Pro-VGF-derived peptides induce penile erection in male rats: Involvement of paraventricular nitric oxide

The effect of four peptides derived from the C-terminal portion of rat pro-VGF(556-617) (VGF(556-576), VGF(588-617), VGF(599-617), and VGF(588-597)), on penile erection and nitric oxide production in the paraventricular nucleus of the hypothalamus was studied in male rats after injecting into this hypothalamic nucleus. VGF(588-617) (0.5, 1 and 2 microg), VGF(599-617) (0.5, 2 and 5 microg) and, to a lower extent, VGF(588-597) (2 and 5 microg) induced penile erection episodes when injected into the paraventricular nucleus and concomitantly increased paraventricular nitric oxide production, while VGF(556-576) (5 microg) was ineffective. VGF(588-617)-induced nitric oxide production was reduced by N(G)-nitro-l-arginine methylester (l-NAME) (20 microg), a nitric oxide synthase inhibitor, which also reduced penile erection when injected in the paraventricular nucleus 15 min before the VGF peptide. The oxytocin receptor antagonist d(CH(2))(5)Tyr(Me)-Orn(8)-vasotocin (1 microg) also effectively reduced VGF(588-617)-induced penile erection when given into the lateral ventricles, but not when injected into the paraventricular nucleus. In both experimental conditions, d(CH(2))(5)Tyr(Me)-Orn(8)-vasotocin was unable to influence nitric oxide production in the paraventricular nucleus. The present results confirm that C-terminal pro-VGF-derived peptides induce penile erection when injected into the paraventricular nucleus and show that this effect is mediated by an increased nitric oxide production in this hypothalamic nucleus. Apparently, this causes the activation of paraventricular oxytocinergic neurons projecting to extra-hypothalamic brain areas and mediating penile erection, as found with dopamine agonists, oxytocin, excitatory amino acids and hexarelin analogue peptides.     

Oxytocin: an extremely potent inducer of penile erection and yawning in male rats

The intracerebroventricular (i.c.v.) injection of oxytocin, in doses ranging from 5 to 90 ng (5–90 pmol) induced penile erection and yawning in male rats. Such response was not induced by doses of the peptide higher than 100 ng, nor by equimolar doses of i.c.v. [Arg⁸]vasopressin, ACTH-(1–24), -MSH, rat corticotropin-releasing factor (rCRF), delta sleep-inducing peptide, neurotensin or substance P. Oxytocin-induced penile erection and yawning were prevented by atropine and morphine, but not by methylatropine or the opiate antagonist naloxone. Haloperidol, a dopamine receptor antagonist, was ineffective at low doses; it partially prevented penile erection but not yawning at high doses. Since oxytocin is present not only in the neurohypophysis but also in other brain areas, our results suggest that oxytocin is implicated in the regulation of penile erection and yawning, and provide further evidence that oxytocin acts as a neuropeptide in the central nervous system.     

The cannabinoid receptor antagonist SR-141716A induces penile erection in male rats: involvement of paraventricular glutamic acid and nitric oxide

The cannabinoid CB1 receptor antagonist SR141716A (0.5, 1 and 2 microg) induces penile erection when injected into the paraventricular nucleus of male rats. The pro-erectile effect of SR 141716A occurs concomitantly with an increase in the concentration of NO2- and NO3- in the paraventricular dialysate obtained by means of intracerebral microdialysis. Both penile erection and NO2- increase induced by SR 141716A were reduced by the prior injection into the PVN of the cannabinoid CB1 agonists WIN 55,212-2 (5 microg) or HU 210 (5 microg), given into the paraventricular nucleus at doses unable to induce penile erection or to modify NO2- concentration. SR 141716A responses were also reduced by nitro-L-arginine methylester (20 microg), a non-selective NO synthase inhibitor, S-methyl-L-thiocitrulline (20 microg), a selective neuronal NO synthase inhibitor, the excitatory amino acid NMDA receptor antagonist dizocilpine ((+)MK 801) (1 microg), or the GABAA receptor agonist muscimol (0.2 microg) injected into the PVN 15 min before SR 141716A. In contrast, the inducible NO synthase inhibitor L-N(6)-(1-iminoethyl)lysine (20 microg), the GABAB receptor agonist baclofen (0.2 microg), the mixed dopamine receptor antagonist cis-flupenthixol (10 microg), and the oxytocin receptor antagonist d(CH2)5Tyr(Me)-Orn8 -vasotocin (1 microg), were ineffective. Despite its inability to reduce penile erection and NO2- increase induced by SR 141716A when injected into the PVN, d(CH2)5Tyr(Me)-Orn8 -vasotocin (1 microg) reduced almost completely penile erection without reducing paraventricular NO2- increase when injected into the lateral ventricles 15 min before SR 141716A. The present results show that SR 141716 induces penile erection by a mechanism (possibly activation of excitatory amino acid neurotransmission), which causes the activation of neuronal NO synthase in paraventricular oxytocinergic neurons mediating penile erection.     

Oxytocin-induced penile erection and yawning in male rats: effect of neonatal monosodium glutamate and hypophysectomy

Penile erection and yawning induced by the intracerebroventricular (ICV) injection of oxytocin (10–1000 ng) was studied in hypophysectomized rats and in rats neonatally treated with monosodium glutamate (MSG), a treatment that depletes hypothalamic opiomelanocorticotropinderived peptides without altering their pituitary and circulating concentration. Oxytocin effect was strongly reduced by hypophysectomy, but not by neonatal MSG. Testosterone replacement (50 /kg/day for 23 days) partially reversed the effect of hypophysectomy on penile erection, but not on yawning. The present results suggest that oxytocin does not induce penile erection and yawning by releasing an ACTH-derived peptide from hypothalamic opiomelanotropinergic neurons, and that the pituitary gland exerts a permissive role on the expression of the above behavioural responses induced by oxytocin.     

Hypophysectomy prevents yawning and penile erection but not hypomotility induced by apomorphine

A small dose of apomorphine (25 or 50 μg/kg, SC) induced repeated episodes of yawning, penile erection, genital grooming and a decrease in locomotor activity in rats. Hypophysectomy almost completely abolished yawning, penile erection and genital grooming but failed to modify the hypomotility induced by apomorphine. These results suggest that pituitary hormones are directly or indirectly involved in the apomorphine-induced yawning, penile erection and genital grooming but not in the sedative response to this drug.     

Cycloheximide prevents apomorphine-induced yawning,penile erection and genital grooming in rats

Apomorphine (50 μg/kg) induced repeated episodes of yawning, penile erection and genital grooming in rats. A dose of cycloheximide, which inhibited brain protein synthesis by 50% totally prevented apomorphine-induced yawning and reduced by approximately 50% the occurrence of episodes of penile erection and genital grooming. However, this treatment failed to modify the stereotyped behaviour induced by 200 μg/kg of apomorphine. These results suggest that protein synthesis is required for the behavioural effects of small doses of apomorphine.     

Oxytocin induces penile erection when injected into the ventral subiculum: Role of nitric oxide and glutamic acid

Oxytocin (100 ng) induces penile erection when injected unilaterally into the ventral subiculum of the hippocampus of male rats. The pro-erectile effect started mostly 30 min after treatment and occurred 15 min after an increase in both nitric oxide (NO) production, measured by the concentration of NO₂⁻ and NO₃⁻, the main metabolites of newly formed NO, and extra-cellular glutamic acid concentration in the dialysate obtained from the ventral subiculum by intracerebral microdialysis. These responses were abolished by d(CH₂)₅Tyr(Me)²-Orn⁸-vasotocin (2 μg), an oxytocin receptor antagonist, S-methyl-l-thiocitrulline (SMTC), a selective inhibitor of neuronal NO-synthase (25 μg), and haemoglobin, a NO scavenger (25 μg), given into the ventral subiculum before oxytocin. Unlike d(CH₂)₅Tyr(Me)²-Orn⁸-vasotocin, SMTC and haemoglobin, (+)MK-801 (5 μg), a noncompetitive antagonist of NMDA receptors abolished oxytocin-induced penile erection, but reduced only partially the increase in NO production and extra-cellular glutamic acid. As NMDA (0.25-1 μg) injected into the ventral subiculum induces penile erection episodes, which also occurred with an increase of NO production and extra-cellular glutamic acid, and NMDA responses were abolished by (+)MK-801 (5 μg), but not by SMTC (25 μg) or haemoglobin (25 μg), injected into the ventral subiculum, these results show that oxytocin injected into the ventral subiculum increases NO production by activating its own receptors. NO in turn increases glutamic acid neurotransmission, leading to penile erection, possibly through neural (glutamatergic) efferent projections from the ventral subiculum to extra-hippocampal brain areas (e.g., prefrontal cortex) modulating the activity of mesolimbic dopaminergic neurons.     

Association of spontaneous and dopaminergic-induced yawning and penile erections in the rat

In a Sprague-Dawley-derived line of rats, selectively bred to establish a high incidence of spontaneous yawning behavior, the simultaneous and systematic monitoring of yawning and penile erections, during observation periods of one hour, demonstrates a linear correlation between these two behavioral patterns. Dose-effect curves of yawning and penile erections elicited by apomorphine and bromocriptine, and their inhibition by metoclopramide are quite similar. These results strongly suggest that yawning and penile erection are subject to some common regulating and modulating mechanisms, one of which seems to involve dopaminergic pathways.     

Role of nitric oxide in penile erection and yawning induced by 5-HT1c receptor agonists in male rats

The effect of the intracerebroventricular (i.c.v.) administration of N^G-nitro-l,-arginine methyl ester and N^G-monomethyl-l.-arginine, two inhibitors of nitric oxide (NO) synthase, on penile erection and yawning induced by 1-(3-chlorophenyl)-piperazine (m-CPP)- and N-(3-trifluoromethylphenyl)-piperazine (TFMPP), two selective 5HT_1c receptor agonists, was studied in male rats. Both NO synthase inhibitors (50–500 g i.c.v.) prevented dose-dependently the behavioural responses induced by m-CPP (0.5 mg/kg s.c.) or by TFMPP (I mg/kg s.c.), but N^G-nitro-l-arginine methyl ester was about 4–5 times more potent than N^G-monomethyl-l,-arginine. The D-isomer of N_G-monomethyl-l-arginine, which does not inhibit nitric oxide synthase, was ineffective. The inhibitory effect of N^G-nitro-l-arginine methyl ester on m-CPP- and TFMPP-induced responses was prevented by the administration of l-arginine (1 mg i.c.v.). In contrast, N^G-nitro-l-arginine methyl ester (20 g) was ineffective when injected in the paraventricular nucleus of the hypothalamus, a brain area that plays a key role in the expression of these behavioural responses. m-CPP- and TFMPP-induced penile erection and yawning was prevented also by the i.c.v. administration of LY 83583 (50–200 g) or methylene blue (50–400 g), two inhibitors of guanylate cyclase but not by reduced hemoglobin (50–400 g), a NO scavenger. The results suggest that central nitric oxide is involved in the expression of penile erection and yawning induced by 5-HT_1c receptor agonists.     

Stimulation of dopamine receptors in the paraventricular nucleus of the hypothalamus of male rats induces penile erection and increases extra-cellular dopamine in the nucleus accumbens: Involvement of central oxytocin

The effect of a pro-erectile dose of apomorphine, a mixed dopamine receptor agonist, and of PD-168077 (N-[4-(2-cyanophenyl)piperazin-1-ylmethyl]-3-methylbenzamide maleate), a selective dopamine D4 receptor agonist, injected into the paraventricular nucleus of the hypothalamus on the concentration of extra-cellular dopamine and its main metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) in the dialysate from the nucleus accumbens was studied in male rats. As expected, apomorphine (0.1microg) and PD-168077 (0.1microg) induced penile erection episodes, which occurred concomitantly to an increase in extra-cellular dopamine and DOPAC concentration in the dialysate from the shell of the nucleus accumbens, as measured by intracerebral microdialysis. When induced by apomorphine, these effects were reduced by 80% by raclopride, a selective D2/D3 receptor antagonist (1microg) and only by 40-45% by L-745,870 (1microg), a selective dopamine D4 receptor antagonist. When induced by PD-168077, these effects were reduced by more than 80% by L-745,870 (1microg), but only by 35-40% by raclopride. Irrespective of the dopamine agonist used to induce penile erection, the pro-erectile effect and the concomitant increase in dopamine and DOPAC concentration in the nucleus accumbens dialysate were almost completely abolished by d(CH(2))(5)Tyr(Me)(2)-Orn(8)-vasotocin(1microg), a potent oxytocin receptor antagonist, given into the lateral ventricles. The present results suggest that stimulation of dopamine receptors (mainly of the D2 to D4 subtype) in the paraventricular nucleus induces the release of oxytocin in brain areas that influence the activity of mesolimbic dopaminergic neurons mediating the appetitive and reinforcing effects of sexual activity. This provides evidence for a role of oxytocin in neural circuits that integrate the activity of neural pathways controlling the consummatory aspects of sexual behaviour (e.g., penile erection) with those controlling sexual motivation and sexual arousal.     

Prevention by morphine of apomorphine- and oxytocin-induced penile erection and yawning: site of action in the brain.

The effect of morphine administered systemically or into the paraventricular nucleus of the hypothalamus (PVN) on penile erection and yawning induced either by oxytocin or by the dopaminergic agonist apomorphine was studied in male rats. Systemic morphine (0.5 to 5 mg/kg intraperitoneally [IP]) prevented in a dose-dependent manner penile erection and yawning induced by the intracerebroventricular injection (ICV) of oxytocin (30 ng) or by the subcutaneous (SC) administration of apomorphine (80 micrograms/kg). Morphine (0.1 to 5 micrograms), but not U-69,593 (5 micrograms), injected into the PVN 10 minutes before oxytocin or apomorphine, was found to be able to prevent penile erection and yawning induced by the unilateral PVN microinjection of oxytocin (10 ng) or apomorphine (50 ng). The morphine-induced prevention of these behavioral responses was abolished by pretreatment with naloxone (3 mg/kg IP) 15 minutes before morphine. The present results suggest that morphine prevents apomorphine- and oxytocin-induced penile erection and yawning by inhibiting the activity of oxytocinergic neurons through mu-type receptors in this hypothalamic nucleus.     

Effects of GABA-ergic drugs on penile erection induced by apomorphine in rats

The effects of GABA agonists and antagonists on penile erection (PE) induced by apomorphine were investigated in rats. Subcutaneous (SC) administration of apomorphine (0.01–0.1 mg/kg) induces a dose-dependent PE in rats. The maximum effect was obtained with 0.1 mg/kg of the drug. The response was decreased with increasing doses of apomorphine from 0.1 to 0.5 mg/kg. The response induced by apomorphine (0.1–0.5 mg/kg) was decreased in animals pretreated with either the GABA-A agonist muscimol or the GABA-B agonist baclofen. Combination of muscimol with baclofen caused a stronger inhibitory effect on apomorphine-induced PE. Bicuculline or picrotoxin but not phaclofen reduced the inhibitory effect of muscimol on PE induced by apomorphine, whereas phaclofen but not GABA-A antagonists decreased the inhibitory action of baclofen on apomorphine-induced PE. Pretreatment of animals with higher doses of the GABA-A antagonists bicuculline and picrotoxin or the GABA-B antagonist phaclofen elicited inhibition of apomorphine-induced PE. However, the inhibitory effects of GABA-A and GABA-B antagonists are lost on combination. Administration of GABA-A and GABA-B receptor stimulation inhibit PE induced by dopaminergic mechanism(s).     

Post-synaptic 5-HT1A receptor involvement in yawning and penile erections induced by apomorphine,physostigmine and mCPP in rats

Apomorphine and mCPP induced yawning associated with penile erections in rats, whereas physostigmine induced only yawns. Apomorphineinduced yawning and penile erections were antagonized by low doses of raclopride, whereas physostigmineinduced yawning and mCPP-induced effects were only partly inhibited at high doses of raclopride. Scopolamine as well as clozapine antagonized yawning and penile erections induced by apomorphine, mCPP and physostigmine. Similarly, the 5-HT_1A agonists 8-OH-DPAT and S 14506 inhibited yawning and penile erections induced by apomorphine, mCPP and physostigmine, and at similar doses induced lower lip retraction and hyperreactivity to handling. The /5-HT_1A antagonist tertatolol reversed the inhibitory effects of 8-OH-DPAT and S 14506 on drug-induced yawning and penile erections and increased apomorphine-and physostigmine-induced yawn frequency but not penile erection frequency. Like tertatolol, propranolol increased apomorphine- and physostigmine-induced yawn frequency, whereas ICI 118551 increased only physostigmine-induced yawning. 8-OH-DPAT-and S 14506-induced lower lip retraction and hyperre-activity to handling were also significantly antagonized by tertatolol. Finally,p-chlorophenylalanine pretreatment produced about 95% depletion in 5-HT in hypothalamus, hippocampus, striatum and frontal cortex and modified neither the responses of the inducing drugs nor the inhibitory effects of 8-OH-DPAT and S 14506 on drug-induced yawning and penile erections. These data suggest (i) that a final cholinergic mechanism blocked by scopolamine and clozapine is involved in drug-induced yawning and penile erections, (ii) that the effects of S 14506 depend upon stimulation of 5-HT_1A receptors, (iii) that the inhibitory effects of 5-HT_1A agonists on yawning and penile erections probably occurred at final steps on the pathways involved in the expression of yawning and penile erections and that these effects could be related to other effects of the 5-HT_1A agonists, (iv) that a tonic inhibitory influence could interfere with the expression of yawning but not with that of penile erections and (v) that presynaptic 5-HT_1A receptors do not seem to play an important role in the inhibitory effects of 5-HT_1A agonists on drug-induced yawning and penile erections in rats.     

The role of nitric oxide in diabetes-induced changes of morphine tolerance in rats

Several neuroendocrine complications including diabetes change the morphine antinociception and the development of tolerance to the drug. Morphine antinociception was reduced significantly in morphine tolerant diabetic rats compared to the non-diabetic animals. The exact mechanism of this effect is not known. This study was performed to determine the role of nitric oxide (NO) on morphine tolerance in diabetic state. Nociceptive responses in alloxan-induced diabetic morphine tolerated rats were measured by the hot-plate test. The urinary nitric oxide level was measured spectrophotometrically with Griess reagent. For the conversion of nitrate to nitrite, vanadium chloride was used. The results showed that experimental diabetes increased morphine analgesia. Conversely, degree of tolerance to morphine was diminished in diabetic state. The urinary nitrite content in diabetic morphine tolerated rats was higher than non-diabetic groups. L-arginine significantly increased the NO production in diabetic morphine tolerated animals, whereas aminoguanidine decreased it. Appropriately, L-arginine increased the latency time of reaction to noxious stimuli in diabetic compared to non-diabetic rats. L-arginine-treated animals also showed more tolerance to morphine analgesia. As expected, aminoguanidine deducted the level of morphine tolerance in diabetic animals. It is suggested that NO has a modulatory role in the effects of diabetes on morphine analgesia and tolerance.     

Contribution of cGMP but not peroxynitrite to negative feedback regulation of penile erection elicited by nitric oxide in the hippocampal formation of the rat

We established previously that nitric oxide (NO) in the hippocampal formation (HF) participates actively in negative feedback regulation of penile erection. This study further evaluated whether this process engaged soluble guanylyl cyclase (sGC)/cGMP cascade or peroxynitrite in the HF. Intracavernous pressure (ICP) recorded from the penis in adult, male Sprague-Dawley rats anesthetized with chloral hydrate was employed as our experimental index for penile erection. Microinjection bilaterally of a NO-independent sGC activator, YC-1 (0.1 or 1 nmol) or a cGMP analog, 8-Bromo-cGMP (0.1 or 1 nmol), into the HF elicited a significant reduction in baseline ICP. Bilateral application into the HF of equimolar doses (0.5 or 1 nmol) of a sGC inhibitor, LY83583 or a NO-sensitive sGC inhibitor, ODQ significantly antagonized the decrease in baseline ICP induced by co-administration of the NO precursor, L-arginine (5 nmol), along with significant enhancement of the magnitude of papaverine-induced elevation in ICP. In contrast, a peroxynitrite scavenger, L-cysteine (50 or 100 pmol), or an active peroxynitrite decomposition catalyst, 5,10,15,20-tetrakis-(N-methyl-4'-pyridyl)-porphyrinato iron (III) (10 or 50 pmol), was ineffective in both events. These results suggest that NO may participate in negative feedback regulation of penile erection by activating the sGC/cGMP cascade in the HF selectively.     

5-HT1A receptor agonists prevent in rats the yawning and penile erections induced by direct dopamine agonists

The new compound (+) S-20499, an amino chromane derivative (8[-4[N-(5-methoxychromane-3yl)N-propyl]aminobutyl] azaspiro[4–5] décane-7,9 dione), is a high affinity full 5-HT_1A agonist. We have investigated its effects on dopaminergic transmission. (+) S-20499 displayed a 10^–8 M affinity for D₂ dopamine (DA) receptors, 100 fold lower than for 5-HT_1A receptors. The hypothermic effect of the drug was reversed by haloperidol in mice, suggesting that it behaves as a direct dopamine agonist. However, increasing doses of (+) S-20499 induced neither yawning nor penile erections, which constitute characteristic responses of direct DA agonists administered at low doses. In addition, (+) S-20499 prevented the apomorphine (100 µg/kg SC) induced yawning and penile erections. This inhibition appears to result from the stimulation of 5-HT_1A receptors since it is an effect shared by both buspirone (from 5 mg/kg) and 8-OH-DPAT (from 0.10 mg/kg). In addition, when rats are treated with the 5-HT_1A receptor antagonist tertatolol (2–5 mg/kg; SC), increasing doses of (+) S-20499 elicit the expected yawns and penile erections. It is concluded that the 5-HT_1A agonist property opposes to that of D₂ dopamine receptor stimulation with regard to yawning and penile erections.     

一氧化氮及一氧化氮合酶在成年与老年大鼠前列腺中的变化

目的:研究一氧化氮(NO)及一氧化氮合酶(NOS)在成年与老年大鼠前列腺中的变化,探讨在大鼠前列腺老年化过程中的临床意义。方法:取4月龄及20月龄SD雄性大鼠各6只,分别取前列腺组织匀浆,检测其NO与NOS活性。结果:老年组大鼠的NO与NOS活性明显低于成年组(P<0.05)。结论:老年大鼠前列腺组织中NO水平及NOS活性的降低可能与前列腺良性增生及功能减退有关。     

Erection induced by Tx2-6 toxin of Phoneutria nigriventer spider: Expression profile of genes in the nitric oxide pathway of penile tissue of mice

The peptides Tx2-5 and Tx2-6, isolated from the whole venom of “armed-spider” Phoneutria nigriventer venom, are directly linked with the induction of persistent and painful erection in the penis of mammals. The erection induced by Tx2-6 has been associated with the activation of nitric oxide synthases. There is a scarcity of studies focusing on the outcome of Tx2-6 at the molecular level, by this reason we evaluated the gene profile activity of this toxin at the nitric oxide (NO) pathway. After microarray analyses on cavernous tissue of mice inoculated with Tx2-6 we found that only 10.4% (10/96) of these genes were differentially expressed, showing a limited effect of the toxin on the NO pathway. We found the genes sparc, ednrb, junb, cdkn1a, bcl2, ccl5, abcc1 over-expressed and the genes sod1, s100a10 and fth1 under-expressed after inoculation of Tx2-6. The differential expressions of sparc and ednrb genes were further confirmed using real-time PCR. Interestingly, ednrb activates the l-arginine/NO/cGMP pathway that is involved in the relaxation of the cavernous body. Therefore the priapism induced by Tx2-6 is a consequence of a highly specific interference of this neurotoxin with the NO pathway.     

Hypothalamic sites sensitive to morphine and naloxone: effects on feeding behavior

Three experiments investigated the feeding response of brain cannulated rats to hypothalamic injection of norepinephrine (NE), the opiate agonist morphine sulfate (MO) and the opiate antagonist naloxone (NAL). Morphine elicited feeding in a dose-dependent manner when injected into the paraventricular nucleus (PVN) of satiated rats, at doses of 0.78 to 100 nmoles, with a threshold dose of 1.56 nmoles. Naloxone, at doses of 3.13 to 200 nmoles, was injected into the PVN of food-deprived rats and was found to produce a dose-dependent suppression of feeding (threshold dose of 6.25 nmoles). Animals with brain cannulas aimed at the PVN, the perifornical hypothalamus (PFH), the dorsomedial (DMN) and ventromedial (VNM) nuclei were compared for their sensitivity to the feeding stimulatory effects of NE and MO (except in the DMN) and the feeding suppressive effects of NAL. Consistent with earlier reports, the PVN-cannulated animals exhibited a reliable increase in feeding after NE injection; the VMN cannula yielded a small feeding response, whereas the DMN and PFH were insensitive to NE. Morphine, in contrast, strongly stimulated eating after administration into PFH, as well as the PVN, apparently dissociating the NE and MO eating responses. The VMN, however, was generally unresponsive to both MO and NE. With regard to NAL's suppressive effect on feeding, the PVN and PFH, which were sensitive to MO, also exhibited responsiveness to opiate antagonism suggesting the existence in these areas of opiate receptors that modulate feeding.(ABSTRACT TRUNCATED AT 250 WORDS)     

剥夺性弱视大鼠视中枢NO与NOS变化及bFGF对其表达的影响

目的研究不同培养条件下剥夺性弱视大鼠视中枢中一氧化氮(NO)及一氧化氮合酶(NOS)的变化,从而探讨NO在弱视形成过程中的作用并讨论碱性成纤维细胞因子(bFGF)对其表达的影响。方法14d大鼠30只随机分为3组,每组10只,Ⅰ、Ⅱ组为实验组,缝合其单侧眼睑30d,造成剥夺性弱视模型,Ⅲ组为正常对照组,同等条件下饲养30d后,3个组均切取外侧膝状体,Ⅰ组用bFGF培养液培养,Ⅱ、Ⅲ组用普通对照培养液培养,1周后取材作NO及NOS生化指标的测定。结果与Ⅲ组相比,单眼剥夺后,Ⅰ、Ⅱ组大鼠剥夺眼对侧外侧膝状体的NOS量显著降低(P<0.01),且Ⅰ组比Ⅱ组更低(P<0.01)。结论生后早期单眼剥夺可造成大鼠外侧膝状体中NO及NOS含量的降低,bFGF有清除氧自由基的作用,可降低体外培养的外侧膝状体中NO及NOS的含量。