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PubMed1993

Hormone-induced rise in cytosolic Ca2+ in axolotl hepatocytes: extracellular origin and control by cAMP.

In amphibian liver, signal transduction of [Arg8]vasotocin (AVT), a "classical" Ca(2+)-dependent hormone in rat liver, is mediated via the generation of adenosine 3',5'-cyclic monophosphate (cAMP) and not via inositol 1,4,5-trisphosphate [Ins(1,4,5)P3]. In isolated hepatocytes from axolotl, hormones that stimulated cAMP formation (the order of efficacy was glucagon > isoprenaline > epinephrine > or = AVT) also provoked a pronounced increase in cytosolic Ca2+, as indicated from changes in fura 2 fluorescence. 8-Bromoadenosine 3',5'-cyclic monophosphate at 100 microM was as potent as maximally effective concentrations of glucagon. Ins(1,4,5)P3 mobilized Ca2+ from the endoplasmic reticulum of saponin-permeabilized axolotl hepatocytes with a half-maximal effect at 0.65 microM, as did GTP (20 microM), even in the absence of polyethylene glycol. However, the hormonally induced increase in cytosolic Ca2+ was not due to a mobilization of the cation from internal stores by Ins(1,4,5)P3, but to an increased inflow from the extracellular medium. We conclude that in axolotl liver, in contrast to rat liver, hormones stimulate the production of cAMP that, in addition to stimulating processes such as glycogenolysis, also regulates the opening of an ion gate in the plasma membrane, which allows the inflow of Ca2+. To our knowledge this is the first demonstration of a second messenger-operated Ca2+ channel in a splanchnic tissue.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1994

Antidiuretic hormone-responding nonselective cation channel in distal nephron epithelium (A6).

Arginine vasotocin (AVT, 70 mU/ml) added from the basolateral side transiently activated a nonselective cation (NSC) channel with a single-channel conductance of 28.5 pS and almost identical selectivity for Na+ and K+ in the apical membrane of distal nephron cells (A6) cultured on permeable supports for 10-12 days in media containing 10% fetal bovine serum without supplemental aldosterone. The open probability (Po) of the NSC channel at the apical resting membrane potential in cell-attached patches was approximately 0.09 and increased when the apical membrane depolarized. The Po of the NSC channel was decreased by a rise in cytosolic Ca2+ concentration within a range of 30 nM-1 microM but not affected by cytosolic pH within a range of 6-8. The channel was activated by the application of negative pressure (10-60 cmH2O) into the patch pipette. Gadolinium (2 microM), an inhibitor of stretch-activated channels, decreased the Po by 40%. This blocking action of gadolinium was more effective after the channel was activated by stretch, i.e., 2 microM gadolinium decreased the Po by 70% when a negative pressure (60 cmH2O) was applied into the patch pipette. Amiloride (10 and 100 microM) showed a blocking action on the channel only when the NSC channel was activated by stretch.

Amiloride↗

PubMed1990

Ca2+ release and InsP3 production in avian uterine cells: effects of PGF2 alpha and AVT.

Primary cultures of smooth muscle cells isolated from the shell gland ("uterus") of the domestic hen were permeabilized with digitonin and loaded with 45Ca2+ in the presence of ATP. When these cells were stimulated with prostaglandin F2 alpha (PGF2 alpha), arginine vasotocin (AVT), or D-myo-inositol 1,4,5-trisphosphate [Ins(1,4,5)P3], there was a rapid, biphasic, and dose-related release of 45Ca2+ from nonmitochondrial pools. 2-Nitro-4-carboxyphenyl-N,N-diphenylcarbamate, an inhibitor of phospholipase C, had no effect on PGF2 alpha - and Ins(1,4,5)P3-promoted 45Ca2+ efflux, whereas it significantly inhibited AVT-stimulated and a stable analogue of GTP-stimulated 45Ca2+ release. In fura-2-loaded intact cells, both PGF2 alpha and AVT increased intracellular Ca2+ levels [( Ca2+]i) in a dose-related manner in the presence of extracellular Ca2+. However, omission of extracellular Ca2+ prevented a PGF2 alpha, but not AVT-induced, rise in [Ca2+]i In D-myo-[3H]inositol-labeled cells, 10 nM AVT caused a rapid, two- to threefold increase in [3H]-Insp3, whereas PGF2 alpha up to 1 microM was infective. Raising PGF2 alpha to 10 microM increased total inositol phosphates by 22% over controls (P less than 0.05). These results point to marked differences in the mechanisms by which AVT and PGF2 alpha regulate [Ca2+]i in uterine smooth muscle cells. It is suggested that the two agonists act in concert to initiate oviposition.

Animals↗

PubMed2005

Exposure to chronic stress downregulates corticosterone responses to acute stressors.

We used captive European starlings (Sturnus vulgaris) to test whether corticosterone responses differed in birds held under normal laboratory conditions or conditions of chronic stress. Surprisingly, both basal corticosterone concentrations and corticosterone responses to acute stress were significantly reduced when birds were chronically stressed. To determine the mechanism underlying this reduced response, animals under both conditions were injected with lactated Ringer's solution (control), adrenocorticotropin (ACTH), arginine vasotocin (AVT), or dexamethasone (DEX). ACTH increased corticosterone concentrations above stress-induced levels in both cases, although maximum responses were lower in chronically stressed birds. AVT did not augment the corticosterone response under nonchronically stressed conditions, but it did under chronically stressed conditions. DEX reduced maximal corticosterone concentrations in both cases. Neither ovine nor rat corticotropin-releasing factor (CRF) altered normal stress responses. These data indicate that changes in responsiveness of the hypothalamic-pituitary-adrenal axis to ACTH and AVT serve to downregulate corticosterone responses during chronic stress. Furthermore, these data lead to the following hypothesis: ACTH output from the pituitary limits maximum corticosterone concentrations under normal conditions, but reduced AVT release from the hypothalamus regulates lower corticosterone concentrations under chronic stress conditions.

Acute Disease↗

PubMed1986

Diluting segment in avian kidney. II. Water and chloride transport.

The mammalian-type nephrons of avian kidneys contain a Henle's loop that runs parallel to the collecting ducts and the vasa recta. Thus we examined whether the thick ascending limb (TAL) of Henle's loop of the avian kidney acts as a diluting segment by measuring water and Cl transport in the isolated and perfused TAL of the quail, Coturnix coturnix. The TAL showed a lumen-positive transepithelial voltage (Vt) (+9.4 +/- 0.4 mV, n = 28). Net water flux (Jv) was nearly zero when the TAL was perfused and bathed with isosmotic solution. When the osmotic gradient was imposed, Jv increased only slightly, and thus the osmotic water permeability (Lp) was low. Arginine vasotocin (AVT) added to the hyperosmotic bath did not alter either Jv, Lp, or Vt. Cl efflux (lumen to bath, 370.4 +/- 27.7 peq X mm-1 X min-1) was higher than Cl influx (bath to lumen, 98.6 +/- 14.3 peq X mm-1 X min-1) when measured in the different tubules. AVT showed no effect on Cl efflux. These results indicate that in the TAL of the quail osmotic water permeability is low while net Cl reabsorption is present, suggesting that the TAL functions as a diluting segment.

Animals↗

PubMed1986

Neurohypophysial peptide potencies in cultured anuran epithelia (A6).

To characterize the V2 receptor (for antidiuretic hormone), we have studied the effect of a number of neurohypophysial hormone analogues on cyclic AMP (cAMP) accumulation and short-circuit current in cultured epithelia formed by A6 cells. A6 is the designation of a continuous cell line derived from the kidney of Xenopus laevis. The order of potency for stimulating cAMP accumulation and short-circuit current in A6 epithelia is like that for stimulating water permeability in toad urinary bladder. As anticipated, arginine vasotocin (AVT), the antidiuretic hormone of Amphibia, is more potent than arginine vasopressin (AVP), the antidiuretic hormone of most mammals. The two hormones differ only in the third amino acid (Phe-3 in AVP is a substitution for Ile-3 in AVT). However, there are a number of striking differences in the responsiveness of these amphibian V2 receptors and mammalian V2 receptors to changes in the 7th, 8th, and 9th amino acids where AVT and AVP are identical. 1) Substitution of Lys-8 for Arg-8 in AVP results in marked loss of potency in Amphibia, whereas there is only modest loss of potency in mammals. 2) Desglycinamide AVP is nearly as potent as AVP in Amphibia, whereas it is inactive in mammals. 2) Tocinoic acid, lacking amino acids 7, 8, and 9, has activity in Amphibia, but pressinoic acid, lacking the same three amino acids, is inactive.

Amino Acids↗

PubMed1990

Ontogeny of vasoconstrictor neurohypophysial hormone function in rats.

This in vitro study examined the ontogeny of arginine vasopressin (AVP) and arginine vasotocin (AVT) compared with norepinephrine (NE)-mediated contraction in rat thoracic aortas. Aortas from three age groups (2-3 days, 6-7 days, and 12 wk) of Sprague-Dawley rats were used. Ring segment resting length was adjusted to optimize tension developed to a dose that produces half-maximal tension of NE in Krebs solution (pH 7.4, 37 degrees C) and gassed with 95% O2-5% CO2. Cumulative dose-response curves were generated for KCl (5-100 mM), NE (10(-10)-10(-5) M), AVP, and AVT (both 10(-10)-10(-6) M) in the presence and absence of a selective V1 vasopressinergic inhibitor, [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid), 2-(O-methyl)tyrosine]arginine vasopressin ([d(CH2)5Tyr(Me)]AVP). A progressive increase in sensitivity among all age groups was found for KCl and NE. There was a slight decrease in sensitivity to both AVP and AVT in the 1st wk. Maximum contractile response to NE increased between 2-3 and 6-7 days, whereas no change was observed for KCl, AVP, or AVT. AVP- and AVT-mediated contractions were selectively inhibited by [d(CH2)5Tyr(Me)]-AVP. These results suggest 1) receptor-mediated contractility is present from 2 days of age for NE, AVP, and AVT; 2) sensitivity to KCl and NE increases progressively during postnatal development, whereas sensitivity to AVP and AVT slightly decreases in the 1st wk with no progressive age-related increase by 12 wk; 3) AVP and AVT mediate contraction via a similar V1-like receptor.

Aging↗

PubMed1990

ADH, renal, and circulatory responses to adrenergic stimulation in anterior third ventricle.

The anterodorsal part of the third ventricle of conscious ducks was perfused intracerebroventricularly (icv) for 10 min with norepinephrine (NE) or with its agonists phenylephrine (alpha 1, Phe), isoproterenol (beta, Iso), and clonidine (alpha 2, Clo) in artificial CSF (aCSF). Their effects on the plasma level of antidiuretic hormone (AVT, arginine vasotocin in birds), urine excretion, heart rate (HR), and mean arterial pressure (MAP) were investigated in steady-state water diuresis. The correct position of the icv cannula was confirmed by enhanced AVT release and antidiuresis in response to icv perfusion of aCSF made hypertonic (400 mosmol/kgH2O) by adding NaCl. Icv perfusion with hypertonic aCSF and 750 ng/min NE had comparable effects on AVT release and urine excretion, but hypertonic aCSF caused small increases in MAP and HR, whereas NE depressed both MAP and HR. Antidiuresis and circulatory depression caused by NE icv perfusion was dose dependent. Among the adrenergic agonists perfused at similar doses (188 ng/min), only Iso stimulated AVT release. Iso and Phe had small depressive effects on MAP and HR (less than 10%). Clo depressed circulation by greater than 20% for longer than 60 min, and AVT release became significantly reduced 30 min after the start of icv perfusion. The consistent results in ducks contrast with the equivocal data hitherto reported for central stimulations with NE or its agonists in mammals and may be due to the concentric perfusion system used in our study for localized stimulations in the vicinity of the paraventricular nucleus.

Animals↗

PubMed1994

Na+ transport and pH in principal cells of frog skin: effect of antidiuretic hormone.

Intracellular pH (pHi), apical membrane potential (Va), and fractional apical membrane resistance (FRa) were measured in principal cells of isolated frog skin (Rana pipiens) with double-barreled microelectrodes under short-circuit conditions. Basolateral exposure to 10 mU/ml arginine vasotocin (AVT) depolarized Va by 30 mV, decreased FRa by 33%, increased short-circuit current (Isc) by 17 microA, and increased pHi by 0.17 pH units. The response of Va, Isc, and pHi occurred concurrently. Forskolin, theophylline, and 8-(4-chlorophenyl-thio)-adenosine 3',5'-cyclic monophosphate caused similar changes in Va, Isc, and pHi. The enhanced response of Isc, Va, and FRa to short pulses of apical amiloride applied during AVT or cAMP exposure suggests an increase in apical Na+ conductance. The presence of cAMP agonists also enhanced the response of pHi to amiloride. We conclude that the AVT- and cAMP-induced increase in Na+ transport across the apical cell membrane is associated with a change in pHi. These data are consistent with the hypothesis that changes in pHi may play a role in the second messenger cascade initiated by the antidiuretic hormone.

Amiloride↗

PubMed1994

The exercise pressor reflex is attenuated by intrathecal oxytocin.

We tested the hypothesis that oxytocin (Oxt) acts in the lumbar spinal cord to attenuate reflex pressor (mean arterial pressure, MAP) and heart rate (HR) responses to static hindlimb contraction (i.e., the exercise pressor reflex). Thus we compared MAP and HR responses to electrically stimulated hindlimb static contraction in the anesthetized cat before and after intrathecal injection of Oxt (30 pmol, n = 3; 300 pmol, n = 6; or 3 nmol, n = 6). The 300-pmol dose was most effective; it attenuated the pressor response to static contraction by 39 +/- 10% but had no effect on HR. In three other cats, contraction-induced increases in MAP and HR were monitored before and after intrathecal injection of 300 pmol of Oxt + 300 nmol of the selective Oxt receptor antagonist [d(CH2)5(1),O-Me-Tyr2,Thr4,Tyr9,Orn8]vasotocin. Pretreatment with the antagonist eliminated the effect of Oxt on MAP. In an additional 10 cats, increases in these same variables in response to static contraction were compared before and after intrathecal injection of the Oxt antagonist (30 nmol, n = 3 or 300 nmol, n = 7) into the lumbar spinal cord (L1-L7). Whereas 30 nmol of the Oxt antagonist had no effect, the 300-nmol dose augmented the contraction-induced pressor and HR responses by 28 +/- 7 and 32 +/- 17%, respectively. These data imply that endogenous Oxt modulates the exercise pressor reflex by its action on Oxt receptors in the lumbar spinal cord that can attenuate sensory nerve transmission from skeletal muscle.

Animals↗

PubMed1995

Effect of acute manipulation of blood volume and osmolality on plasma [AVT] in seawater flounder.

Chronically cannulated seawater (SW)-adapted flounder (Platichthys flesus) were used unanesthetized and unrestrained in an experimental series that acutely manipulated blood volume and plasma osmolality to determine their influence on plasma arginine vasotocin (AVT) concentrations. Immunoreactive AVT was measured using a radioimmunoassay validated for flounder and other teleosts. After hemorrhage-induced hypovolemia or hypervolemia produced by saline infusion, no major changes in plasma AVT concentrations were detected. Raising plasma osmolality by intraperitoneal injection of 1 M NaCl compared with control 150 mM NaCl-injected fish (329.4 +/- 3.4 vs. 320.4 +/- 3.0 mosmol/kgH2O, P < 0.05) produced an increase in plasma AVT concentration (6.7 +/- 1.2 vs. 4.2 +/- 0.2 fmol/ml, P < 0.05). In a separate study, plasma composition in a large number of uncannulated SW-adapted flounder was determined. This demonstrated a positive linear relationship between the natural variation in plasma AVT concentrations and plasma osmolality and Na+ and Cl- concentrations observed between fish. These data indicate that AVT secretion in SW-adapted flounder is closely related and perhaps directly sensitive to changes in plasma tonicity.

Animals↗

PubMed1996

Water transport in collecting ducts of Japanese quail.

Previously, we reported that the countercurrent urine concentration mechanism in birds appears to operate by recycling of a single solute (NaCl), in which the thick ascending limb of looped nephrons provides an energy source. To determine the importance of the medullary collecting duct (MCD) in the countercurrent multiplier system, we examined in isolated and perfused MCDs from Japanese quail, Coturnix coturnix, the osmotic and/or diffusional water permeability and whether arginine vasotocin (AVT) regulates water permeability. We noted that dark cells that possess electron-dense cytoplasm and numerous mitochondria and light mucus-secreting cells exist in the cortical collecting duct (CD), whereas only mucus-secreting cells are present in the MCDs. The volume flux (Jv) in the MCDs from intact birds and that from the water-deprived birds were nearly zero; after exposure to a hyperosmotic bath and AVT (2 x 10(-5) M), the Jv was significantly higher in water-deprived birds. The diffusional water permeability (Pdw) was moderately high in MCDs bathed in an isosmotic bath in which the Pdw was increased slightly by AVT (10(-5) M, bath) and more markedly (10(-5) M) by forskolin (Fsk), whereas 1,9-dideoxy Fsk (an inactive analogue) showed no effect. Furthermore, the basal adenosine 3',5'-cyclic monophosphate (cAMP) levels were higher in the medulla than in the cortex and were stimulated only slightly by AVT (10(-5) M) and markedly by Fsk (10(-4) M) in both the cortex and medulla. These results in the C. coturnix CD indicate the following. 1) Two types of cells are present; whereas dark cells resemble mammalian intercalated cells morphologically, it is not certain whether mucus-secreting cells are equivalent to principal cells. 2) AVT increases Pdw via a cAMP mechanism; the relatively high basal Pdw and minor effect of AVT on Jv and Pdw suggest, however, that diffusional water movement across the MCD may occur without significant direct control by AVT.

Animals↗

PubMed2001

Hormonal regulation of chicken intestinal NHE and SGLT-1 activities.

The effects of aldosterone and arginine vasotocin (AVT) on intestinal Na(+)/H(+) exchange (NHE) and Na(+)-sugar cotransport (SGLT-1) activities have been investigated using brush-border membrane vesicles isolated from Hubbard chicken small and large intestines, and they were compared with those induced by either Na(+) depletion or dehydration. Na(+) depletion was induced by feeding the chickens with either a low- or a high-Na(+) diet for either 0.5, 1, 2, 4, or 8 days. Ileal and colonic NHE2 activity increased with the duration of the Na(+) depletion, whereas that of intestinal SGLT-1 decreased, reaching a plateau after 2 days of treatment. Three-hour incubation of the intestine with aldosterone produced the same effects on NHE activity as does Na(+) depletion, without altering SGLT-1 activity. However, 3-h incubation of the intestine with AVT increased intestinal SGLT-1 activity, without affecting intestinal NHE activity. It is concluded that aldosterone regulates apical ileal and colonic NHE2 activity, whereas that of SGLT-1 is regulated by AVT.

Aldosterone↗

PubMed1995

ADH-evoked [Cl-]i-dependent transient in whole cell current of distal nephron cell line A6.

The effect of antidiuretic hormone (ADH) on a distal nephron cell line (A6) was studied using the whole cell patch-clamp technique. A6 cells were cultured on a permeable support filter for 10-14 days in media containing 10% fetal bovine serum without supplemental aldosterone. In the unstimulated condition A6 cells had very small conductances of Na+,K+, and Cl-. Arginine vasotocin (AVT, 140 mU/ml, 280 nM) evoked a "transient" increase in whole cell currents as did dibutyryl-adenosine 3',5'-cyclic monophosphate (5 mM). These transients consisted of two components; one was the nonselective cation conductance, and the other was the Cl- conductance. Activation of these conductances was dependent on intracellular Cl- concentration ([Cl-]i). At low [Cl-]i (< or = 50 mM) both conductances were activated, whereas when [Cl-]i was 80 mM, only the Cl- conductance was activated. At high [Cl-]i (125 mM), both conductances were inhibited. It seems likely that the [Cl-]i maintained at a low level (< or = 50 mM) is an important requirement for A6 cells to respond to AVT.

Animals↗

PubMed1998

Microtubule disruption inhibits AVT-stimulated Cl- secretion but not Na+ reabsorption in A6 cells.

The effects of microtubule disruption on arginine vasotocin (AVT)-stimulated Na+ and Cl- transport were studied in A6 cells by measuring short-circuit currents (Isc) across cell layers grown in tissue culture on permeable supports. Microtubule disruption inhibited an AVT-stimulated secretory Cl- current but did not prevent activation of amiloride-sensitive Na+ transport. This AVT-stimulated secretory Cl- current was significantly inhibited by glibenclamide, an inhibitor of the cystic fibrosis transmembrane conductance regulator (CFTR). Reverse transcription of RNA isolated from A6 cells followed by polymerase chain reaction (PCR) using primers designed to amplify a portion of the R-domain of CFTR cloned from Xenopus laevis skin and immunocytochemistry demonstrated the presence of CFTR in A6 cells and an apparent recruitment of cytoplasmic CFTR to the apical cell surface after AVT stimulation. In contrast, indirect immunofluorescent labeling of Na+ channels using a polyclonal antibody raised against a biochemically isolated Na+ channel complex from bovine renal medulla labeled the apical plasma membrane but failed to demonstrate intracellular labeling of Na+ channels (except in subconfluent cells) or recruitment of Na+ channels to the apical membrane region after AVT stimulation.

Animals↗

PubMed2006

Stimulation of the hypothalamic paraventricular nucleus modulates cardiorespiratory responses via oxytocinergic innervation of neurons in pre-Botzinger complex.

Previously we reported that oxytocin (OT)-containing neurons of the hypothalamic paraventricular nucleus (PVN) project to the pre-Bötzinger complex (pre-BötC) region and phrenic motoneurons innervating the diaphragm (D). The aim of these studies was to determine pathways involved in PVN stimulation-induced changes in upper airway and chest wall pumping muscle activity. In addition, we determined the role of OT-containing neurons in the PVN in mediating increased respiratory output elicited by PVN stimulation. Neuroanatomical experiments, using pseudorabies virus (PRV) as a transneuronal tracer in C8 spinalectomized animals showed that PVN neurons project to hypoglossal motoneurons innervating the genioglossus (GG) muscle. Furthermore, microinjection of the PVN with bicuculline, a GABA(A) receptor antagonist, significantly increased (P < 0.05) peak electromyographic activity of GG (GG(EMG)) and of D(EMG), frequency discharge, and arterial blood pressure (BP) and heart rate. Prior injection of OT antagonist [d-(CH(2))(5),Tyr(Me)(2),Orn(8)]-vasotocin intracisternally or blockade of OT receptors in the pre-BötC region with OT antagonist l-368,899, diminished GG(EMG) and D(EMG) responses and blunted the increase in BP and heart rate to PVN stimulation. These data show that PVN stimulation affects central regulatory mechanisms via the pre-BötC region controlling both respiratory and cardiovascular functions. The parallel changes induced by PVN stimulation were mediated mainly through an OT-OT receptor signaling pathway.

Animals↗

PubMed2001

Electrophysiological evidence for vasopressin V(1) receptors on neonatal motoneurons, premotor and other ventral horn neurons.

Prominent arginine-vasopressin (AVP) binding and AVP V(1) type receptors are expressed early in the developing rat spinal cord. We sought to characterize their influence on neural excitability by using patch-clamp techniques to record AVP-induced responses from a population of motoneurons and interneurons in neonatal (5-18 days) rat spinal cord slices. Data were obtained from 58 thoracolumbar (T(7)-L(5)) motoneurons and 166 local interneurons. A majority (>90%) of neurons responded to bath applied AVP (10 nM to 3 microM) and (Phe(2), Orn(8))-vasotocin, a V(1) receptor agonist, but not V(2) or oxytocin receptor agonists. In voltage-clamp, postsynaptic responses in motoneurons were characterized by slowly rising, prolonged (7-10 min) and tetrodotoxin-resistant inward currents associated with a 25% reduction in a membrane potassium conductance that reversed near -100 mV. In interneurons, net AVP-induced inward currents displayed three patterns: decreasing membrane conductance with reversal near -100 mV, i.e., similar to that in motoneurons (24 cells); increasing conductance with reversal near -40 mV (21 cells); small reduction in conductance with no reversal within the current range tested (41 cells). A presynaptic component recorded in most neurons was evident as an increase in the frequency but not amplitude (in motoneurons) of inhibitory and excitatory postsynaptic currents (IPSCs and EPSCs), in large part due to AVP-induced firing in inhibitory (mainly glycinergic) and excitatory (glutamatergic) neurons synapsing on the recorded cells. An increase in frequency but not amplitude of miniature IPSCs and EPSCs also indicated an AVP enhancement of neurotransmitter release from axon terminals of inhibitory and excitatory interneurons. These observations provide support for a broad presynaptic and postsynaptic distribution of AVP V(1) type receptors and indicate that their activation can enhance the excitability of a majority of neurons in neonatal ventral spinal cord.

2-Amino-5-phosphonovalerate↗

PubMed2001

Social and neural modulation of sexual plasticity in teleost fish.

Teleost fishes are the 'champions' of sexual plasticity among vertebrates. Several species have two male reproductive morphs with distinct suites of behavioral, somatic, neuronal, endocrinological, and life history traits. Here, we consider recent studies of the social and neural modulation of sexual plasticity for such species with a focus on two neuropeptides, gonadotropin releasing hormone (GnRH) and arginine vasotocin (AVT, teleostean analogue of mammalian arginine vasopressin). The major premise of this review is that phenotypic changes in GnRH and AVT expression in the brain can orchestrate events leading to changes in either sexual status or the expression of morph specific display behaviors important in reproduction.

Animals↗