The effects of congenital brain serotonin deficiency on responses to chronic fluoxetine.

The importance of reversing brain serotonin (5-HT) deficiency and promoting hippocampal neurogenesis in the mechanisms of action for antidepressants remain highly controversial. Here we examined the behavioral, neurochemical and neurogenic effects of chronic fluoxetine (FLX) in a mouse model of congenital 5-HT deficiency, the tryptophan hydroxylase 2 (R439H) knock-in (Tph2KI) mouse. Our results demonstrate that congenital 5-HT deficiency prevents a subset of the signature molecular, cellular and behavioral effects of FLX, despite the fact that FLX restores the 5-HT levels of Tph2KI mice to essentially the levels observed in wild-type mice at baseline. These results suggest that inducing supra-physiological levels of 5-HT, not merely reversing 5-HT deficiency, is required for many of the antidepressant-like effects of FLX. We also demonstrate that co-administration of the 5-HT precursor, 5-hydroxytryptophan (5-HTP), along with FLX rescues the novelty suppressed feeding (NSF) anxiolytic-like effect of FLX in Tph2KI mice, despite still failing to induce neurogenesis. Thus, our results indicate that brain 5-HT deficiency reduces the efficacy of FLX and that supplementation with 5-HTP can restore some antidepressant-like responses in the context of 5-HT deficiency. Our findings also suggest that feeding latency reductions in the NSF induced by chronic 5-HT elevation are not mediated by drug-induced increments in neurogenesis in 5-HT-deficient animals. Overall, these findings shed new light on the impact of 5-HT deficiency on responses to FLX and may have important implications for treatment selection in depression and anxiety disorders.

Deficient serotonin neurotransmission and depression-like serotonin biomarker alterations in tryptophan hydroxylase 2 (Tph2) loss-of-function mice.

Probably the foremost hypothesis of depression is the 5-hydroxytryptamine (5-HT, serotonin) deficiency hypothesis. Accordingly, anomalies in putative 5-HT biomarkers have repeatedly been reported in depression patients. However, whether such anomalies in fact reflect deficient central 5-HT neurotransmission remains unresolved. We employed a naturalistic model of 5-HT deficiency, the tryptophan hydroxylase 2 (Tph2) R439H knockin mouse, to address this question. We report that Tph2 knockin mice have reduced basal and stimulated levels of extracellular 5-HT (5-HT(Ext)). Interestingly, cerebrospinal fluid (CSF) 5-hydroxyindoleacetic acid (5-HIAA) and fenfluramine-induced plasma prolactin levels are markedly diminished in the Tph2 knockin mice. These data seemingly confirm that low CSF 5-HIAA and fenfluramine-induced plasma prolactin reflects chronic, endogenous central nervous system (CNS) 5-HT deficiency. Moreover, 5-HT(1A) receptor agonist-induced hypothermia is blunted and frontal cortex 5-HT(2A) receptors are increased in the Tph2 knockin mice. These data likewise parallel core findings in depression, but are usually attributed to anomalies in the respective receptors rather than resulting from CNS 5-HT deficiency. Further, 5-HT(2A) receptor function is enhanced in the Tph2 knockin mice. In contrast, 5-HT(1A) receptor levels and G-protein coupling is normal in Tph2 knockin mice, indicating that the blunted hypothermic response relates directly to the low 5-HT(Ext). Thus, we show that not only low CSF 5-HIAA and a blunted fenfluramine-induced prolactin response, but also blunted 5-HT(1A) agonist-induced hypothermia and increased 5-HT(2A) receptor levels are bona fide biomarkers of chronic, endogenous 5-HT deficiency. Potentially, some of these biomarkers could identify patients likely to have 5-HT deficiency. This could have clinical research utility or even guide pharmacotherapy.

Regulation of cAMP by the p75 neurotrophin receptor: insight into drug design of selective phosphodiesterase inhibitors.

Subcellular compartmentalization of PDEs (phosphodiesterases) is a major mechanism for the regulation of cAMP signalling. The identification of the proteins that recruit specific PDE isoforms to subcellular compartments can shed light on the regulation of spatial and temporal cAMP gradients in living cells and provide novel therapeutic targets for inhibiting functions of PDEs. We showed recently that p75(NTR) (p75 neurotrophin receptor) interacts directly with a single PDE isoform, namely PDE4A4/5, via binding to its unique C-terminal region, and targets cAMP degradation to the membrane. The purpose of this review is to present the biological significance of PDE4A compartmentalization by p75(NTR) and discuss the potential of inhibiting the interaction between p75(NTR) and PDE4A for the development of an isoform-specific inhihibitor for PDEs.

Contextual approaches to the physiology and classification of erectile function, erectile dysfunction, and sexual arousal.

This paper offers a reexamination of some long-held beliefs relating to the physiology of erectile function and dysfunction, including the idea that there is a singular physiology of erection. Rather, there appear to be plural neural, neurochemical, and endocrine mechanisms whose participation in erectile function depends on the behavioral context in which erection occurs. The best examples of this context-dependent physiology come from research on rats. For example, the medial amygdala is essential for noncontact erection in response to inaccessible estrous females, but not for erection during copulation. Also, androgen is necessary for touch-based and noncontact erection, but not for erection during copulation. Even the specific dopamine receptors important to erection may differ, depending on the context. If there is not a singular physiology of erection, then it follows that the physiology of erectile dysfunction may also vary from context to context. Thus, some disorders of the central nervous system may not be manifested in sleep-related erection, and therefore may be misinterpreted as "psychogenic" erectile dysfunction. This term belies the axiom that all psychological processes have a somatic basis; therefore, there can be no psychogenic dysfunction that does not involve organic processes which may respond to pharmacotherapy. A revised classification of erectile dysfunction based on this premise is offered. Finally, closer attention to erectile context may also illuminate male "sexual arousal" and its relation to "sexual motivation". The former term has so many meanings in current usage as to impede research, especially into the physiology of sexual arousal, which depends on comparisons between animals and humans. It is proposed that attention be given to two variables: whether or not erection occurs and whether or not the context is sexual. The occurrence of penile erection within a sexual context is viewed as the only case in which sexual arousal may be inferred unambiguously.

Female presence during postejaculatory interval facilitates penile erection and 22-kHz vocalization in male rats.

During the postejaculatory interval (PEI), male rats exhibit prolonged immobility, 22-kHz vocalization, and penile erections. To test whether females modulate these behaviors, females were removed after the first or second ejaculation or left in the test chamber. Female presence during the PEI delayed exploratory behavior and facilitated vocalization and erection. Female stimulation of vocalization is consistent with the hypothesis that vocalization has a communicative function, not just a thermoregulatory one. The timing of the effect of females on erection suggests that males are sexually arousable well before they resume copulation. Therefore, erection may be better than vocalization as an indicator of the male's sexual refractoriness. The findings also challenge the conventional view that the PEI comprises absolute and relative sexual refractory periods marked, respectively, by the presence and absence of 22-kHz vocalization.

Neuronal Fos activation in olfactory bulb and forebrain of male rats having erections in the presence of inaccessible estrous females.

Volatile odors from estrous female rats are necessary and sufficient to induce non-contact penile erections in male rats. It is not known whether these pheromones are detected by the accessory as opposed to the main olfactory system or whether they are processed by forebrain regions that receive olfactory inputs. Using nuclear Fos immunoreactivity as a marker of neuronal activation, we asked how the detection and processing of distal cues from inaccessible estrous females, which elicited non-contact penile erections, compared with the processing of sensory cues from soiled estrous bedding which did not elicit non-contact penile erections. In Experiment 1, groups of sexually experienced males were given one of five treatments. A control group was placed on clean bedding. A second group displayed non-contact penile erections when exposed to the smell, sight and sound of an estrous female restrained behind a permeable barrier. A third group was exposed to the same stimuli as the second (an estrous female) but failed to exhibit non-contact penile erections during the first hour of testing. A fourth group was placed on soiled estrous bedding, and a fifth group was allowed two ejaculations with an estrous female. All males were perfused with 4% paraformaldehyde 2 h after the onset of these respective treatments, and their brains were later processed for Fos immunoreactivity. Non-contact penile erections were observed in males that were exposed to distal cues from an estrous female but not in males exposed to soiled estrous bedding. Males that displayed non-contact penile erections or that were exposed to estrous bedding showed significantly more neuronal Fos immunoreactivity than clean-bedding controls in the nucleus accumbens core and shell, anterior and posterior medial amygdala, bed nucleus of the stria terminalis and the medial preoptic nucleus. Even greater neuronal Fos responses occurred in these regions in mated males. In Experiment 2 these same treatments were given to another cohort of sexually experienced males. Increased neuronal Fos immunoreactivity was observed in the granule and mitral cell layers of the accessory olfactory bulb of males that were either mated or exposed to estrous bedding, but not in males that displayed non-contact penile erections in response to distal cues from an estrous female. The volatile odors which presumably caused non-contact penile erections failed to stimulate significant neuronal Fos immunoreactivity in five main olfactory bulb sites examined. Even so, it seems likely that these pheromones are detected via the main olfactory system and are subsequently processed by the same projection circuit that responds to other pheromones present in estrous bedding that are incapable of eliciting non-contact penile erections.

Regulation of noncontact erection in rats by gonadal steroids.

Male rats exhibit erections in the presence of inaccessible estrous females, and we investigated which gonadal steroids regulate these noncontact erections (NCEs). Sexually experienced Wistar males (n >/= 8/group) were tested for NCE four times (every 3 days) before castration, after castration, and after receiving subcutaneous implants of 10-mm Silastic capsules that were empty or filled with crystalline testosterone propionate (TP), dihydrotestosterone (DHT), estradiol benzoate (EB), or DHT + EB (10 mm each). Before castration, males responded with NCE in approximately 50% of tests. No males had NCEs after castration, beginning 3 days after surgery. Also, no males responded after treatment with EB or empty capsules. After receiving implants of TP, DHT, or DHT + EB, 50% of males had NCEs, beginning with the first test 3 days after treatment. On every measure of NCE, males treated with DHT or DHT + EB were indistinguishable from each other and from TP-treated males. Among the sexual responses of male rats, NCE appears to be more sensitive than other behaviors to changes in gonadal condition. In its profile of response to gonadal steroids (testosterone+, dihydrotestosterone+, estradiol-), NCE is similar to reflexive erection, for which spinal systems are sufficient, and unlike copulation (T+, DHT-, E+), which depends on discrete areas of the brain. We nonetheless conclude that NCE depends on androgen-sensitive systems in the brain, but androgen-sensitive neurons in the lumbosacral spinal cord may also play a role.

Peripheral nerves mediating penile erection in the rat.

We examined the effects in male rats of bilateral transection of two nerves previously implicated in erectile function, the viscerocutaneous branch of the pelvic nerve (Vc) and the hypogastric nerve (HgN). In Experiment 1 (conducted in Storrs), males underwent simultaneous or successive section of Vc and HgN and were tested for copulation, reflexive erection, and noncontact erection (NCE), i.e. in response to remote cues from estrous females. NCE is considered to be analogous to 'psychogenic' erection in humans, for which the HgN has been ascribed a significant role. In all three types of test, males had a moderate to severe deficit in erectile function after Vc transection. Section of HgN alone had no apparent pro- or anti-erectile effect in any context, nor did it affect the decrement resulting from Vc surgery. Regardless of treatment, all groups retained some erectile potential in each type of test. The loss of bladder function after Vc surgery and of seminal plug deposition after HgN section gave evidence that the targeted nerves were in fact severed. In Experiment 2 (conducted in Xalapa), males were tested only for NCE, but (a) they were tested every 3 days beginning 3 days after each surgery, (b) the interval between the two surgeries was more than 2 weeks, rather than 1 week as in Experiment 1, to allow more time for recovery from general effects of surgery and for hypothetical plasticity of neural function. In the first test after the first surgery, all groups had a modest reduction in the proportion of males displaying NCE, relative to sham-operated males. However, this deficit did not extend to measures of NCE latency or number, and was absent after the second test. After the second surgery, when all males except those with sham operations had both nerves cut, none of the groups exhibited a significant deficit in NCE, and all groups had at least one test in which at least half the males responded. Thus, (a) HgN section did not significantly impair NCE, reflexive erection, or copulation; (b) Vc section impaired, but did not eliminate, erection in all three contexts, but even those effects may be transient; and (c) transection of both nerves, simultaneously or successively, did not cause a greater impairment in erection than did cutting just the Vc. We infer that the HgN may have no pro-erectile role in erection in rats, even in a model analogous to psychogenic erection. The Vc is probably the most important nerve mediating pro-erectile function in NCE, as in reflexive erection and copulation, but this nerve may not be essential for erection in rats in any context, at least in some males.

Erectile function in male rats after lesions in the lateral paragigantocellular nucleus.

In previous research on rats, lesions of the lateral paragigantocellular nucleus (LPGi) in the medulla have facilitated the display of reflexive erection and ejaculation. The present research sought to replicate and extend these findings by determining whether LPGi lesions would also promote erection during copulation and during exposure of the male to inaccessible females, i.e. non-contact erections (NCEs). As expected, males with LPGi lesions (n = 10) had a greater incidence of reflexive erection than males with sham lesions (n = 8), and during copulation LPGi-damaged males required fewer intromissions before ejaculation. However, the lesions did not change the copulatory intromission ratio, a partial measure of erectile function, nor did they change the incidence, latency, or number of NCEs displayed. More direct measures of erection will be necessary to determine whether the inhibitory role of LPGi on sexual reflexes is absent in some erectile contexts, or whether its role in some contexts is too small to be evident in behavioral measures.

Intracavernous pressure during erection in rats: an integrative approach based on telemetric recording.

To better understand the similarities and differences in the neural control of penile erection occurring in different contexts, we recorded intracavernous pressure (ICP) in conscious rats using a miniaturized telemetric device. ICP changes during reflexive, noncontact, and apomorphine-induced erections were characterized by a plateau increase surmounted by peaks. Plateaus were also elicited by cavernous nerve stimulation in anesthetized rats, suggesting that the cavernous nerve represents the final common proerectile autonomic pathway in these contexts and that it responds similarly to information originating in the periphery or in supraspinal nuclei. During reflexive, noncontact, and apomorphine-induced erections, activation of spinal autonomic nuclei, considered the spinal generators of erection, would take place first, representing a prerequisite for the occurrence of peaks. Suprasystolic peaks would result from the addition of pudendal motoneuron activity. In contrast, only peaks were recorded during copulation. In this context, the convergence of peripheral and supraspinal information apparently elicits the best temporal arrangement of autonomic and somatic outflows, reflecting a highly organized and integrated spinal activity.

Sexual behavior in male rats after radiofrequency or dopamine-depleting lesions in nucleus accumbens.

Considerable neurochemical evidence links dopamine (DA) in nucleus accumbens (NAcc) to male sexual behavior. The present experiments were conducted to extend this information to the male's sexual response to remote stimuli from estrous female (noncontact erection; NCE). Male rats were tested for copulation and NCE after either 6-hydroxydopamine (6-OHDA) or radiofrequency (RF) lesions in NAcc). Males with an average 78% depletion of DA in NAcc had a lower incidence of NCE, longer latency to display NCE, and fewer erections. DA-depleted males also had less locomotor activity after injections of d-amphetamine, and reductions in apomorphine-induced yawning, but a normal incidence of penile erection. Males with RF lesions of the NAcc had longer NCE latencies. All males copulated to ejaculation after either 6-OHDA or RF lesions with little or no deficit, although the 6-OHDA-treated males had longer intromission latencies. The NCE deficit supports the hypothesized role of NAcc DA in arousal processes in responding to remote cues from estrous females. The minimal effect of lesions on copulation suggests that the presence of additional proximal stimulation during copulation may overcome the deficits induced by DA depletions or lesions in NAcc.

Importance of the medial amygdala in rat penile erection evoked by remote stimuli from estrous females.

Effects of medial amygdala lesions (MAL) were examined on rat penile erection in three different experimental situations. Only sexually vigorous males, as identified by preoperative mating tests, were used. Bilateral radiofrequency lesions were confined to the posterior medial amygdala, with little systematic damage to anterior medial amygdala or to adjacent structures. Lesion electrodes were withdrawn without current application in sham-operated animals (SHAM). After recovery for brain surgery, males were tested for (1) noncontact erection (NCE) that occurs when males were placed in proximity to inaccessible estrous females, (2) reflexive erection evoked in supine males by retraction of the penile sheath, and (3) copulatory behaviour with receptive females. In the NCE test, none of the MAL males showed penile erection during the 20 min observation, whereas 70% of the SHAM males showed it (P < 0.001). In contrast, no erectile dysfunction in the MAL males was detected in the other two tests. MAL males displayed more penile-body erections (flips) than SHAM males in the reflexive-erection test (P <0.05). In the copulation test, most of the MAL males achieved intromission, but their intromission ratio, a partial measure of erectile function, was marginally lower than that of SHAM males (P = 0.051). MAL males had longer intervals between intromissions (P < 0.001); as a result, none of them ejaculated during the 30 min period that followed the first intromission. The results suggest that the posterior medial amygdala plays an essential role in the regulation of NCE, and it may also contribute to the regulation of erection in other contexts.

Mounting and brief noncontact exposure of males to receptive females facilitate reflexive erection in rats, even after hypogastric nerve section.

In three experiments, reflexive erection in male rats was facilitated by housing the males for 2 min with inaccessible sexually receptive females. In Experiment 1, males were sexually naive or experienced and received two reflexive erection tests, 1 week apart, immediately after the males were exposed to receptive females, to unreceptive females, or to no females (n = 8 per group). In both tests, experienced males exposed to estrous females had the shortest reflexive erection latencies; in Test 1 the differences among groups were of borderline significance (p = 0.057), but in Test 2 the differences among groups were highly reliable (p<0.01). Further analysis indicated that only experienced males exposed to receptive females were significantly different from other groups. In Experiment 2, sexually experienced males (n = 11) received four reflexive erection tests: after being with no female, and 0, 5, or 10 min after exposure to estrous females. As the interval between exposure and test increased, the males had progressively shorter erection latencies (p<0.01) and more intense glans erections (p<0.03). Experiments 1 and 2 may be viewed as demonstrating the psychogenic facilitation of reflexive erections. In Experiment 3, males underwent sham surgery (sham, n = 10) or bilateral transection of the hypogastric nerves (HgNx, n = 10), which are conventionally viewed as mediating psychogenic erection. After males mounted a receptive female for 5 min without intromission or had 2 min of non-contact exposure to receptive females, the males had shorter erection latencies (p<0.001) and more erections (p<0.02). These facilitative effects of pretest stimulation were unaffected by HgN transection. During copulation tests, HgNx males had longer ejaculation latencies (p<0.05) and lower intromission ratios (p<0.05), possible signs of impaired erectile function. However, in Experiment 4, other males were tested twice for reflexive erection and copulation after sham (n = 8) or HgNx (n = 9) surgery, and there were no significant effects of surgery on reflexive erection or copulatory behavior. Collectively, these experiments indicate (a) that brief noncontact exposure of sexually experienced males to estrous females facilitates reflexive erection, (b) that this facilitation increases for at least 10 min after the females are removed, and (c) that the hypogastric nerves do not mediate these facilitative effects. The evidence for a role for the HgN in copulation was inconclusive.

Importance of the medial amygdala in rat penile erection evoked by remote stimuli from estrous females.

Effects of medial amygdala lesions (MAL) were examined on rat penile erection in three different experimental situations. Only sexually vigorous males, as identified by preoperative mating tests, were used. Bilateral radiofrequency lesions were confined to the posterior medial amygdala, with little systematic damage to anterior medial amygdala or to adjacent structures. Lesion electrodes were withdrawn without current application in sham-operated animals (SHAM). After recovery for brain surgery, males were tested for (1) noncontact erection (NCE) that occurs when males were placed in proximity to inaccessible estrous females, (2) reflexive erection evoked in supine males by retraction of the penile sheath, and (3) copulatory behaviour with receptive females. In the NCE test, none of the MAL males showed penile erection during the 20 min observation, whereas 70% of the SHAM males showed it (P < 0.001). In contrast, no erectile dysfunction in the MAL males was detected in the other two tests. MAL males displayed more penile-body erections (flips) than SHAM males in the reflexive-erection test (P < 0.05). In the copulation test, most of the MAL males achieved intromission, but their intromission ratio, a partial measure of erectile function, was marginally lower than that of SHAM males (P = 0.051). MAL males had longer intervals between intromissions (P < 0.001); as a result, none of them ejaculated during the 20 min period that followed the first intromission. The results suggest that the posterior medial amygdala plays an essential role in the regulation of NCE, and it may also contribute to the regulation of erection in other contexts.

Erection evoked in male rats by airborne scent from estrous females.

In the presence of inaccessible estrous females, male rats display penile erections and associated stereotypic behavior indicative of sexual arousal. The effective stimuli for these noncontact erections (NCEs) had not been determined, but bedding soiled by estrous females was known to be ineffective. The present experiments tested for a potential role for volatile olfactory cues in evoking NCE. In Experiment 1, sexually naive male rats were observed for NCEs when tested with inaccessible, estrous females, upwind (n = 20) or downwind (n = 20) from them under conditions that permitted or prevented visual communication. After half the males in each condition had copulatory experience, they were tested under the same conditions. In each test, only on male of 20 responded with females downwind, whereas about half the 20 males displayed NCEs with females upwind, irrespective of barrier type or, in Test 2, of sexual experience. Olfactory cues from estrous females were apparently necessary to induce NCE, whereas visual and auditory stimuli from estrous were not sufficient to evoke NCE, nor did they affect the response to olfactory stimulation. In Experiment 2, males were downwind from estrous females (n = 10) or anestrous females (n = 10) that were behind opaque barriers and were anesthetized to preclude auditory communication. Results indicated that olfactory cues were also sufficient to provoke NCE in sexually experienced males. Receptive female rats apparently broadcast a volatile pheromone that promotes erection. Pheromones are well known to attract potential mates and to act in concert with other stimuli to promote mating. However, this is the first mammalian evidence for a volatile pheromone acting alone to evoke a sexual fixed-action pattern and, in that sense, acting as an airborne aphrodisiac.

Lesions in medial preoptic area and bed nucleus of stria terminalis: differential effects on copulatory behavior and noncontact erection in male rats.

The goal of these studies was to assess the regulatory roles of the medial preoptic area (MPOA) and the bed nucleus of the stria terminalis (BST) in sexual arousal, inferred from noncontact erection (NCE) evoked in male rats by remote cues from estrous females. NCE and copulatory behavior were recorded before and after quinolinic acid or radiofrequency (RF) lesions were made in the MPOA (Experiments 1-3) or RF lesions were made in the BST (Experiment 4). All males with MPOA lesions, particularly in the rostral region, displayed severe deficits in copulation but little or no decrement in NCE. In contrast, BST lesions caused relatively moderate deficits in copulation, but they severely impaired NCE. Animals with larger BST lesions, including rostral and caudal medial regions, had more deficits in both copulatory behavior and NCE than did males with smaller lesions confined to the rostral medial BST. These results suggest that (1) the MPOA is critical for copulatory behavior but not for NCE, (2) males that stop copulating after MPOA lesions are still sexually aroused by estrous females, and (3) the BST plays an important role in mediating NCE.

Effects of p-chlorophenylalanine on reflexive and noncontact penile erections in male rats.

To clarify the role of serotonin in penile erection, testosterone-primed castrated male rats were treated with the serotonin-synthesis inhibitor, p-chlorophenylalanine (pCPA), and reflexive erection (RE; male supine, penile sheath retracted) and noncontact erection (NCE; penile erection evoked by remote sexual stimuli) tests were performed. Half the males were injected with 100 mg/kg pCPA 4 times before each test; control males were treated with saline instead of pCPA. In the RE test, compared to the control group, pCPA-treated males had a shorter erection latency, but they also displayed fewer erections. NCE tests were conducted as a 2 x 2 factorial experiment: pCPA or saline, and estrous female present or absent. Only the pCPA-female Group had a high proportion of responders (68%), compared to 14-27% in the other Groups (p < 0.02). These results suggest that the serotonergic system exerts facilitative and inhibitory influences on different systems in regulating reflexive erection. On the other hand, serotonin appears to play an inhibitory role in the induction of noncontact erection, because pCPA did not directly induce erection, but rather facilitated the response to females.

Impaired sexual response after lesions of the paraventricular nucleus of the hypothalamus in male rats.

N-methyl-D-aspartic acid (NMDA) or radiofrequency (RF) lesions were made in the paraventricular nucleus of the hypothalamus (PVH) of male rats. The rats were tested for copulation, noncontact erection (NCE) evoked by remote cues from estrous females, and (after RF lesions) reflexive erection. NMDA, which destroyed parvocellular but spared magnocellular neurons, caused no deficits in copulation but caused longer NCE latencies and fewer NCEs. Rats with RF lesions had parvo- and magnocellular neuron damage; these males copulated to ejaculation, but they had lower intromission ratios and longer ejaculatory latencies. RF-lesioned rats also had longer NCE latencies, and a smaller proportion of males displayed reflexive erection. Results indicate that the PVH participates in mediating erectile function in copula and ex copula, and that the parvo- and magnocellular PVH neurons may have different roles in mediating erection.

Penile erection in response to remote cues from females: albino rats severely impaired relative to pigmented strains.

Male rats have been observed to display erections when exposed to inaccessible estrous females, and it was suggested that these "noncontact erections" (NCEs) represent a species-typical response that may index sexual arousal. Initial efforts in other laboratories to repeat and extend this research were unsuccessful, and it appeared that differences in the rat strains being used might be responsible. To address this question NCE tests were given to rats of two albino strains, Wistar and Sprague-Dawley, and two pigmented strains, hooded Long-Evans and inbred Brown Norway. A high proportion of Long-Evans and Brown Norway rats displayed NCEs, whereas Wistar and Sprague-Dawley albino rats rarely did. Additional experiments did not reveal the reasons for the strain difference in NCE, but they provided evidence against hypotheses based on the relative erectogenic effect of albino and hooded estrous females, the attention paid to estrous females, the motor repertoire, or erectile function per se. Albinism-related neural pathology, possibly outside of the visual system, may contribute to the deficit in NCE in albino rats.