days after ovulation or at 270 days of age if they were not cyclic earlier. The percentage of gilts reaching puberty before 225 days of age was significantly higher in Treatment I (7 19 ) than in Treatment O (0 19 ) even though the average age at puberty was similar (I, 231 +/- 24 days; O, 243 +/- 12 days; mean +/- SD). Age at puberty and the number of days between mature female introduction and puberty differred significantly between the pens of gilts in Treatment O but not in Treatment I. Ovarian weights, ovulation rate and percentage of gilts with silent estrus were similar in the two treatments. Thus, the occurrence of pubertal estrus may be influenced by contact with an older, cyclic female or with other contemporary females raised in the same pen.

Journal Article↗
PubMed1982

Studies on the central effect of prolactin in inducing precocious puberty in the female rat.

Implantation of prolactin (PRL) into the median eminence (PRL-ME implants) of 23 day old female rats markedly advanced the onset of puberty, as measured by the age at vaginal opening and at first ovulation. Precocious puberty was preceded by steroidogenic activation of the ovary, as reflected by increases in uterine weight and an enhanced in vitro steroidal responsiveness of the ovary to hCG. The stimulatory effect of PRL-ME implants could not be attributed to alterations in the release of LH, FSH, GH or TSH from the anterior pituitary. Likewise, the PRL effect was neither exerted through the adrenal gland nor involved activation of a direct neural, vagal-mediated influence on the ovary. Furthermore, the effect of PRL-ME implants was not due to a decrease in pituitary secretion of opioid substances, which appear to restrain chronically gonadotropin release during female prepubertal development. These latter experiments also showed that administration of the opioid agonist, morphine, can delay the onset of puberty in the female rat. Although local exposure of the medial basal hypothalamus to high PRL levels is extremely effective in accelerating puberty, the mechanisms by which this effect is exerted remains to be elucidated.

Animals↗
PubMed1988

Hypothalamus and puberty.

The effect of a transitory increase in plasma FSH and LH levels during the prepubertal period on puberty has been investigated. Twenty-day-old rats had been bilaterally ovariectomized and 24 hr later they received two ovaries of infantile rats beneath the kidney capsule. These rats exhibited precocious puberty. Animals into which two additional ovaries had been transplanted first and the next day their own ovaries removed showed puberty at the same time as controls. Additional investigations provided evidence that the ovariectomized and ovary implanted rats plasma FSH and LH levels were in the control range four days after implantation. The findings support the assumption that the hypothalamic lesion-induced precocious puberty is due rather to a transitory enhanced release of gonadotropin releasing hormone by the lesion than to the destruction of sex-steroid sensitive structures inhibiting the release of gonadotropic hormones in prepubertal rats.

Animals↗
PubMed2006

The onset of puberty in North American bison (Bison bison) bulls.

Prepubertal testicular development was evaluated in young North American bison (Bison bison) bulls over a 12 months period, by following various parameters of semen quality intended to measure sexual maturity level. The study goals were to characterize bison male reproductive development and to define the age and onset of puberty. Semen was collected by electro-ejaculation from 12 bulls once a month for a period of 12 months, from 13 through 24 months of age. Volume, density, gross motility, individual motility, morphology, live/dead ratio, and concentration were used to judge the quality of the ejaculates. Abnormal sperm were classified into categories according to descriptions used for bovine evaluations and guidelines created by the Western Canadian Association of Bovine Practitioners were used for determining satisfactory semen quality. Minimums of 60% progressive motility and 70% normal sperm cells identified samples as satisfactory. Puberty was defined as the point in testicular development where an ejaculate contains a minimum of 50 x 10(6)sperm cells, showing at least 10% progressive motility. Fecal samples collected from bulls prior to electro-ejaculation for testosterone determination by a commercial testosterone specific antibody radioimmunoassay showed no significant changes in mean fecal testosterone concentrations over time. Changes in mean body weights over the study period were calculated, the average body weight at 13 and 24 months of age were 263+/-18.6 and 475+/-52.2 kg, respectively. Under these experimental conditions, age was determined to be the most significant factor in determining the onset of puberty. On average, bulls reached puberty at 16.5+/-2.5 months. There was a significant increase in the number of normal sperm with increasing bull age as well as significant decreases in proximal cytoplasmic droplets and head defects, but no significant changes in midpiece and principal piece defects. There were significant increases with age in individual progressive motility, gross motility, concentration, density, and volume but not in the percent of live sperm. Bison bulls used for breeding should be capable of passing a breeding soundness evaluation by 24 months of age. The commercial bison industry semen tests, and possibly rejects, many developmentally incomplete bulls between 19 and 21 months of age. We suggest that these may actually be developing normally and should not be hastily discarded; it may be worth testing again at 24 months.

Age Factors↗
PubMed2006

The effect of a short-term delay of puberty on trabecular bone mass and structure in female rats: a texture-based and histomorphometric analysis.

Accrual of bone mass and strength during development is imperative in order to reduce the risk of fracture later in life. Although delayed pubertal onset is associated with an increased incidence of stress fracture, evidence supports the concept of "catch up" growth. It remains unclear if deficits in bone mass associated with delayed puberty have long-term effects on trabecular bone structure and strength. The purpose of this study was to use texture-based analysis and histomorphometry to investigate the effect of a delay in puberty on trabecular bone mass and structure immediately post-puberty and at maturity in female rats. Forty-eight female Sprague-Dawley rats (25 days) were randomly assigned to one of four groups; (1) short-term control (C-ST), (2) long-term control (C-LT), (3) short-term GnRH antagonist (G-ST) and (4) long-term GnRH antagonist (G-LT). Injections of either saline or gonadotropin-releasing hormone antagonist (GnRH-a) (100 microg/day) (Cetrotide, Serono, Inc.) were given intraperitoneally for 18 days (day 25-42) to both ST and LT. The ST groups were sacrificed after the last injection (day 43) and the LT groups at 6 months of age. Pubertal and gonadal development was retarded by the GnRA antagonist injections as indicated by a delay in vaginal opening, lower ovarian and uterine weights and suppressed estradiol levels in the short-term experimental animals (G-ST). Delayed puberty caused a transient reduction in trabecular bone area as assessed by histomorphometry. Specifically, the significant deficit in bone area resulted from a decreased trabecula number and an increase in trabecular separation. Texture analysis, a new method to assess bone density and structural anisotropy, correlated well with the standard histomorphometry and measured significant deficits in the density measure (M(Density)) in the G-ST group that remained at maturity (6 months). The texture energy deficit in the G-ST group was primarily in the 0 degrees orientation (-13.2%), which measures the longitudinal trabeculae in the proximal tibia. However, the deficit in the G-LT group was in the 45 degrees and 135 degrees orientations. These results suggest that any "catch-up" growth following the cessation of the GnRH-antagonist injection protocol may be directed in trabeculae oriented perpendicular to 0 degrees at the expense of trabeculae in other orientations.

Animals↗
PubMed2004

Effects of low doses of dietary lead on puberty onset in female mice.

Female Swiss mice typically display signs of puberty at about 33-37 days of age. In the present investigation (96 female mice tested in 8 Pb exposure levels, n=12 per exposure level), the time to puberty onset was markedly influenced by exposure to dietary lead. While modest increases in blood lead concentrations from a normal background of 2-3 to 13.2 microg/dl delayed the onset of puberty by 15-20% to about 40-43 days, reducing blood lead from 2-3 to 0.7 microg/dl was associated with an acceleration of puberty to 21 days, an enhancement by over 30%. This dose-response relationship represents novel findings of possible ecological as well as public health significance and indicates that lead is able to induce biologically significant changes at blood lead levels previously thought to be without effect.

Administration, Oral↗
PubMed2006

Low doses of dietary lead are associated with a profound reduction in the time to the onset of puberty in female mice.

We report results from a replication in second and third generation female mice of accelerated time to puberty associated with low Pb exposure levels . Mice in the 2nd generation study are offspring of mice from the initial study; the 3rd generation mice are offspring from mice in the 2nd generation study. For each generation the time to puberty onset was markedly influenced by exposure to dietary lead. Modest increases in blood lead concentration from a normal background of 2-3 to 8-13 micro g/dl delayed the onset of puberty by 10-20% from a normal of 33-35 days to about 40-43 days; reducing blood lead from 2-3 to 0.7 micro g/dl was associated with profound acceleration of puberty to 21 days, an enhancement by over 30%. This dose-response relationship, which replicates previous novel findings, has possible ecological as well as public health significance and indicates that lead is able to induce biologically significant changes at blood lead levels previously thought to be without effect.

Administration, Oral↗
PubMed2005

Treating heifers with GnRH from 4 to 8 weeks of age advanced growth and the age at puberty.

In heifer calves, an early transient increase in circulating concentrations of LH is associated with early follicular development and is thought to regulate the timing of puberty. In an attempt to hasten the onset of sexual maturity, the early rise in LH concentration was advanced by injecting heifer calves with 120 ng/kg of GnRH (n=6) twice daily from 4 to 8 weeks of age; control calves received saline (n=6). Blood samples were collected every 15 min for 10h at 4, 8, 14, 20, 26, 32, 38, 44 and 50 weeks of age. Treatment with GnRH increased mean circulating concentrations of LH at 8 weeks of age (P<0.05), LH pulse frequency at 4 and 8 weeks of age (P<0.05), and reduced the mean age at puberty by 6 weeks (56.8+/-1.7 versus 62.8+/-2.4 weeks of age, for GnRH treated and control calves, respectively; P=0.04). Body weight gain was greater in GnRH-treated calves than control calves (P<0.05), and the rate of weight gain was shown to be a significant covariate within age at puberty. In conclusion, we suggest that the timing of the early rise in LH concentrations is a critical signal involved in the timing of puberty in heifers.

Aging↗
PubMed2002

Neuroendocrine mechanisms that delay and initiate puberty in higher primates.

This paper highlights a series of studies using the male rhesus monkey that has led to a model for the control of the onset of puberty in higher primates. The model proposes that the timing of puberty in these species is governed by the duration of a central brake that, during juvenile development, holds in check the hypothalamic network of gonadotropin-releasing hormone (GnRH) neurons, which, in the adult, drive the pituitary-gonadal axis. The neurobiology of this hypothalamic brake, and the physiological mechanisms that time its application and removal, are incompletely understood. Nevertheless, the pubertal resurgence of pulsatile GnRH release, which terminates the juvenile phase of primate development and triggers the initiation of puberty in man and monkeys, is associated with structural and molecular remodeling of the hypothalamus. A major component of this developmental plasticity appears to involve neuropeptide Y (NPY). NPY inhibits GnRH release, and NPY gene expression in the hypothalamus is elevated during juvenile development when GnRH release is restrained. Since the changes in hypothalamic function and morphology that trigger primate puberty unfold in the absence of gonadal steroid feedback, the possibility is raised that, in addition to activating the pituitary-gonadal axis at this stage of development, they may also contribute directly to the causation of behaviors and affective states that emerge at adolescence.

Animals↗
PubMedDate not supplied

Excitatory amino acid receptors and puberty.

Glutamate is an important excitatory signal in the hypothalamus for the steroid-mediated preovulatory gonadotropin surge. Steroids may exert this action by regulating glutamate receptor levels or glutamate release, or both. Work in our laboratory found no changes in NMDA and kainate receptor binding in the hypothalamus of castrated or castrated plus steroid-replaced male and female rats. Likewise, we found that NMDA and kainate binding did not change over the onset of puberty in the female rat. A competitive quantitative RT-PCR assay using exogenous internal standards was used to measure NMDAR1, GluR1, and beta-actin mRNAs levels. NMDAR1 and GluR1 expression was examined in the preoptic hypothalamic area and in the medial basal hypothalamus at Postnatal Days 10, 15, 20, 25, 30, 32, 34, 36, 40, and 63. A transient increase in GluR1 mRNA levels in the preoptic hypothalamic area was observed on Day 20, with all other time points showing comparable levels. NMDAR1 levels in the POA and medial basal hypothalamus did not change significantly at any of the time points; in contrast, however, AMPA receptor binding levels were increased in the hypothalamus at the time of puberty in the female rat. Thus, in addition to the previously reported elevation of glutamate release rates in the hypothalamus at the time of puberty, AMPA receptors may also be elevated and play a role in mediating glutamate regulatory effects on the timing of puberty in the female rat.

Animals↗
PubMed2002

Impact of boar exposure on puberty attainment and breeding outcomes in gilts.

We examined the most effective method of boar exposure for the attainment of puberty in 89 gilts. At 160 days of age, we allocated gilts to daily direct contact with a vasectomized boar after movement of pen groups of gilts to a detection-mating area (DGB: n = 30); daily direct contact with boars in the gilt home pens (DBG: n = 31); or daily fenceline contact between boars and gilts housed in individual gilt stalls (FBG: n = 28). DGB gilts were younger (P < or = 0.05) than FBG gilts at puberty. Direct boar contact reduced the interval from initial boar contact to puberty in DGB and DBG gilts, compared to fenceline contact in FBG gilts (P < 0.05). There was no difference (P > or = 0.05) between treatment for pubertal weight, backfat, lifetime growth rate, or duration of first pubertal estrus. Backfat depth and leptin concentration at 160 days of age were positively correlated (P < or = 0.05). We detected no relationships between leptin or IGF-1 concentration at 160 days of age and the interval from initial exposure to a vasectomized boar to puberty (P > 0.05). Based on objective criteria, fenceline contact with a boar (BC) during artificial insemination improved the quality of artificial insemination compared to no boar contact (NC) (P < 0.05).

Adipose Tissue↗
PubMed1997

Neonatal hypothalamic c-fos expression in an excitotoxicity-induced model of precocious puberty.

We have used immunocytochemical detection of c-fos expression (FOS-like immunoreactivity, FLI) to establish the site of action of monosodium glutamate (MSG) in neonatal rats in a model of lesion-induced precocious puberty. The primary target appears to be the hypothalamic arcuate nucleus (ARC) but other circumventricular organs (CVO) are also affected (e.g. subfornical organ). Single injections of MSG (1-4 mg/g single dose, postnatal day 2 (P2)) which result in precocious puberty induce an area of edema, surrounded by a ring of FLI in the basal hypothalamus. In contrast, a maximal sub-lethal dose of NMDA (N-methyl-D-aspartate; 3 mg/kg) which produces a different pattern of ARC FLI, without edema, has no effect on puberty. Multiple doses of MSG (4 mg/g P2, P4, P6, P8), consistent with severe ARC damage and resultant sterility, markedly attenuates the FLI response by P8, with no visible edematous reaction following the final injection. In efforts to block the effect of MSG, pretreatment with the NMDA receptor-specific antagonist MK-801 (dizocilpine maleate) prevented the appearance of edema, as well as the onset of precocious puberty. However, MK-801 did not completely eliminate the FLI, but transformed the pattern of staining so that the original edematous area now contained many FOS-positive cells. This remaining MSG-induced FLI could not be eliminated by higher doses of MK-801 or by the non-NMDA antagonist DNQX (6,7-dinitroquinoxaline-2,3-dione). The combination of MK-801 and DNQX was also ineffective. MK-801 or DNQX had no effect on FLI when injected alone (i.e., without MSG) or in combination. The receptor which mediates MSG-induced c-fos expression, in the presence of MK-801 or DNQX, needs to be identified. We conclude, in conjunction with our previous work, that MSG induces precocious sexual maturation via an MK-801-sensitive mechanism associated with an edematous response of the basal hypothalamus. Whether the appearance of edema is indicative of an excitotoxic action of MSG, resulting in the removal of neurons inhibitory to sexual maturation, remains to be established.

Animals↗
PubMed2000

Sexually dimorphic cognitive style in rats emerges after puberty.

In a water maze (WM), rats employ different and sexually dimorphic behavioral strategies to solve a place-learning task, a test of cognitive/propositional ability. Puberty is the last step in brain development and marks an important phase with regard to sexually dimorphic cognitive performance and behavior. The present study assessed possible sex differences in cognitive style before and after puberty in a WM place-learning task. Since nitric oxide (NO) is implicated in spatial learning and hippocampal function, and since brain NO(-)(2) + NO(-)(3) levels (stable metabolites of NO) display region-specific sex differences in rat brain, NO(-)(2) + NO(-)(3) levels were determined after behavioral testing. The sex-related style difference emerged very clearly but only in the adult rats, which suggests that the female behavioral strategy in the WM place-learning task requires the presence of female sex hormones at puberty. Although NO(-)(2) + NO(-)(3) levels were higher in the adult rats and males compared to prepubertal and female rats, respectively, no significant correlations emerged between brain NO and behavior. The fact that the behavioral sexually dimorphic cognitive-style effect observed here and in previous studies appears to emerge only after puberty suggests that awareness of such postpubertal sex differences may also be important in human educational and therapeutic contexts.

Adaptation, Psychological↗
PubMed1997

Failure of melatonin implants to alter onset of puberty in gilts.

Forty crossbred gilts (Hampshire x Yorkshire x Landrace x Duroc) weighing 55.4 +/- 0.5 kg at 4.2 +/- 0.1 months of age received either melatonin implants (N = 20) or served as controls (N = 20). Gilts were housed in a temperature controlled room (21 degrees C) with a light (L):dark (D) cycle of 10L:14D. Initially, four implants (12 mg melatonin each, Wildlife Pharmaceuticals, Ft. Collins, CO) were placed in one ear subcutaneously. At 2-week intervals, five, six, seven or eight implants were placed in ears of the gilts (one implant per 11.8 kg body weight). Throughout the trial, blood samples were collected twice weekly by jugular venipuncture. All gilts were exposed to mature boars for 15 min on alternate days. Age of puberty was determined from serum concentrations of progesterone and visual observations of estrus. Serum concentrations of melatonin were elevated (5-10 fold) throughout the trial in those gilts that received melatonin implants. Average daily gain (P = 0.51) and age at puberty (P = 0.57) were similar between gilts that received melatonin implants or no implants. Even though gilts continued to receive melatonin after they attained puberty, elevated serum concentrations of melatonin did not alter the length of subsequent estrous cycles (P = 0.90). These data indicate that elevation of serum concentrations of melatonin via implants did not alter the onset of puberty or length of subsequent estrous cycles.

Aging↗
PubMed1999

A unique urinary constituent, 6-hydroxy-6-methyl-3-heptanone, is a pheromone that accelerates puberty in female mice.

BACKGROUND: Olfactorily mediated puberty acceleration in female mice (measured by an increase in uterine weight) has been observed since the 1960s without the active chemosignal being structurally identified. There are many controversies in the literature as to whether this male-originated pheromone is a volatile substance. We investigated the chemical nature of the urinary fractions that are responsible for the characteristic uterine weight increases. RESULTS: The active pheromone was identified as 5,5-dimethyl-2-ethyltetrahydrofuran-2-ol and/or its open-chain tautomer (6-hydroxy-6-methyl-3-heptanone). A series of cyclic vinyl ethers were isolated from chromatographically active fractions of the urine. Because these compounds did not accelerate puberty, we postulated that these ethers were degradation products of a lactol (5,5-dimethyl-2-ethyltetrahydrofuran-2-ol). The lactol was then detected directly in the mouse urine extract using a silylation agent. Synthetic 6-hydroxy-6-methyl-3-heptanone had strong biological activity, whereas its close structural analogs did not. CONCLUSIONS: The male house mouse excretes into its urine a large quantity of a volatile substance that has a unique lactol/hydroxyketone structure. This substance is capable of binding to the less volatile urinary constituents, such as proteins or peptides, and is active in puberty-acceleration bioassays. The controversies regarding the volatility of the puberty-accelerating pheromones can now be explained by considering a complex of volatile lactol/hydroxyketone and urinary proteins.

Animals↗
PubMed2002

A possible association between dietary intake of copper, zinc and phosphate and delayed puberty in heifers in Sudan.

Zinc and copper deficiencies have been reported in heifers of various breeds at four different locations in Sudan. These were Kuku (5 km north of Khartoum), Seleit (20 km northwest of Khartoum), Medani (180 km south of Khartoum) and El Obeid (600 km west of Khartoum). Phosphorus deficiency was only observed in the serum of heifers at El Obeid. The heifers at all locations showed delayed puberty, stunted growth and infertility. The heifers of the local breeds at El Obeid only attained puberty by 1530 days of age compared with 840 days for the pure Friesian heifers at Seleit. The crossbred animals at Kuku and Medani attained puberty at 1440 and 1020 days of age, respectively. The marginal or low zinc and copper contents in pasture, soil or animal feed may have been predisposing factors for the observed deficiencies and might have been responsible for the delayed age of puberty.

Animal Feed↗
PubMed1999

Sexual dimorphism in circulating monomeric and dimeric inhibins in normal boys and girls from birth to puberty.

BACKGROUND AND OBJECTIVE: Inhibins are peptides, mainly of gonadal origin, that suppress FSH production. Dimeric forms of inhibin (A and B) have been proposed as peripheral markers of Sertoli and granulosa cell function. The aim of this study was to establish the relationship between circulating dimeric and monomeric inhibins, and gonadotrophins and sex steroids, in normal boys and girls from birth to puberty. SUBJECTS: One hundred and forty-six normal children (females: 57; males: 89) were studied. MEASUREMENTS: Serum LH and FSH were measured by an immunofluorometric assay. Serum oestradiol and testosterone were measured by radioimmunoassay. Serum inhibin A and B, and Pro-alphaC, were measured by specific two-site enzyme-linked immunosorbent assays. RESULTS: In boys from birth to 6 months of age, the mean serum inhibin B concentration was as high (477 +/- 53.7 ng/l) as that found at puberty (400 +/- 70.2 ng/l). After the first year, inhibin B gradually decreased to reach its lowest concentration (153 +/- 23.6 ng/l) at age 4-6 years. At approximately age 10, it rose progressively to reach pubertal concentrations. Pro-alphaC showed a similar pattern but at lower concentrations. Inhibin A was not detected at any age. In girls from birth to 6 months, inhibin B levels (83.0 +/- 18.3 ng/l) were approximately 50% lower than those found at puberty (181 +/- 25.7 ng/l). After 6 months of age, these levels dropped (17.5 +/- 1.6 ng/l) and remained low until the prepubertal years. Thereafter, they increased to pubertal concentrations. The serum inhibin A concentration after birth (29.9 +/- 8.7 ng/l) was similar to that found at puberty (18.3 +/- 5.7 ng/l); after 6 months, it fell to undetectable levels until the prepubertal years. CONCLUSION: The sex difference in serum levels of gonadotrophins is associated with sex differences in the levels and proportions of circulating dimeric and monomeric inhibins.

Adolescent↗
PubMed1999

GnRH mRNA increases with puberty in the male Syrian hamster brain.

Puberty in the male Syrian hamster (Mesocricetus auratus) is characterized by decreased responsiveness to testosterone mediated negative feedback, but the neural mechanism for this change remains elusive. We hypothesized that decreased inhibition of the gonadotropin-releasing hormone (GnRH) system results in increased neurosecretory activity, which includes an increase in GnRH gene expression. This study examined GnRH mRNA in male hamsters before and after puberty, and sought to determine if any increase in mRNA was specific to particular subpopulations of GnRH neurones. Brains were collected from 21-day-old prepubertal males (n = 5) and 56-day-old postpubertal males (n = 5). Alternate 10 microm coronal sections from fresh-frozen brains were collected throughout the septo-hypothalamic region, and 25% of those sections were processed for in-situ hybridization histochemistry using an 35S-riboprobe complementary to hamster GnRH. No differences were observed in the number of GnRH mRNA expressing cells in any region, but in the diagonal band of Broca (DBB)/organum vasculosum of the lamina terminalis (OVLT) there was a significant increase in labelling intensity (defined as area of the cell occupied by silver grains) in postpubertal males. A second analysis compared the frequency distributions of cells based on labelling intensity between prepubertal and postpubertal males. This analysis revealed significant differences between the two frequency distributions in all areas analysed (DBB/OVLT, medial septum (MS), and preoptic area (POA)). Furthermore, examining the distribution of cells in these regions revealed a shift to the right in the postpubertal population of cells, which indicated an increased number of GnRH neurones with greater labelling intensity. These data clearly demonstrate increased GnRH mRNA during puberty. Furthermore, they suggest that the previous observation of brain region specific pubertal decreases in GnRH-immunoreactivity only within the DBB/OVLT and MS but not the POA are not due to differential levels of GnRH gene expression, but could indicate increased release from these neurones during puberty.

Aging↗