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Biomedical subjects

C D Ingram

Publications and source records attributed to C D Ingram.

At least 37 records · Page 2Linked to original sources
PubMed2000

Abnormal expression of cell cycle regulatory proteins in ductal and lobular carcinomas of the breast.

In a previous study, we demonstrated that the G1 cell cycle checkpoint in carcinomas of the breast is frequently abrogated by loss of p16, the product of the CDKN2/INK4A gene, and, to a lesser extent, by loss of pRB, the product of the retinoblastoma gene. The purpose of the present study was to determine whether other mechanisms of cell cycle deregulation exist in breast cancers which have retained RB and p16 function. Paraffin sections of 81 invasive breast carcinomas (49 ductal, 26 lobular, 6 mixed) were reacted with monoclonal antibodies against cyclin D1 and p53, using optimized immunohistochemical staining protocols. The staining results were correlated with the expression of p16 and pRB, and with a variety of pathological parameters and DNA ploidy. Twenty-five tumors (31%) accumulated (presumably mutant) p53 and 28 (35%) overexpressed cyclin D1; 7 carcinomas (not including any pure lobular cancers) abnormally expressed both proteins. p53 accumulation correlated with nuclear, mitotic, and overall grade, but not with tumor size, lymph node involvement, or DNA ploidy. Overexpression of cyclin D1 was not associated with any of the patho-biological variables. There was an inverse correlation between loss of p16 and high levels of p53, but not cyclin D1. The G1 cell cycle checkpoint, which is controlled by RB, cyclin D1, and p16, was abrogated in 65% of carcinomas, and only p53 was abnormal in an additional 17%. The number of abnormally expressed genes correlated with mitotic activity and overall tumor grade, but not with tumor histology, size, or nodal status, suggesting that cell cycle deregulation is an early event in breast tumorigenesis. Only 18% of the carcinomas showed a normal level of expression of the four genes tested, and p16 appeared to be the most common target of cell cycle deregulation. These data point to the importance of cell cycle regulatory protein abnormalities in human breast cancer.

Breast Neoplasms↗
PubMed2000

Chronic iodine deprivation attenuates stress-induced and diurnal variation in corticosterone secretion in female Wistar rats.

Many millions of people throughout the world are at risk of developing iodine deficiency-associated disorders. The underlying effects of iodine deficiency on neuroendocrine function are poorly defined. We have studied stress-induced and diurnal variation in corticosterone secretion in female rats rendered chronically hypothyroid by feeding them an iodine-free diet for 6 months. Corticosterone secretory responses in iodine deficient animals were compared to those seen in animals rendered hypothyroid with propylthiouracil and untreated controls. By using a well-validated, automated blood sampling system to collect small samples of blood over the complete daily cycle in unrestrained animals, we have demonstrated for the first time that the normal diurnal rhythm of corticosterone secretion is lost in chronic iodine deficiency and that the corticosterone secretory response to the psychological stress of 10 min exposure to white noise is attenuated. Despite restoration of circulating triiodothyronine and thyrotropin releasing hormone- and thyroid stimulating hormone beta-transcript prevalence in the hypothalamus and pituitary, respectively, 1 month after restoration of normal iodine-containing diet both the diurnal variation in corticosterone levels and the corticosterone secretory response to the noise stress remained reduced in amplitude compared to control animals. Thus, chronic hypothyroidism induced by iodine deficiency significantly attenuates hypothalamo-pituitary-adrenal axis activity, an effect that persists after functional recovery of the thyroid axis.

Acoustic Stimulation↗
PubMed1999

Differential effects of psychological and immunological challenge on the hypothalamo-pituitary-adrenal axis function in adjuvant-induced arthritis.

Inability to mount a suitable glucocorticoid response to a stressor can be life-threatening. Rats with hind-paw inflammation, associated with the development of adjuvant-induced arthritis (AA), are unable to mount a hypothalamo-pituitary-adrenal (HPA) axis response to acute stress. In the present study we have compared the effects of acute psychological stress (noise) and acute immunological challenge (lipopolysaccharide [LPS] injection), on the activation of the HPA axis in rats with the chronic inflammatory stress of AA. We conclude that the increase in HPA axis activity in AA is principally due to an increase in corticosterone pulse frequency and not to any alteration in pulse magnitude. The lack of response to acute stress can be accounted for by the increase in pulse frequency and the associated refractory period following each pulse, producing dramatic but specific changes in basal HPA function. These changes may account for the loss of responsiveness to acute stress, but not to acute immunological challenge, because the HPA axis is able to respond to LPS in male rats with AA. However, there appears to be an impaired adrenal responsiveness in female rats with AA that is not inherent, but occurs as a consequence of the development of inflammation.

Animals↗
PubMed1999

Hypothalamo-pituitary-adrenal axis responses to lipopolysaccharide in male and female rats with adjuvant-induced arthritis.

We have previously demonstrated that rats with adjuvant-induced arthritis (AA) are unable to mount a hypothalamo-pituitary-adrenal (HPA) axis response to either psychological or physical stress. In the present study we have taken male and female rats with AA and injected these with lipopolysaccharide (LPS) as an acute immune challenge and assessed the effects of this challenge at all levels of the HPA axis. We have demonstrated that, in contrast to acute stress, there is an activation of the HPA axis in male AA rats in response to acute immune challenge which occurs at all levels of the HPA axis. The hypothalamic and pituitary response to LPS is intact in the female AA rat. However, there appears to be an impaired adrenal responsiveness in the AA female given LPS. The non-AA female is able to respond to LPS suggesting that this defect is not inherent but is a reaction to the development of inflammation. This hyporesponsiveness has major implications for the ability of the organism to survive infections or immune challenges which are potentially life threatening in the absence of release of anti-inflammatory glucocorticoids from the adrenal cortex. The implications of these changes in the female on the subsequent development of the disease and the mechanisms mediating these effects may provide a better understanding of the gender differences underlying susceptibility to autoimmune diseases.

Adrenocorticotropic Hormone↗
PubMed1999

Chronic treatment with oestradiol does not alter in vitro LTP in subfield CA1 of the female rat hippocampus.

Population excitatory post-synaptic potentials (pEPSPs) were recorded in vitro from subfield CA1 of the hippocampus of female rats which had been ovariectomized and treated for 14 days with either oil or 17beta-oestradiol (10 microg/day). The currents applied to the Schaffer collateral-commissural input necessary to induce threshold, maximum and 50% maximum pEPSP responses did not differ between groups. Application of trains of pulses (0.1-1 s; 100 Hz) evoked post-tetanic and long-term (> 60 min) potentiation of pEPSP responses, the magnitude of which was related to stimulus duration in both groups. However, the degree of potentiation induced by near-threshold (0.1, 0.15 and 0.2 s) and saturating (1 s) stimuli did not differ between groups. Thus, despite reports that oestradiol can modulate synaptic spine density and glutamatergic and GABAergic components of the inputs to CA1, these data suggest that chronic oestradiol treatment has no effect on either the excitability or induction of LTP in the Schaffer collateral-commissural-CA1 pathway.

Animals↗
PubMed1999

Effect of gonadal steroids on the oxytocin-induced excitation of neurons in the bed nuclei of the stria terminalis at parturition in the rat.

Experiments were undertaken to examine the role of ovarian steroids in peripartum programming of oxytocin sensitivity of limbic neurons implicated in oxytocin-induced facilitation of the milk-ejection reflex. In vivo recordings of neurons in the bed nuclei of the stria terminalis and ventrolateral septum of pre-parturient rats which had undergone prior ovariectomy and hysterectomy showed that oestradiol significantly increased the excitatory responses of bed nuclei/ventrolateral septum neurons to intracerebroventricular oxytocin, compared to oil-treated controls. Oestradiol also increased the excitation of bed nuclei neurons to the selective oxytocin agonist, [Thr4,Gly7]oxytocin in brain slices from steroid pre-treated ovariectomized hysterectomized rats, so that both the proportion of responsive neurons, and the magnitude of their responses were significantly increased. Parallel autoradiographic studies showed that oxytocin binding in the medial bed nuclei and ventrolateral septum was selectively increased following oestradiol treatment. Progesterone pre-treatment had no effect on either oxytocin sensitivity of bed nuclei/ventrolateral septum neurons recorded in vivo, or on oxytocin binding in the medial bed nuclei and ventrolateral septum, compared to oil-treated controls. Mean responses to [Thr4,Gly7]oxytocin in bed nuclei neurons recorded in slices from progesterone-treated rats were larger than controls, but this effect was highly variable. These results demonstrate that oestradiol greatly enhances oxytocin receptor expression and sensitivity of bed nuclei/ventrolateral septum neurons to oxytocin over the peripartum period, consistent with involvement of this steroid in enhancing oxytocin regulation of neuroendocrine and behavioural adaptations required for lactation.

Animals↗
PubMed1999

The hypothalamic-pituitary-adrenal axis response to endotoxin is attenuated during lactation.

Pregnancy and lactation are times of prolonged physiological changes affecting the neuroendocrine and immunological systems. One well-characterized change is the neuroendocrine hyporesponsiveness to acute stressful stimuli. We have now designed studies to see whether there is an alteration in the response of the hypothalamic-pituitary-adrenal (HPA) axis to an immunological inflammatory challenge and to ascertain whether lactating animals show altered neural and endocrine responses to inflammatory stimuli. Lactating (day 9-12 postpartum) or virgin control Sprague-Dawley female rats were injected with either 200 microg of endotoxin (lipopolysaccharide, LPS ) or sterile saline given i.p. Trunk blood or jugular blood was collected from the animals at 2 h or hourly over 6 h after injection. Both plasma adrenocorticotropic hormone (ACTH) and corticosterone concentrations were significantly higher in saline treated lactating animals compared with the virgin group. LPS significantly elevated circulating levels of plasma ACTH and corticosterone in both virgin and lactating animals compared with saline controls, however, hormone responses to LPS were significantly reduced in lactating animals relative to virgin controls. Corticosterone-binding globulin concentrations were lower in lactating animals compared to virgin animals and LPS decreased concentrations in virgin, but not lactating rats. Analysis of cfos mRNA in the paraventricular nucleus (PVN) of the hypothalamus revealed that 2 h following injection there was a increase in cfos expression only in the virgin animals treated with LPS, compared to all other treatment conditions. Corticotropin-releasing hormone (CRH) mRNA expression was overall greater in virgin animals, but was increased to similar extent in both virgin and lactating animals treated with LPS. Primary arginine vasopressin (AVP) mRNA transcripts were increased 2 h following LPS injection, but a greater increase in expression was seen in virgin animals. These data demonstrate that there is a lower level of free circulating glucocorticoid in response to inflammatory stimuli and suggests that communication between the immune and endocrine systems may be altered during lactation.

Adrenocorticotropic Hormone↗
PubMed1998

Electrophysiological effects of oxytocin within the bed nuclei of the stria terminalis: influence of reproductive stage and ovarian steroids.

The bed nuclei of the stria terminalis (BNST) is a target site for the central actions of oxytocin (OT) in promoting behavioural and neuroendocrine responses involved in female reproduction, and binding studies suggest that OT sensitivity may be modulated over the peripartum period. Electrophysiological recordings from brain slices in vitro showed that OT sensitivity of BNST neurones is relatively low in late pregnancy, but is high during lactation. In vivo studies over the immediate peri-partum period revealed that although BNST neurones can be excited by i.c.v. OT at day 22 of pregnancy, there is a 5-10 min delay in their response which is not present in lactation. This delay can be reversed by naltrexone, or lesioning the stria terminalis, and may involve an inhibitory opioid input to the BNST from the amygdala. Examination of the role of steroids in regulating OT responses of BNST neurones showed that oestradiol pre-treatment in late pregnant ovariectomized rats increased OT excitation of BNST neurones in vitro, and a similar result was observed with in vivo recordings. Progesterone also augmented OT excitation of BNST neurones in vitro, but no such effect was observed in vivo. This difference could indicate that an additional effect of progesterone is to potentiate extraneous inhibitory inputs to the BNST, or may reflect the ability of this steroid to suppress OT sensitivity by a direct membrane action. Changes in the response of BNST neurones to OT may have functional implications for the action of central OT in facilitating the neuroendocrine milk-ejection reflex (i.e. increasing milk-ejection frequency), an effect which first appears at around day 3 of lactation. Studies involving steroid treatment of late pregnant ovariectomized rats showed that this facilitatory mechanism can be induced to appear early (i.e. on day 22 of pregnancy) by oestradiol, but not progesterone treatment. Collectively, these results support this view, that the action of OT in the BNST is regulated by the changing levels of steroids towards the end of pregnancy, thereby ensuring appropriate neuroendocrine responses necessary for motherhood.

Animals↗
PubMed1998

Vasopressin neurotransmission and the control of circadian rhythms in the suprachiasmatic nucleus.

Vasopressin (VP) is one of the principal transmitters in the suprachiasmatic nucleus (SCN). Approximately 20% of neurones in the dorsomedial division of the SCN synthesize the peptide and a high proportion of SCN neurones (> 40%) are excited by VP acting through the V1 receptor. This suggests that VP may act as a feedback regulator of electrical activity within the nucleus. Such an intrinsic excitatory signal can be demonstrated by perifusion with a V1 antagonist which reduces spontaneous neural activity. As the synthesis and release of VP occurs in a circadian manner, this leads to a variable feedback excitation which may contribute to the circadian pattern of activity of the neural clock. This role in amplifying rhythmicity is supported by observations that animals deficient in VP show a reduced circadian amplitude of behavioural rhythms (e.g. locomotor and cortical electroencephalographic rhythms). VP expression declines during ageing and although aged animals show no change in the proportion of SCN neurones excited by VP, the rhythm of spontaneous electrical activity shows a progressive decline, consistent with the reduced endogenous excitatory feedback. However, the homozygous Brattleboro rat which lacks any VP expression still maintains rhythms of electrical activity, indicating that VP is not the sole factor generating circadian activity. The generation of this rhythmicity may depend upon the interaction of VP with other transmitter systems, such as the inhibitory transmitters somatostatin and GABA which show a circadian variation in efficacy. In addition to its role in feedback amplification of the endogenous rhythm of electrical activity, VP also functions as part of the efferent signal to the rest of the CNS where it potentially regulates a number of behavioural and physiological rhythms, including the circadian activity of the hypothalamo-pituitary-adrenal axis. Thus, the combined amplification and signalling functions makes VP an important component of the neuronal clock function in mammals.

Animals↗
PubMed1998

The pulsatile characteristics of hypothalamo-pituitary-adrenal activity in female Lewis and Fischer 344 rats and its relationship to differential stress responses.

The dynamic patterns of basal and stimulated hypothalamo-pituitary-adrenal (HPA) activity of freely moving female Lewis and Fischer 344 rats were compared using an automated blood-sampling system. Both strains showed pulsatile corticosterone release throughout the 24 h cycle. Lewis rats showed clear circadian variation in both pulse frequency (8.4 +/- 0.4 pulses between 1700-2300 h vs. 5.3 +/- 0.8 pulses between 0500-1100 h; P < 0.05) and height (198 +/- 27 ng/ml between 1700-2300 h vs. 107 +/- 14 ng/ml between 0500-1100 h; P < 0.05). Fischer rats exhibited pulses of similar frequency and height to those in Lewis rats during the evening, but showed no circadian variation, resulting in higher mean daily corticosterone concentrations. Although both strains showed behavioral and HPA responses to white noise stress (10 min; 114 dB), Fischer rats showed much greater increases in total activity, grooming, and rearings, and two important differences in the corticosterone responses were observed. First, in Lewis rats a clear relationship existed between basal and stimulated HPA activities, in that a significant response was seen only when the stress coincided with the rising (secretory active) phase of a basal pulse. Noise stress coinciding with a falling (nonsecretory) phase elicited no significant response. In contrast, Fischer rats showed similar responses regardless of the underlying pulse phase. Second, after the peak response at 20 min (Lewis, 237 +/- 67 ng/ml; Fischer, 390 +/- 57 ng/ml), corticosterone levels fell rapidly in Lewis rats, but remained maximally elevated for 20 min in Fischer rats, resulting in a significantly greater integrated response. The corticosterone response to i.v. CRF was unaffected by pulse phase in both strains, suggesting that a suprapituitary mechanism mediates the phase-dependent response to stress in the Lewis strain. CRF-induced corticosterone levels rose more rapidly in Fischer rats, peaking at 10 min (473 +/- 95 ng/ml) compared with 30 min (390 +/- 75 ng/ml) in Lewis rats, suggesting greater pituitary sensitivity in this strain. Thus, differences in both central and pituitary control of the HPA axis contribute to the strain difference in stress responsiveness between female Lewis and Fischer rats.

Animals↗
PubMed1998

Ultradian rhythm of basal corticosterone release in the female rat: dynamic interaction with the response to acute stress.

The present study investigated the dynamic regulation of the hypothalamo-pituitary-adrenal axis and its significance to acute stress responsiveness in the female rat. An automated, frequent blood-sampling technique allowed the circadian rhythm of corticosterone to be resolved into a series of pulses. These were equally distributed (mean interval, 50.9 +/- 3.7 min) throughout the 24-h cycle, but their magnitude varied significantly, being higher between 1800-2200 h (137 +/- 9 ng/ml) than between 0600-1000 h (75 +/- 17 ng/ml). This pattern of release indicates continuous, but variable, activity of the axis throughout the day. The pulsatile ultradian rhythm suggested alternate periods of secretion and inhibition, which were found to have a profound effect on the corticosterone responses to acute stress. Noise stress (10 min, 114 decibels) evoked a transient increase in corticosterone, which reached a maximum (377 +/- 87 ng/ml) 20 min after onset. However, within this group (n = 26) the response varied depending on the underlying basal activity. When stress coincided with a rising (secretory) phase of a pulse, corticosterone concentrations rose to 602 +/- 150% of mean basal concentrations (P < 0.001). In contrast, when stress coincided with a falling (nonsecretory) phase of a pulse, a significantly smaller response, no greater than a basal pulse, was evoked. Thus, the alternate periods of secretion and inhibition generating basal hypothalamo-pituitary-adrenal activity are an important determinant of responses to acute stress.

Activity Cycles↗
PubMed1997

Region-specific immediate-early gene expression following the administration of corticotropin-releasing hormone in virgin and lactating rats.

Central administration of corticotropin-releasing hormone (CRH) induces immediate-early gene (IEG) expression (c-fos and NGFI-B) in forebrain structures in a pattern similar to that observed following restraint stress. Lactating rats display modified neuroendocrine and behavioural responses to stress which have been hypothesized to be at least partially mediated through changes within the circuitry converging on the PVN, including CRH activated pathways. Quantitative measures of regional expression of c-fos and NGFI-B mRNA representative of two classical intracellular pathways, were used to define modification of the circuitry involved in the altered response to central CRH in the lactating female. Compared to saline controls, virgin female rats injected with 5 micrograms CRH i.c.v. displayed significantly increased immediate-early gene expression in the hypothalamic paraventricular nucleus (PVN), arcuate nucleus, lateral septum, bed nucleus of the stria terminalis, central, medial and cortical nuclei of the amygdala, and all subfields of the hippocampal formation. In lactating rats treated with CRH there was a significant increase in c-fos gene expression in the CeA and in the hippocampal subfields CA1, CA4 and dentate gyrus but not in the other areas examined. The i.c.v. administration of CRH significantly increased NGFI-B expression in the PVN, arcuate nucleus, medial amygdala and all hippocampal subfields of virgin rats. Lactating rats treated with CRH failed to show a significant increase in NGFI-B expression in the PVN, median eminence, arcuate nucleus, medial amygdala, CA2 and CA3 subfields of the hippocampus. These results further suggest that changes in specific neural circuits might at least partially underlie the modified responses to CRH and perhaps to stress in the lactating female.

Amygdala↗
PubMed1997

Pharmacological characterisation of oxytocin binding sites in the ovine pineal gland.

Both oxytocin (OT) and [Arg8]vasopressin (AVP) are found within the ovine pineal gland and may function to modulate melatonin secretion. However, the receptors which mediate the actions of these peptides have yet to be characterised. Preliminary studies of ovine pineal microsomal cell membranes showed binding of [3H]OT (79+/-9 fmol/mg) 10 times greater than binding of [3H]AVP (8+/-3 fmol/mg). Saturation studies using either [3H]OT or the selective OT receptor ligand [125I]d(CH2)5[Tyr(Me)2,Thr4,Orn8,Tyr-NH2(9)]-vasotocin (OTA) revealed high affinity, single site kinetics (Kd = 1.72+/-0.32 nM; Bmax = 68+/-18 fmol/mg). Binding of [3H]AVP was more effectively displaced by OT than AVP, suggesting that binding may be due to cross-reaction with the OT binding site. Displacement of [3H]OT using a range of selective agonists and antagonist analogues revealed pharmacological characteristics similar to [3H]OT binding sites in the ovine and rat uterus. These data show that the ovine pineal expresses a high density of OT binding sites which may participate in the regulation of melatonin secretion.

Animals↗
PubMed1997

Evidence for independent hypertensive effects of oxytocin and vasopressin in the rat dorsal vagal complex.

Infusion of OT or the V1 agonist [Phe2,Orn8]-vasotocin (POVT) (50 ng) into the dorsal vagal complex of urethane-anaesthetized male rats induced a sustained hypertension. Simultaneous infusion of the V1 antagonist d(CH2)5[Tyr(Me)2]-VP blocked the effect of POVT, but not of OT. The OT antagonist d(CH2)5[Tyr(Me)2,Thr4,Orn8,Tyr-NH(9)2]-vasotocin blocked the effect of OT, but not of POVT. The OT agonist [Thr4,Gly7]-OT had no effect. This suggests that OT-induced hypertension involves mechanisms independent of V1 and uterine-type OT receptors.

Animals↗
PubMed1997

Changing pattern of oxytocin-induced excitation of neurons in the bed nuclei of the stria terminalis and ventrolateral septum in the peripartum period.

Oxytocin acts within the limbic system (bed nuclei of the stria terminalis and ventrolateral septum) to induce maternal behaviour and to facilitate neuroendocrine activity at specific times during the peripartum period. Studies were undertaken to determine whether the timing of these effects arises from modulation of the oxytocin-induced excitation of limbic neurons. Extracellular activity of single units was recorded on urethane-anaesthetized rats and neurons were tested for responses to intracerebroventricular injection of 1.1 ng oxytocin. In the first part, animals were recorded on days 19 and 22 of pregnancy and on days 3 and 5 of lactation. No significant differences in the basal firing rates or in the proportion of oxytocin-responsive neurons were detected, but responses by neurons on day 22 of pregnancy occurred after a significant delay (10.7 +/- 2.0 min), resulting in a smaller overall response compared to the other groups. These differences in the pattern of response were not due to changes in density of oxytocin binding in the limbic areas studied, since autoradiographic detection of oxytocin binding sites using the iodinated antagonist [125I]d(CH2)5[Tyr(Me)2, Thr4, Orn3, Tyr-NH2(9)]-vasotocin showed no differences between the pregnant and postpartum animals. In the second part, parturient animals (day 22 of pregnancy) received intravenous injection of the long-acting opioid antagonist naltrexone, or unilateral knife-cut lesions to the stria terminalis, a source of inhibitory inputs (including enkephalinergic) to the bed nuclei of the stria terminalis and ventrolateral septum. Both treatments abolished the characteristic delay of oxytocin-induced excitation in non-treated animals on day 22 of pregnancy, and increased the overall excitatory response. Thus, during the peripartum period, a population of limbic neurons sensitive to oxytocin display a dynamically changing pattern of excitatory responses, apparently modulated by an endogenous opioid cone and independent of changes in oxytocin receptor expression. The attenuated neuronal response to central oxytocin seen on the day of parturition could account for the absence of a facilitatory effect of oxytocin on neuroendocrine activity at this time.

Animals↗
PubMed1997

Endocrine and behavioural responses to noise stress: comparison of virgin and lactating female rats during non-disrupted maternal activity.

The behavioural and endocrine responses to a 10 min white noise stress have been characterized in female virgin and undisturbed lactating Sprague-Dawley rats. Animals were continuously video-taped and frequent blood samples were collected using an automated sampling system. Noise stress caused hypothalamo-pituitary-adrenal (HPA) activation, as indicated by a rapid increase in plasma corticosterone and ACTH in the virgins: corticosterone concentrations peaked 20 min after initiation of the stress before declining rapidly back to basal concentrations. In contrast, noise stress had no significant effect on either plasma corticosterone or ACTH concentrations in the lactating animals. However, 72 h after weaning the corticosterone response of the ex-lactating rats was of comparable magnitude, but longer duration to that seen in the virgins. Plasma prolactin concentrations were significantly higher in the lactating animals and declined in response to the noise whereas, a transient but reproducible increase was seen in the virgin group. In situ hybridization revealed a significantly lower basal expression of CRF mRNA in the paraventricular nucleus of lactating rats as compared to the virgins, but noise stress had no further effect. Virgin animals showed behavioural responses to the stress, including an increase in the total activity, exploratory behaviours (rearing) and displacement behaviours (grooming). Lactating animals also showed behavioural responses to the noise, but their activities were principally directed towards the pups. These data show that although lactating rats showed normal behavioural reactivity to a psychological stress they showed no statistically significant activation of the HPA axis, suggesting a dissociation of behavioural and neuroendocrine responses to this mild stress.

Adrenocorticotropic Hormone↗
PubMed1997

Central oxytocin administration reduces stress-induced corticosterone release and anxiety behavior in rats.

Endocrine responses to noise stress and anxiety-related behaviors were measured in groups of ovariectomized, estradiol-treated female rats given central infusions of oxytocin. Control animals receiving isotonic saline showed a large increase in plasma corticosterone concentrations in response to 10 min of white noise. This response to noise stress was significantly and dose dependently decreased by oxytocin administered intracerebroventricularly at 10 or 100 ng/h for 5 days. Oxytocin also significantly decreased rearing behavior during this stress. When a second noise stress was given 3 days after cessation of oxytocin infusion, corticosterone responses did not differ between the control and previously oxytocin-infused animals. Administration of vasopressin had no significant effect on either the corticosterone or behavioral responses to noise stress. Anxiety-related behaviors were measured on the elevated plus-maze. No significant differences were seen in maze exploration between saline- and oxytocin-treated animals when housed and tested in the same environment. However, when animals were mildly stressed by testing in an unfamiliar environment, oxytocin-treated animals showed a higher proportion of open arm entries and spent significantly more time in the open arms of the maze. Thus, oxytocin exerts a central anxiolytic-like effect on both endocrine and behavioral systems and could play a role in moderating behavioral and physiological responses to stress.

Animals↗