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C F Ferris

Publications and source records attributed to C F Ferris.

At least 55 records · Page 3Linked to original sources

An iodinated vasopressin (V1) antagonist blocks flank marking and selectively labels neural binding sites in golden hamsters.

An arginine-vasopressin (AVP) derivative, [d(CH2)5,Sar7]AVP (SAVP), has been characterized as an antagonist to vasopressin V1 receptors. Using AVP-dependent flank-marking behavior as a bioassay, it was possible to verify that iodinated SAVP (I-SAVP) retains biological activity within the central nervous system, as the antagonist blocked the behavior. Furthermore, 125I-SAVP was used to localize specific V1 binding sites in the brain. The resulting binding was localized to discrete anatomical sites, and highly specific to V1-like receptors. While we confirmed previous findings using 3H-AVP in golden hamsters, we also identified binding in many areas previously unreported (e.g., arcuate and paraventricular nuclei of the hypothalamus, tenia tecta, posteromedial cortical nucleus of the amygdala, and zona incerta), suggesting that 125I-SAVP provides a greater level of resolution. In addition, specific binding was observed in the lateral septum, anterior hypothalamus, and midbrain central gray, areas that have previously been shown to trigger flank marking in response to AVP microinjection. The presence of AVP binding sites in limbic and mesencephalic areas involved in the regulation of flank marking suggests that this neuropeptide may play an important role as a neurotransmitter at multiple levels in the neural circuits controlling this behavior.

Animals↗

Distribution of corticotropin-releasing hormone immunoreactivity in golden hamster brain.

The distribution of corticotropin-releasing hormone-immunoreactive (CRH-IR) neurons and fibers was observed in golden hamsters. CRH-IR neurons and fibers were observed within the hypothalamus, thalamus, amygdala, cortex, midbrain, and hindbrain. The largest numbers of CRH-IR neurons were seen within the magno- and parvocellular divisions of the paraventricular nucleus of the hypothalamus and within the septum, bed nucleus of the stria terminalis, preoptic area continuum. The highest density of immunoreactive fibers was observed in the external zone of the median eminence. In addition, many immunoreactive fibers were observed within the bed nucleus of the stria terminalis and the preoptic area. The distribution obtained in hamsters was compared with previously reported distributions from rats, and both were generally similar.

Animals↗

Arginine-vasopressin immunoreactivity is not altered by photoperiod or gonadal hormones in the Syrian hamster (Mesocricetus auratus).

The present study examined whether gonadal hormones or photoperiodic control influence arginine-vasopressin (AVP) immunoreactivity in the Syrian hamster (Mesocricetus auratus) as has been reported in several other rodent species. Male hamsters were castrated or sham-castrated and exposed to LD 14/10 or LD 6/18 for 13 weeks. Photoperiod and castration significantly altered body weight and the levels of circulating testosterone. In sham-castrates, testis width was significantly reduced in hamsters housed in LD 6/18. In contrast, photoperiod and castration produced no detectable alterations in AVP immunoreactivity in various CNS sites including the bed nucleus of the stria terminales, the lateral septum and medial preoptic-anterior hypothalamus when measured by immunocytochemistry and radioimmunoassay of tissue punches. These data provide no evidence that AVP is regulated by either gonadal hormones or photoperiodic mechanisms in the Syrian hamster.

Animals↗

Acute and repeated exposure to social conflict in male golden hamsters: increases in plasma POMC-peptides and cortisol and decreases in plasma testosterone.

The purpose of the present study was to characterize the hormonal response of dominant and submissive male hamsters to acute and repeated exposure to social conflict. We found that submissive, but not dominant, males exhibited elevated plasma levels of adrenocorticotropin (ACTH), cortisol, and beta-endorphin (beta-EP) following one exposure to an agonistic encounter. After five exposures to a dominant opponent, submissive males showed smaller, but still significant, elevations in these plasma hormones. After nine exposures, submissive hamsters showed significant elevations only in plasma ACTH and beta-EP. Plasma testosterone was significantly suppressed in submissive males that fought nine times. We conclude that hamsters are a useful species with which to study the neuroendocrine correlates of social behavior.

Adrenocorticotropic Hormone↗

Steroid-specific regulation of agonistic responding in the anterior hypothalamus of male hamsters.

The agonistic behaviors of adult male golden hamsters (N = 108 dyads) were examined 5 min after stereotaxic microinjection of adrenal and gonadal steroids into the anterior hypothalamus. Flank marks, attacks, bites, and retreats were scored over a 15 min test period during which steroid-injected animals were paired in a neutral arena with vehicle-injected conspecifics. Animals microinjected with either 10(-6) M cortisol or 10(-6) M beta-estradiol displayed significantly (p less than 0.05) higher levels of flank marking than other steroid-treated animals. Animals microinjected with 10(-6) M cortisol displayed significantly higher levels of aggression than their opponents. In contrast, the behavior of the vehicle-injected animals paired with 10(-6) M cortisol-treated opponents was characterized by submissive responding. This profile of the 10(-6) M cortisol treatment, i.e., promoting aggression in a steroid-treated animal while eliciting submission from its vehicle-treated opponent, was not observed in pairs in which steroid-injected animals were treated with equimolar concentrations of testosterone, dihydrotestosterone, progesterone, beta-estradiol, or deoxycorticosterone. These findings suggest steroids exert immediate effects on agonistic responding in the anterior hypothalamus of male hamsters. The immediate action(s) of cortisol appear to include facilitating aggression and flank marking, while the immediate action(s) of beta-estradiol appears to be confined to the communicative aspect of agonistic responding in this species.

Aggression↗

[3H]arginine-vasopressin binding sites in the CNS of the golden hamster.

Tritiated arginine8-vasopressin [( 3H]AVP) was used to identify specific binding sites for this neuropeptide in the CNS of the golden hamster. [3H]AVP binding sites were concentrated in the dorsal, ventral and lateral septum, bed nucleus of the stria terminalis (BNST), central amygdala, hippocampus, dorsal thalamic nuclei, anterior cingulate gyrus and endopiriform nucleus. Septal-BNST [3H]AVP binding sites were further characterized using membrane preparations. Saturation analysis in septal-BNST membranes resulted in a Bmax of 12.4 +/- 0.82 fmol/mg protein and a Kd of 2.5 +/- 0.36 nM. Pharmacological studies indicate that the binding site in the septum-BNST membranes shows selectivity similar to a V1-type vasopressin receptor. Binding characteristics were similar to those obtained from crude septal membranes prepared from adult Long-Evans rat.

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Evidence for a functional and anatomical relationship between the lateral septum and the hypothalamus in the control of flank marking behavior in Golden hamsters.

Golden hamsters with established dominant/subordinate relationships communicate their social status by rubbing pheromone-producing flank glands against objects in the environment. This behavior, called flank marking, is controlled by vasopressin-sensitive neurons localized to the anterior hypothalamus. Vasopressinergic magnocellular neurons in the nucleus circularis and medial aspect of the supraoptic nucleus are thought to be a source of neurotransmitter for the initiation of flank marking. The present study was undertaken to examine the extrahypothalamic control of flank marking. The anatomical and functional connections between the lateral septum and the vasopressin-containing nuclear groups in and around the anterior hypothalamus were examined by: (1) tracing afferent and efferent connections following microinjection of horseradish peroxidase and Phaseolus vulgaris-leucoagglutinin into the lateral septum, and (2) recording odor-induced flank marking prior to and following ibotenate lesions in the septum. The greatest number of perikarya retrogradely labeled with horseradish peroxidase were found lateral to the anterior hypothalamus and ventral to the fornix in the area of the lateral hypothalamus. The vasopressin-containing nuclear groups, e.g., paraventricular, supraoptic, suprachiasmatic nuclei, and the nucleus circularis, were devoid of labeled perikarya. Nerve terminals anterogradely labeled with Phaseolus vulgaris-leucoagglutinin were primarily localized to the anterior hypothalamus, in and around the nucleus circularis, and the medial aspect of the supraoptic nucleus. The lateral aspect of the supraoptic nucleus was devoid of nerve terminals as were the paraventricular and suprachiasmatic nuclei. The anatomical connections between the lateral septum and the hypothalamus appear to be necessary for the control of flank marking, since the microinjection of ibotenate into this limbic site significantly reduced odor-induced flank marking as compared to control microinjections of 0.9% NaCl.

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Vasopressin in the septal area of the golden hamster controls scent marking and grooming.

Microinjection of arginine vasopressin into the lateral septum and bed nucleus of the stria terminalis of male hamsters stimulates intense flank marking and flank gland grooming, while microinjections of vasopressin in sites immediately adjacent to these areas or in the lateral ventricle are ineffective. Microinjections of oxytocin, angiotensin II and the behaviorally active C-terminal fragment of vasopressin, metabolite neuropeptide, by comparison, do not stimulate flank marking. Effective sites for vasopressin injection are clearly superimposable upon autoradiographically defined sites of high V1-receptor density. Furthermore, vasopressin-sensitive neurons in the lateral septum and bed nucleus of the stria terminalis are necessary for the expression of naturally elicited flank marking since the microinjection of a V1-receptor antagonist into these sites was able to temporarily block flank marking triggered by odors from conspecifics.

Animals↗

Exocrine secretion and processing of pro-xenopsin in rat gastric lumen.

This study examines the effects of acid, acid secretagogues, and pepstatin on gastric luminal concentrations of xenopsin-like immunoreactivity (XPLI) by in situ luminal perfusion of the stomach in anesthetized rats. During perfusion with saline over a 2-h period, the concentration of XPLI fell in parallel with acid output. Levels of XPLI fell more rapidly when the saline contained 20 micrograms/ml pepstatin A and when phosphate-buffered saline (pH 7.0) was used. These treatments did not, however, alter acid output. After a basal condition was established at 90 min, intravenous injection of carbachol, pentagastrin, or histamine stimulated acid and pepsin secretion and also led to an increase in XPLI concentration, which was pepstatin sensitive. Acid itself was also a stimulus for pepsin and XPLI output, which were correlated at various levels of acidity. Although pepstatin blocked the effect of acid on XPLI output, it did not lead to an accumulation of xenopsin (XP) precursor in the luminal fluid. However, the decrement in acid-stimulated XPLI output seen in the presence of pepstatin was matched by an increment in XP precursor associated with the mucosal surface. During high-pressure liquid chromatography, approximately 70% of the acid-generated XPLI eluted at the position of mammalian XP. These data support the notion that, during heightened acid output, XP is secreted by a pepsin-dependent process or generated by the action of pepsin on XP precursor present on the mucosal surface of the rat stomach.

Animals↗

Vasopressin immunoreactivity in the anterior hypothalamus is altered during the establishment of dominant/subordinate relationships between hamsters.

When paired for 15-min periods for 5-8 consecutive days, castrated, testosterone-treated hamsters consistently assumed the dominant status, based on a higher aggression index (18 +/- 3) and frequency of flank marking (15 +/- 3) as compared to their castrated, untreated subordinate partners (-1.3 +/- 1 and 2.4 +/- 1, respectively). In addition to these hamsters with established dominant/subordinate relationships, control hamsters with no social interactions were killed, and in all animals the vasopressin level in the anterior hypothalamus-medial preoptic area was assessed by counting vasopressin immunoreactive perikarya following immunocytochemistry, or by radioimmunoassay of vasopressin from tissue punches. In the socialized pairs the subordinate hamsters had a significantly (P less than 0.01) lower number of vasopressin staining perikarya in the anterior hypothalamus, specifically the area of the nucleus circularis, than their dominant partners (n = 6 pairs). There was also a significantly (P less than 0.001) lower level of vasopressin immunoreactivity in punches taken from the area of the nucleus circularis in subordinate hamsters as compared to their dominant partners (n = 14 pairs). However, there were no significant differences in the number of perikarya or the concentration of immunoreactive vasopressin between subordinate and dominant hamsters in the supraoptic nucleus, paraventricular nucleus, suprachiasmatic nucleus or bed nucleus of the stria terminalis. The number of perikarya (n = 5 pairs) and concentration of vasopressin (n = 8 pairs) for all vasopressin immunoreactive sites, including the nucleus circularis, were similar for testosterone-treated and untreated hamsters that remained isolated and not subjected to daily aggressive encounters.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Evidence that neurotensin participates in the central regulation of the preovulatory surge of luteinizing hormone in the rat.

Neurotensin (NT) has been implicated in the central regulation of LH and PRL secretion in the rat. We investigated the importance of NT release to the neural events that trigger the preovulatory LH surge and coincident PRL surge, using as our animal model ovariectomized (OVX) rats treated with estrogen and progesterone to induce reliable and robust surges. To interfere with the action of endogenous NT in the basal forebrain, we administered a NT antiserum (NTAS) in a series of bilateral microinjections aimed at the anterior border of the medial preoptic area. One week after OVX, rats bearing cerebral guide cannulae received Silastic capsules (3 x 15 mm; sc) containing 17 beta-estradiol. Two days later, beginning at 0830 h, conscious rats were administered either NTAS or control serum bilaterally in a series of four 100-nl injections spaced at 30-min intervals. After an initial blood sample, rats received progesterone (4 mg, sc) at 1200 h; blood samples were then taken at 1-h intervals from 1400-2100 h. Blood samples were obtained from conscious, freely moving rats via a chronic atrial catheter implanted previously. Plasma levels of LH and PRL were measured by RIA, and the location of microinjection sites was verified histologically. Administration of NTAS caused a 66% reduction in the magnitude of the LH surge without altering its timing, whereas the PRL surge was unaffected. These results provide strong evidence that NT in the basal forebrain participates in the steroid-induced LH surge and suggest that NT plays a role in the preovulatory LH surge.

Animals↗

Inhibition of vasopressin-stimulated flank marking behavior by V1-receptor antagonists.

Flank marking, a form of olfactory communication displayed by hamsters, is dependent upon vasopressin-sensitive neurons in the anterior hypothalamus. In the present study two vasopressin type-1 (V1) receptor antagonists, d(CH2)5Tyr(Me)AVP and dPTyr(Me)AVP were tested for their ability to block flank marking stimulated by the microinjection of arginine vasopressin (AVP) into the anterior hypothalamus. Dose-response curves were established for AVP and flank marking in the presence or absence of different concentrations of each antagonist. DPTyr(Me)AVP was microinjected into the anterior hypothalamus 1 h before the microinjection of AVP while d(CH2)5Tyr(Me)AVP and AVP were prepared together and delivered as a single microinjection. This procedure was necessary because dPTyr(Me)AVP, but not d(CH2)5Tyr(Me)AVP, had agonist activity when initially injected into the anterior hypothalamus in concentrations ranging from 0.90-900 microM. The ED50 values (microM) for dPTyr(Me)AVP and AVP were 17.9 and 0.90, respectively. The initial agonist activity of dPTyr(Me)AVP was always followed by blocker activity. Both V1-receptor antagonists caused a dose-dependent decrease in AVP-stimulated flank marking. Maximal inhibition of AVP-stimulated flank marking was produced with approximately 1.0 mM of either antagonist. Both antagonists blocked AVP-stimulated flank marking behavior for over 12 h following their microinjection.

Animal Communication↗

Testosterone alters the behavioral response of the medial preoptic-anterior hypothalamus to microinjection of arginine vasopressin in the hamster.

The medial preoptic-anterior hypothalamus (MPOA-AH) is necessary for expression of several testosterone-dependent behaviors including a form of hamster scent marking, called flank marking. Since arginine vasopressin (AVP) plays a critical role in the control of flank marking by the MPOA-AH the present study examined whether testosterone can influence the amount of flank marking produced by AVP microinjected into the MPOA-AH. The dose-dependent induction of flank marking by AVP was found to be reduced by approximately 50% in castrated male hamsters when compared to intact or testosterone-treated castrates. These data demonstrate that testosterone influences the amount of flank marking produced by AVP within the MPOA-AH.

Animals↗

Vasopressin receptor blockade in the anterior hypothalamus suppresses aggression in hamsters.

Although the anterior hypothalamus has been implicated in the control of aggression in various rodent species, little is known about the neurochemical mechanisms mediating this control. It has been established that flank marking, which occurs with high frequency during agonistic encounters in hamsters, is dependent upon vasopressin-sensitive neurons in the anterior hypothalamus. The present study was undertaken to determine whether intraspecific aggression in this species is similarly influenced by vasopressin in this area of the hypothalamus. Adult male hamsters, surgically implanted with guide cannulae aimed at the anterior hypothalamus, were microinjected with three different concentrations of the V1-receptor antagonist d(CH2)5Tyr(Me)AVP or a vehicle control of 0.9% NaCl. Sixty minutes after each microinjection a smaller male hamster was introduced into the home cage of the treated hamster. The resident hamsters showed a significant dose-dependent reduction in the number of biting attacks on the intruders over the 10 minute test period. The V1-receptor antagonist also caused a significant increase in the resident hamster's latencies to attack the intruder. However, the resident hamsters' total contact time with the intruder was unaffected by drug treatment suggesting that the reduction of aggression was not due to a generalized effect upon social behavior. The specificity of the drug treatment was further supported by the observation that it did not affect resident hamsters' sexual motivation or ability to mount a receptive female. These data suggest that vasopressin-sensitive neurons in the anterior hypothalamus are involved in the control of intraspecific aggression in male hamsters.

Aggression↗

Fibronectin extracellular matrix assembly by human epidermal cells implanted into athymic mice.

Human epidermal keratinocytes reorganize into epidermal inclusion cysts when implanted subcutaneously into athymic mice. During the organization and maturation of these cysts, fibronectin accumulates in the surrounding extracellular matrix and the basement membrane proteins bullous pemphigoid antigen and laminin appear at the epithelial-stromal interface. The sequence in which these proteins appear parallels that seen during reepithelialization of a skin wound in vivo. Fibronectin appears during aggregation of the epidermal cells and persists in the area surrounding the cysts for at least 7 days. Bullous pemphigoid antigen and laminin appear later (by 4 and 7 days, respectively) and ultimately become organized into a continuous band at the periphery of the cyst. This distribution of bullous pemphigoid antigen and laminin at the stromal-epithelial interface persists at least 5 weeks, suggesting that the implanted epidermal cells are capable of developing and maintaining a stable basement membrane zone. Fibronectin, which is abundant in the matrix adjacent to the epidermal cysts and in the surrounding stroma during cyst organization and maturation, diminishes to undetectable levels by 5 weeks. While much of the fibronectin derives from the host tissues, species-specific antibodies to human fibronectin reveal that at least a portion of this protein is synthesized and deposited by the implanted epidermal cells.

Animals↗

Light selectively alters vasoactive intestinal peptide and peptide histidine isoleucine immunoreactivity within the rat suprachiasmatic nucleus.

The concentration of vasoactive intestinal peptide (VIP)-, peptide histidine isoleucine (PHI)-, neurotensin (NT)- and substance P (SP)-like immunoreactivity (LI) within the suprachiasmatic nucleus (SCN) were determined by radioimmunoassay in rats housed in LD 14:10 h, constant light or constant dark. No day-night differences were observed in the concentration of VIP-, PHI-, NT- or SP-LI within the SCN. Exposure to constant light significantly depressed the SCN concentrations of VIP- and PHI-LI, but had no significant effects on SCN concentrations of NT- or SP-LI, or VIP- or PHI-LI concentrations within the cortex. These data represent the first evidence that VIP/PHI-containing neurons may be involved in mediating photic information within the SCN.

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