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PubMed1989

Simultaneous immunogold labeling of GABAergic terminals and vasopressin-containing neurons in the rat paraventricular nucleus.

The GABAergic innervation of vasopressin-containing cells in the magnocellular part of the paraventricular nucleus was studied at the electron-microscope level using antibodies against GABA and vasopressin. The detection of both GABA and vasopressin on the same ultrathin section, performed with a double-labeling immunogold method, revealed GABAergic terminals in symmetrical synaptic contact with vasopressin-containing neurons. These GABAergic terminals displayed mitochondria, clear synaptic vesicles and varying numbers of electron-dense vesicles. Vasopressin-immunoreactivity was associated with neurosecretory granules, whereas GABA-immunoreactivity was found above mitochondria, clear synaptic vesicles and some electron-dense vesicles. This study, demonstrating the extensive participation of GABA in the innervation of magnocellular vasopressin-secreting neurons, suggests that this inhibitory neurotransmitter regulates vasopressin secretion at the level of the paraventricular nucleus.

Animals↗
PubMed1994

Modulation of plasma arginine vasopressin during rehydration in the Bedouin goat.

When severely dehydrated Bedouin goats were allowed to drink to satiation their plasma arginine vasopressin concentration immediately dropped from a value of 19.9 +/- 9.4 pmol.l-1 to 9.4 +/- 3.9 pmol.l-1 (P < 0.05). It continued to drop further until a concentration of 1.8 +/- 2.9 pmol.l-1 was recorded, similar to that reported for goats allowed to drink freely. When the goats were shown the water but drinking was denied, plasma arginine vasopressin immediately dropped to 11.7 +/- 4.0 pmol.l-1 (P < 0.05) and further decreased to 10.0 +/- 4.8 pmol.l-1 5 min following their sighting the water. This level, however, was not sustained and 2 h after the initial drop the high pre-trial concentration of plasma arginine vasopressin was regained. Presumably, sighting of water by dehydrated goats induces an abrupt drop in their plasma arginine vasopressin level even before drinking commences. When rehydrated, by introducing water directly to the rumen, circumventing both the sensing of the water and the drinking proper, no immediate drop in the plasma arginine vasopressin concentration of the newly rehydrated goats was observed. A delayed drop in the plasma arginine vasopressin levels took place slowly, concurrently with the drop in osmolality and concentration of Na+ in the plasma. It is suggested that sighting of water by dehydrated goats is involved in the modulation of plasma arginine vasopressin.

Animals↗
PubMed1993

The suprachiasmatic nucleus of the mink (Mustela vison): apparent absence of vasopressin-immunoreactive neurons.

The hypothalamic suprachiasmatic nucleus is centrally involved in generation of several circadian rhythms. Neurons of the mammalian suprachiasmatic nucleus express a number of neuropeptides including vasopressin. The suprachiasmatic nucleus of the mink (Mustela vison) is easily distinguished from neighbouring hypothalamic areas and the underlying optic chiasm as a small nucleus containing densely packed parvocellular neurons. A dorsal and ventral subdivision were clearly recognized within the midportion and caudal part of the nucleus. Using immunohistochemistry, we have identified vasopressin-, neurophysin-, and vasoactive intestinal peptide-immunoreactive neuronal elements in the hypothalamus of the mink. Vasoactive intestinal peptide-immunoreactive neurons can be observed in the ventral aspect of the suprachiasmatic nucleus, but to our surprise, no vasopressin immunoreactive perikarya are found within the suprachiasmatic nucleus, this absence being independent of the experienced annual cycle. The hypothalamic paraventricular and supraoptic nuclei contain large numbers of vasopressin-, neurophysin- and vasoactive intestinal peptide-immunoreactive magnocellular neurons with extensive projections towards the infundibulum and neurohypophysis. A comparative analysis of the distribution of vasopressin-immunoreactive elements in a number of conventional laboratory animals has demonstrated that, in contrast to the rat, golden hamster and Mongolian gerbil, neither vasopressin-containing perikarya in the suprachiasmatic nucleus nor fine calibered immunoreactive fibres entering the adjacent subparaventricular zone are present in the mink. The mink is a photodependent seasonal breeder, and thus vasopressin-immunoreactive neurons in the suprachiasmatic nuclei may not be essential for the photoperiodic regulation of reproduction and seasonal events experienced by this species.

Animals↗
PubMed1980

Evidence for the involvement of a GABA-mediated inhibition in the hypovolaemia-induced vasopressin release.

The influence of GABA and of drugs, known to alter GABA-metabolism, on the hypovolaemia-provoked vasopressin release was investigated in rats. Blood volume was decreased without altering plasma osmolality or arterial blood pressure by i.p. injection of polyethylene glycol and the resulting plasma vasopressin concentration was measured using a radioimmunoassay. I.c.v. injections of GABA (0.4-2 mg) markedly suppressed the hypovolaemia-induced vasopressin release. The central inhibitory effect of GABA could not be related to appropriate changes in peripheral parameters believed to regulate vasopressin release (arterial blood pressure, renin-angiotensin system). Aminooxyacetic acid (9-81 mg kg-1, i.m.) and gamma-vinyl-GABA (1.5 g kg-1, i.p.), two potent inhibitors of GABA aminotransferase and known to increase brain GABA content, reduced vasopressin release to a comparable degree as did GABA (i.c.v.). On the other hand, 3-mercaptopropionic acid (10-90 mg kg-1, i.p.), an inhibitor of the GABA synthetizing enzyme glutamic acid decarboxylase, promoted the release of vasopressin when the rats were killed prior to the onset of convulsions. These results, on the whole, intimate the existence of a GABA-mediated inhibition in the central control of vasopressin release.

3-Mercaptopropionic Acid↗
PubMed1983

Effects of guanine nucleotides on vasopressin-induced water flow and sodium transport of the frog bladder.

In the present study, we examined the effects of guanine nucleotides on vasopressin-induced osmotic water flow and sodium transport in the 14-h preincubated frog bladder. We also examined the effects of the adenylate cyclase-cyclic AMP and cyclic AMP-dependent protein kinase system in the bladder's epithelial cells. Gpp(NH)p significantly enhanced vasopressin-induced water flow while it did not affect cyclic AMP-induced water flow. However, Gpp(NH)p did not enhance the vasopressin-induced increment of sodium transport across the frog bladder. The adenylate cyclase activity of the crude homogenate was enhanced by vasopressin, Gpp(NH)p and NaF. The effects of Gpp(NH)p and vasopressin, at their maximum doses, on the enzyme activities were additive, while other combinations were not. Specific Gpp(NH)p binding sites were found in the pellet fraction after 2,400 X g centrifugation. No direct effect on the protein kinase activity was observed in the presence of 10(-6) M nucleotides, such as GTP, GDP, GMP, CTP, UTP, ITP and Gpp(NH)p. Cyclic AMP stimulated the phosphorylation of discrete protein bands, however, Gpp(NH)p did not influence cyclic AMP-dependent protein phosphorylation of crude homogenate of the bladder's epithelial cells. These results suggest the guanine nucleotides stimulate the vasopressin-induced osmotic water flow in frog bladder by enhancing the vasopressin-mediated adenylate cyclase activity, so that accumulated cyclic AMP might activate cyclic AMP-dependent protein kinase.

Adenylyl Cyclases↗
PubMed1991

Activation of voltage-sensitive Ca2+ currents by vasopressin in an insulin-secreting cell line.

The effect of vasopressin on voltage-sensitive Ca2+ currents in the rat insulinoma cell line RINm5F has been investigated in patch-clamp whole-cell and single-channel current recording experiments. In the whole-cell recording configuration the dominant inward current in the presence of tetrodotoxin was noninactivating and had a high voltage threshold. This current was much enhanced when external Ca2+ was replaced by Ba2+ and was blocked by 1 microM nifedipine. It can therefore be classified as an L-current. Vasopressin enhanced the L-current without changing the voltage threshold of activation or the voltage at which the peak current was observed. Vasopressin effects were seen at concentrations as low as 0.01 nM, and the maximal effect was observed at about 1 nM. In higher concentrations the vasopressin effects were weaker, with effects at 50 nM of about the same magnitude as at 0.01 nM. In single-channel current recording experiments carried out with the cell-attached configuration there were no effects on single L-channel currents when vasopressin was added to the bath solution, but in experiments in which vasopressin (5 nM) was infused into the patch pipette a marked increase in the apparent channel open state probability was observed. We conclude that vasopressin, a peptide that is known to markedly enhance glucose-evoked insulin secretion, stimulates opening of the voltage-sensitive Ca2+ channels in insulin-secreting cells.

Animals↗
PubMed1978

Role of prostaglandin E (PGE) in the modulation of the action of vasopressin on water flow in the urinary bladder of the toad and mammalian kidney.

PGE1 and PGE2 are known to interfere with the water permeability effect of vasopressin in toad bladder and kidney. It has been proposed that endogenous prostaglandin E (PGE), synthesized within cells of vasopressin-sensitive tissues, serves to modulate the permeability changes elicited by the neurohypophyseal hormone. Direct evidence in support of this hypothesis is as follows: vasopressin increases the biosynthesis of PGE2 in renal interstitial cells and in isolated toad bladder. In the latter, inhibition of vasopressin-induced synthesis of PGE by a variety of inhibitors results in a greater water permeability response to vasopressin. It appears that vasopressin has two effects in toad bladder and kidney: (i) it activates adenylate cyclase thereby increasing the concentration of adenosine 3',5' monophosphate (cyclic AMP), the nucleotide responsible for the resultant increase in water permeability; and (ii) it activates a phospholipase that serves to release arachidonic acid, the precursor of PGE2 from intracellular pools. The PGE derived from the arachidonic acid diminishes adenylate-cyclase activity, in consequence of which the response of the enzyme to vasopressin is modulated.

Adenylyl Cyclases↗
PubMedDate not supplied

Comparative physiological features of the regulatory effect of vasopressin on higher nervous activity in an ascending series of mammals.

This report provides comparative physiological data on the features of the regulatory effects of the neurohormone vasopressin on higher nervous activity in an ascending series of mammals consisting of insectivores, rodents, and primates. Administration of vasopressin to hedgehogs produced a general facilitatory effect on conditioned reflex brain activity. The effects of vasopressin on memory processes in hedgehogs was minor. In rabbits, vasopressin had greater regulatory effects on conditioned reflex memory than in hedgehogs. However, this was transient in nature. In monkeys, administration of vasopressin had complex differential effects on simple conditioned responses and different types of memory. The effects of vasopressin on memory processes were long-lasting and were different for corticalized and noncorticalized forms of nervous activity. The question of changes in the nature of the regulatory effects of vasopressin during phylogenesis is discussed, as is the question of the increases in its level of involvement in the regulation of higher nervous functions and memory processes.

Animals↗
PubMed1987

Effects of phorbol esters, A23187 and vasopressin on oleate metabolism in isolated rat hepatocytes.

Studies were conducted to compare the metabolic effects of vasopressin, 4 beta-phorbol-12-myristate-13-acetate (PMA) and A23187 on ketogenesis and oleate metabolism in isolated hepatocytes from fed rats. Vasopressin inhibited the formation of acid-soluble products from [1-14C]oleate (0.25 mM, 0.5 mM and 1 mM), the inhibition being most marked at low (0.25 mM) concentration of oleate. Conversion of [1-14C]oleate into 14CO2 and esterified products was stimulated by vasopressin. The stimulatory effect of this hormone on 14CO2 production was most marked at high (1 mM) concentration of oleate, whereas that on [1-14C]oleate esterification was most marked at low (0.25 mM) concentration of oleate. These vasopressin actions were abolished when hepatocytes were incubated in the absence of calcium in the medium. Our results strongly suggest that both increase in esterification and increase in oxidation to CO2 contribute to the anti-ketogenic action of vasopressin when oleate is added as substrate, although the relative extent of their contribution varies according to the oleate concentration. The anti-ketogenic action of vasopressin was mimicked by PMA but not by A23187. PMA also caused a stimulation of [1-14C]oleate esterification although the effect was diminished at 1 mM [1-14C]oleate. A23187 failed to affect [1-14C]oleate esterification. The metabolic effects of PMA were elicited in the absence of extracellular calcium, too. Conversion of [1-14C]oleate into 14CO2 was only slightly increased by both PMA and A23187 when 1 mM [1-14C]oleate was added as substrate. The marked stimulatory effect of vasopressin on 14CO2 production from [1-14C]oleate was not reproduced even by the combination of PMA and A23187.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2003

Analysis of vasopressin-induced Ca2+ increase in rat hepatocytes.

To analyze vasopressin-induced Ca2+ increase in liver cells, rat hepatocytes were isolated and attached to collagen-coated cover slips. Using fura-2, a Ca2+-sensing dye, changes in intracellular Ca2+ concentration by vasopressin were monitored. Results in this communication suggested that vasopressin-induced Ca2+ increase were composed of both Ca2+ release from internal Ca2+ stores and influx from the plasma membrane. The Ca2+ influx consisted of two distinguishable components. One was dependent on the presence of vasopressin and the other was not. SK&F96365 blocked vasopressin-induced Ca2+ influx in a dose-dependent manner. Vasopressin-induced Ca2+ release from internal stores diminished in a primary culture of hepatocytes according to the culture time. However, changes in vasopressin-induced Ca2+ influx across the plasma membrane differed from changes in the Ca2+ release from internal stores, suggesting two separate signalings from receptor activation to internal stores and to the plasma membrane.

Animals↗
PubMed2005

[Vasopressin and terlipressin in sepsis and systemic inflammatory response syndrome. Effects on microcirculation, oxygen transport, metabolism and organ function].

Vasopressin and terlipressin are increasingly used as alternative non-adrenergic vasopressors for hemodynamic support of septic patients with arterial hypotension. Despite excellent vasopressive effects, vasopressin analogues may potentially impair macro-hemodynamics, oxygen transport and microvascular blood flow. Due to those unwanted side-effects, vasopressin and terlipressin may potentially compromise organ function and possibly foster the development of multiple organ failure. This review article discusses the results of clinical and experimental studies to judge the effects of vasopressin and terlipressin on microcirculation, oxygen supply, metabolism and organ function in patients with sepsis or systemic inflammatory response syndrome (SIRS). Although vasopressin analogues are emerging as promising alternatives to treat catecholamine-refractory hypotension, there is no evidence that vasopressin receptor agonists improve outcome. To date, vasopressin and terlipressin can, therefore, not be recommended for routine clinical use.

Animals↗
PubMed2002

Shear stress modulates vasopressin-induced renal vasoconstriction in rats.

Vasopressin is a potent renal vasoconstrictor in vitro which elicits relatively minor renal vascular effects in vivo. Efficient modulation might occur through shear stress-elicited release of vasodilator compounds from endothelial cells. The aim of this study was to evaluate in vitro, in the isolated perfused kidney, the influence of shear stress and related nitric oxide (NO) release on basal renal vascular tone and on vasopressin-induced renal vasoconstriction. Rat kidneys were perfused at a constant flow rate of 8 ml/min with Tyrode's solution (relative viscosity eta=1) or, in order to increase shear stress, with Tyrode's solution supplemented with 4.7% Ficoll 400 (Ficoll 400; eta=2.3), which is representative of the relative viscosity found in small vessels. Renal shear stress was further elevated during vasoconstriction elicited by vasopressin. Basal renal true vascular conductance, which reflects mean blood vessel radius, was 2.5-fold higher and overall wall shear stress doubled in Ficoll 400 - as compared to Tyrode-perfused kidneys. The decrease in vascular conductance elicited by NO synthase inhibition with N(omega)-nitro-L-arginine (L-NNA) increased with the viscosity of the perfusate. Shear stress was elevated during vasopressin-induced renal vasoconstriction, all the more kidneys were Ficoll 400-perfused. In these kidneys, the concentration-response curve to vasopressin was shifted to the right, giving evidence of hyporeactivity to the peptide. L-NNA potentiated vasoconstriction to vasopressin particularly in Ficoll 400-perfused kidneys, although additional inhibition of cyclooxygenase and/or cytochrome P(450) was without effect. These results provide in vitro evidence that shear stress enhanced by perfusate viscosity increases basal renal vascular conductance by an NO-dependent mechanism. Together with shear stress enhanced during vasoconstriction, it blunts vasopressin-induced renal vasoconstriction.

Animals↗
PubMed2001

Comparative effects of the novel vasotocin analogue F-180 vs. vasopressin and terlipressin on systemic and splanchnic isolated vessels from portal hypertensive rats.

F-180 has been proposed as a new vasopressin analogue for the treatment of portal hypertension. This study investigates the contractile profile of F-180 compared to vasopressin and its analogue terlipressin on isolated systemic and splanchnic vessels from sham-operated and partial portal vein ligated (PPVL) rats. F-180 (10(-9)-10(-6) M), vasopressin (10(-11)-10(-8) M) and terlipressin (10(-9)-10(-4) M) induced contraction of the mesenteric vein, aorta, iliac, tail and mesenteric arteries. The order of potency in these vessels was vasopressin (pD2 approximately 9) > F-180 (pD2 approximately 8) > terlipressin (pD2 approximately 6). Significant (P<0.01) differences between sham-operated and PPVL rats were noticed exclusively in the mesenteric vein, being the maximal effect of the three agonists at least twice greater in PPVL rats than in sham-operated rats. The order of sensitivity to the vasoconstrictors in vessels from PPVL rats was aorta < mesenteric artery << iliac artery approximately equal tail artery approximately equal mesenteric vein. The contractile profile of these peptides in each vessel from PPVL animals was quite similar, except in the mesenteric vein and the aorta. F-180 showed higher efficacy (P<0.01) than terlipressin in the mesenteric vein and lower (P<0.05) efficacy than vasopressin in the aorta. These findings suggest the existence of a vasoconstrictor territorial selectivity for vasopressin and its analogues, which could justify the efficacy of these drugs in portal hypertension therapy. In particular, F-180 appears to be a viable alternative to the classic vasopressin analogues.

Animals↗
PubMed2003

Immunohistochemical evaluation of vasopressin expression in breast fibrocystic disease and ductal carcinoma in situ (DCIS).

We previously found that expression of the vasopressin gene is a common feature of human breast cancer. In the present study we first examined 21 different cases of benign fibrocystic breast disease for vasopressin expression using immunohistochemistry and antibodies directed against vasopressin (anti-VP) and against vasopressin-associated glycopeptide (anti-VAG). All cases examined were negative for vasopressin gene expression using these antibodies. Alternatively, we examined 16 cases of breast ductal carcinoma in situ (DCIS) using the second of these antibodies (anti-VAG), and all of these cases were positive for vasopressin gene expression. Our results suggest that products of vasopressin gene expression are not markers of cellular proliferation in the breast, and might rather represent an early part of the carcinogenic process in this tissue.

Biopsy↗
PubMed1994

Effect of autonomic blockade on pressor responses to vasopressin in pregnant rats.

OBJECTIVE: We tested the hypothesis that gestational changes in reflex neural control of the heart and vasculature contribute to altered cardiovascular responses to vasopressin during pregnancy. STUDY DESIGN: Changes in mean arterial pressure, cardiac output, total peripheral resistance, and heart rate were measured in response to constant infusion of arginine vasopressin (0.15 to 2.5 mU/kg/min) in conscious pregnant and virgin rats (n = 9) with total autonomic blockade plus restoration of baseline hemodynamics by norepinephrine infusion. RESULTS: Resting cardiac output was 40% higher and total peripheral resistance 30% lower in pregnant animals (p < 0.01). Constant infusion of arginine vasopressin evoked equivalent changes in mean arterial pressure in both groups, but the respective contributions of cardiac output and total peripheral resistance to mean arterial pressure differed between groups. Cardiac output was unchanged and the increase in total peripheral resistance was significantly blunted in pregnant vs virgin rats during arginine vasopressin infusion. Control data in nonblocked revealed similar pressor responses to arginine vasopressin in gravid compared with virgin rats but no differences in the contributions of cardiac output and total peripheral resistance to the change in mean arterial pressure. CONCLUSION: These findings suggest that neural modulation of arginine vasopressin-induced hypertension is altered during pregnancy and are consistent with a reduction in intrinsic vascular sensitivity to arginine vasopressin during gestation.

Animals↗
PubMed1988

Vasopressin, phorbol diesters and serum elicit choline glycerophospholipid hydrolysis and diacylglycerol formation in nontransformed cells: transformed derivatives do not respond.

REF52, a rat embryo cell line, and several transformed derivatives were used to examine the lipid-related events associated with agonist treatment (phorbol diesters, vasopressin, fetal bovine serum). Exposure of cells, prelabeled with [3H]glycerol, to TPA (12-O-tetradecanoylphorbol 13-acetate) resulted in 3-4-fold increase in the amount of intracellular diacyl[3H]glycerols as early as 10 min after treatment. Continued incubation (up to 60 min) revealed that the diacyl[3H]glycerol formed was under dynamic metabolic regulation as shown by the production of triacyl[3H]glycerols and free [3H]glycerol. Serum and vasopressin likewise induced the generation of intracellular diacyl[3H]glycerol, thereby illustrating that physiological agents provoke a similar reaction. In the three SV-40-transformed variants examined, the diacylglycerol generative-response to TPA, serum and vasopressin, was greatly diminished or totally absent. Experiments employing REF52 cells prelabeled with [3H]choline demonstrated that both TPA and vasopressin induce the hydrolysis of cellular choline-containing glycerophospholipids; this was measured by both a decrease in cell-associated phosphatidylcholine radioactivity and an increase in the production of water-soluble [3H]choline-containing metabolites in the culture medium. 92-97% of the tritium released to the medium was identified as [3H]choline. Vasopressin treatment of REF52 cells prelabeled with [3H]arachidonic acid elicited an increase of more than 11-fold in the amount of cellular diacyl[3H]glycerol and a concomitant release of arachidonic acid to the culture medium that was 12-fold higher than controls. These data demonstrate that tumor-promoting phorbol esters (agonists of protein kinase C), serum and vasopressin, increase the levels of cellular diacylglycerol by stimulating the hydrolysis of choline-containing glycerophospholipids. This agonist-directed mechanism is inoperable in transformed cells. Further, collateral with vasopressin-induced phosphatidylcholine hydrolysis, the cellular release of arachidonic acid occurs. The participation of these lipid-related responses in the signaling of agonist-directed events and their relation to cellular homeostasis is currently being explored.

Animals↗
PubMed1985

Interaction of vasopressin with the nigro-striatal dopamine system: site and mechanism of action.

The results of the present experiments show that local microinjections of Arg8-vasopressin into the nucl. caudatus cause an increase in the alpha-methyl-p-tyrosine methylester-HCl-induced disappearance of dopamine (DA) at the site of administration of the peptide. It is suggested that the caudate nucleus is the site of action of the peptide with respect to its effect on nigrostriatal DA neurons. This conclusion is corroborated by both the finding that microinjection of Arg8-vasopressin into the A9 region, which contains the cell bodies of the nigrostriatal system, was ineffective, and the results of push-pull experiments which showed an enhancement in apparent DA release in the nucl. caudatus when Arg8-vasopressin was co-perfused through the cannula system. Arg8-vasopressin appears to have a rather modest effect on nucl. caudatus DA synthesis, as was deduced from the results of experiments in which the in vitro conversion of tritiated tyrosine into tritiated DA was measured following in vivo Arg8-vasopressin administration as well as after in vitro incubation with the peptide. In conclusion, the interaction of vasopressin with the nigrostriatal DA system appears to be at the level of the DA terminals in the nucl. caudatus rather than at the level of the substantia nigra, and secondly, Arg8-vasopressin appears to affect DA release in the nucl. caudatus rather than DA synthesis.

Animals↗
PubMed1986

Effects of androgens and estrogens on the vasopressin and oxytocin innervation of the adult rat brain.

Recently we reported that castration of rats eliminates vasopressin immunoreactivity in the lateral septum and other areas that appear to receive vasopressin innervation from the bed nucleus of the stria terminalis. Testosterone treatment counteracts this effect of castration. In the present study, we investigated whether this action of testosterone depends on its androgenic or estrogenic metabolites by treating long-term castrated rats with estradiol (E) and/or 5 alpha-dihydrotestosterone (DHT) or testosterone. The brains were then processed for immunocytochemistry or radioimmunoassay. DHT did not increase vasopressin staining in the lateral septum, although it fully restored the size of the seminal vesicles. E did restore the original fiber density, but individual fibers stained more weakly than in sham-operated males. Only treatment with both E and DHT fully restored the vasopressin innervation. This pattern was also reflected in the radioimmunoassay data. The vasopressin content of the lateral septum decreased about 90% after castration but was fully restored by either testosterone or E + DHT treatment. E alone, however, was only half as effective as E + DHT. The treatments had no effect on the oxytocin content of the septum, or on the vasopressin or oxytocin content of the dorsal vagal complex. The results suggest that E mediates most of the effects of testosterone on the vasopressin innervation of the lateral septum. DHT enhances the response to E but has little effect on its own.

Animals↗