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PubMed1996

Oxidative stress in the brain following intraventricular administration of ethylcholine aziridinium (AF64A).

AF64A is a toxic analog of choline that disrupts high affinity choline transport and produces a persistent presynaptic cholinergic hypofunction. The observed neuroprotectant effects of Vitamin E in the AF64A model suggested that oxidative stress contributed to the cholinotoxicity of AF64A. The studies presented here examined whether intraventricular injection of AF64A produces oxidative stress in the brain of male Wistar rats. Indices of oxidative stress including thiobarbituric acid reactive species (TBARS), free radical generation using hydrogen peroxide-induced, luminol-dependent chemiluminescence (CL) and superoxide scavenging/generating activity were measured in cerebral cortex, hippocampus and the rest of the brain, without cerebellum, 1, 3 or 5 days after bilateral intraventricular injection of 3 nmol of AF64A or artificial CSF (sham surgery). The sham operation itself induced oxidative stress throughout the brain (increased TBARS, CL and superoxide generation). In addition to the oxidative stress of the sham surgery AF64A increased basal TBARS on day 1 and Fe/ascorbate-induced TBARS on days 3 and 5 throughout the brain. AF64A produced compensatory 'antioxidative' changes as well with increased superoxide scavenging activity observed on day 3 and decreased basal TBARS on day 5. AF64A also induced specific changes in the hippocampus including a decrease of CL and an increase of superoxide scavenging activity on day 5. The increased superoxide scavenging activity persisted up to 126 days. The results of the present study provide the first direct evidence that AF64A induces oxidative stress following intraventricular injection.

Animals↗
PubMed1990

Effects of glucose, 2-deoxyglucose, phlorizin, and insulin on food intake of lean and fatty rats.

Glucose, 2-deoxyglucose, phlorizin, and insulin were injected into the third ventricle of lean and fatty rats, and food intake recorded hourly for the next 6 h. In the lean rats, there was a significant but unimpressive decrease in food intake after the intraventricular injection of glucose, but there was no effect of glucose in the fatty rat. Phlorizin in the lowest dose (10 micrograms) increased the food intake in lean animals at 1 and 2 h, and all three doses increased it significantly at 6 h after intraventricular injection. The fatty rat, in contrast, showed no response to phlorizin. 2-Deoxyglucose showed a dose-related stimulation of food intake in the lean rats at 1, 2, 3, and 6 h after injection. In the fatty rat, there was no significant effect on food intake at any dose. The intraventricular injection of insulin had no effect on food intake in either the lean or fatty rats. These studies indicate that glucose-responding systems in the region of the third ventricle are defective in the fatty rat to signals that normally increase or decrease food intake in lean animals.

Animals↗
PubMed1992

A cyclic AMP mechanism mediates the serotonin-induced increase in glutamic acid decarboxylase activity in the preoptic area and hypothalamus.

Previous studies have shown that the injection of 5-hydroxytryptamine (5-HT) into the third ventricle of rats on the afternoon of proestrus increases glutamic acid decarboxylase (GAD) activity in the preoptic area and the hypothalamus. In the present report we examine the adenylate cyclase-cyclic AMP (cAMP) system as mediator of that effect. The increase in GAD activity induced by intraventricular injection of 5-HT was completely blocked by injecting an antiserum against cAMP into the third ventricle 30 min earlier, whereas an injection of serum from normal rabbits was ineffective. On the contrary, activation of adenylate cyclase activity by intraventricular injection of forskolin increased GAD activity, an effect that was also blocked by anti-cAMP serum. Anti-cAMP serum also lowered GAD activity in the preoptic area and hypothalamus when injected on the morning of proestrus but not when injected in the afternoon, when the values of GAD activity were already low. The results suggest that a cAMP mechanism may be involved in the changes in preoptic-area and hypothalamic GAD activity such as the rise in enzyme activity induced by intraventricular injection of 5-HT.

Animals↗
PubMed1999

Estrogen and leptin have differential effects on FSH and LH release in female rats.

Prior experiments have shown that the adipocyte hormone leptin can advance puberty in mice. We hypothesized that it would also stimulate gonadotrophin secretion in adults. Since the secretion of follicle stimulating hormone (FSH) and luteinizing hormone (LH) is drastically affected by estrogen, we hypothesized that leptin might have different actions dependent on the dose of estrogen. Consequently in these experiments, we tested the effect of injection of leptin into the third cerebral ventricle of ovariectomized animals injected with either the oil diluent, 10 microg or 50 microg of estradiol benzoate 72 hr prior to the experiment. The animals were ovariectomized 3-4 weeks prior to implantation of a cannula into the third ventricle 1 week before the experiments. The day after implantation of an external jugular catheter, blood samples (0. 3 ml) were collected just before and every 10 min for 2 hr after 3V injection of 5 microl of diluent or 10 microg of leptin. Both doses of estradiol benzoate equally decreased plasma LH concentrations and pulse amplitude, but there was a graded decrease in pulse frequency. In contrast, only the 50-microg dose of estradiol benzoate significantly decreased mean plasma FSH concentrations without significantly changing other parameters of FSH release. The number of LH pulses alone and pulses of both hormones together decreased as the dose of estrogen was increased, whereas the number of pulses of FSH alone significantly increased with the higher dose of estradiol benzoate, demonstrating differential control of LH and FSH secretion by estrogen, consistent with alterations in release of luteinizing hormone releasing hormone (LHRH) and the putative FSH-releasing factor (FSHRF), respectively. The effects of intraventricularly injected leptin were drastically altered by increasing doses of estradiol benzoate. There was no significant effect of intraventricular injection of leptin (10 microg) on the various parameters of either FSH or LH secretion in ovariectomized, oil-injected rats, whereas in those injected with 10 microg of estradiol benzoate there was an increase in the first hr in mean plasma concentration, area under the curve, pulse amplitude, and maximum increase of LH above the starting value (Deltamax) on comparison with the results in the diluent-injected animals in which there was no alteration of these parameters during the 2 hr following injection. The pattern of FSH release was opposite to that of LH and had a different time-course. In the diluent-injected animals, probably because of the stress of injection and frequent blood sampling, there was an initial significant decline in plasma FSH at 20 min after injection, followed by a progressive increase with a significant elevation above the control values at 110 and 120 min. In the leptin-injected animals, mean plasma FSH was nearly constant during the entire experiment, coupled with a significant decrease below values in diluent-injected rats, beginning at 30 min after injection and progressing to a maximal difference at 120 min. Area under the curve, pulse amplitude, and Deltamax of FSH was also decreased in the second hour compared to values in diluent-injected rats. In contrast to the stimulatory effects of intraventricular injection of leptin on pulsatile LH release manifest during the first hour after injection, there was a diametrically opposite, delayed significant decrease in pulsatile FSH release. This differential effect of leptin on FSH and LH release was consistent with differential effects of leptin on LHRH and FSHRF release. Finally, the higher dose of E2 (50 microg) suppressed release of both FSH and LH, but there was little effect of leptin under these conditions, the only effect being a slight (P < 0.04) increase in pulse amplitude of LH in this group of rats. The results indicate that the central effects of leptin on gonadotropin release are strongly dependent on plasma estradiol levels. These effects are consistent w

Activity Cycles↗
PubMed1964

CENTRAL CARDIOVASCULAR ACTIONS OF GAMMA-AMINOBUTYRIC ACID.

The vasomotor and cardiac effects of gamma-aminobutyric acid (GABA) administered by different routes were studied in cats and dogs. The cat was resistant to the action of GABA administered intravenously or into a vertebral artery. Intrathecal injection of GABA into the cat depressed the vasomotor reponse to spinal compression. In dogs, intravenous, intrathecal or intraventricular injection, or topical application of GABA to the floor of 4th ventricle consistently produced hypotension and depressed the reflex and direct excitability of the vasomotor neurones, located at the supraspinal and spinal levels. Bradycardia observed after intravenous and intraventricular injections of GABA into dogs was abolished by stellate ganglionectomy but not by vagotomy. It has been attributed to depression of the central sympathetic neurones.

Aminobutyrates↗
PubMed1975

Role of brain monoamines in release of gonadotropin before proestrus in the cyclic rat.

To determine whether brain monoaminergic neurons are involved in the release of gonadotropins responsible for estrogen increases before proestrus, various inhibitors and precursors of monoamine biosynthesis were administered subcutaneously or intracranially to the 3rd ventricle at 10.00 or 20.00 on the day before proestrus, the 2nd day of diestrus (DII) in 4-day cycling rats. The inhibitors used were alpha-methyl-p-tyrosine (alpha-MPT) and bis-(4-methyl-1-homopiperazinyl-thiocarbonyl)-disulfide (FLA-63). The effects of these drugs on changes in vaginal cytology, ovulation, uterine weight of uterine intraluminal fluid, and on serum concentrations of LH and FSH were evaluated in selected experiments. (1) Administration of alpha-MPT (150 mg/kg s.c.), an inhibitor of tyrosine hydroxylase, at 10.00 on DII reduced weights of uterus and intraluminal fluid on the day of expected proestrus (P), prevented vaginal cornification on estrus (E), blocked ovulation in all 10 rats, and induced prolonged diestrus. (2) Administration of FLA-63 (10 mg/kg s.c.), an inhibitor of dopamine-beta-hydroxylase, at 10.00 on DII reduced weights of uterus and intraluminal fluid on P, blocked ovulation for a few days but did not prevent vaginal cornification at the expected time of E. (3) Administration of alpha-MPT (200 mg/kg) or FLA-63 (15 mg/kg) at 20.00 on DII blocked ovulation in all of 8 and 7 rats, respectively, but these treatments did not block vaginal cornification at the expected time in any animal. (4) Administration of L-DOPA (100 mg/kg) or dihydroxy-phenylserine (DOPS, 200 mg/kg) with alpha-MPT (200 mg/kg) at 20.00 on DII reversed the blocking effect of alpha-MPT on ovulation in 3 out of 6 and 3 out of 5 rats, respectively. (5) Direct application of crystalline alpha-MPT or FLA-63 (about 3-5 mug) to the 3rd ventricle at 20.00 on DII also blocked ovulation in all of 7 and 5 rats, respectively. (6) Both systemic and intraventricular injections of alpha-MPT at 10.00 on DII reduced serum LH on P but not serum FSH. FLA-63 by intraventricular injection also reduced serum LH but not serum FSH. (7) Injection of 17beta-estradiol (40 mug s.c.) with alpha-MPT or FLA-63 partially removed the ovulatory blockade induced by conditions 1, 2, 3 and 5. Therefore, norepinephrine seems to be an important neurotransmitter in the release of gonadotropin responsible for estrogen secretion before P, but dopamine may also be involved during its early stage as represented by 10.00 on DII.

Animals↗
PubMed1976

Further studies on prostaglandin E2 (PGE2)-induced gonadotropin release: comparison with the effect of 15-methyl PGE2, PGAs, PGBs and prostaglandin endoperoxide analogs.

It is known that PGE2 is a potent stimulus of LH release. To determine if the effect of PGE2 could be enhanced and/or prolonged by retarding its metabolic degradation, a derivative, 15-methyl PGE2 (15-E2) which is more slowly degraded than the natural compound was injected intravenously (i.v.) at various dose levels or into the third ventricle (3rd V) of ether-anesthetized, ovariectomized, estrogen (OVX, Eb)-treated rats and its effect on gonadotropin release was compared with that of PGE2. Both PGs injected i.v. were equally effective in increasing plamsa LH and maintaining the elevated levels, although 15-E2 induced a larger and more sustained increase in plasma FSH than PGE2. By contrast, 3rd V PGE2 was clearly more effective than 3rd V 15-E2 in releasing LH and to a lesser extent, FSH. The effect of 15-E2 on LH was similar to that produced by 3rd V PGE1, injected at a similar dose. However, its effect on FSH was greater than that of PGE1. To evaluate the effect(s) of prostaglandins of the A and B series on gonadotropin release, PGA1, PGA2, PGB1 or PGB2 were injected intraventricularly in OVX, Eb-treated rats. PGBs were injected into conscious, free-moving rats. PGA2 or PGB2 increased plasma LH concentrations although much less effectively than PGE2. Third V PGA1 or PGB1 were ineffective. The 3rd V injection of two cyclic esters (U-44069 and U-46619), stable analogs of the PG endoperoxide PGG2 and PGH2, induced a small, transient increase in LH levels and did not alter plasma FSH in conscious, free-moving animals. PGE2 injected intraventricularly at a similar dose was demonstrated to be mcuh more potent than the analogs in stimulating LH and FSH release. The results indicate that: 1) 15-E2, in spite of its described long-lasting activity, does not appear to be more potent than the natural compound in releasing LH, although when injected i.v., it appeared to induce a more sustained increase in plasma FSH; 2) although PGA2 and PGB2 can also act centrally to stimulate LH release, their low potency suggests that this is a pharmacological effect; and 3) the two analogs of PG endoperoxides tested proved to be poor stimuli for gonadotropin release. The significance of these findings is discussed.

Animals↗
PubMed1998

Lateral ventricular injections of the NK3 agonist senktide affect salt taste-elicited responses.

Central injections of the selective tachykinin NK3 receptor agonist senktide (SENK) suppresses salt appetite. Also, following SENK, intraoral infusions of hypertonic NaCl elicit fewer ingestive taste reactivity responses and more aversive responses than following intraventricular injections of isotonic saline. This pattern of taste reactivity results suggest that SENK affects the oral stimulating properties of salt taste. Before accepting this interpretation, however, alternative explanations need to be examined. The following experiments evaluated whether the effects of intraventricular SENK injection on taste reactivity could be due to: 1) a general oral motor impairment that reduces ingestive responding to tastes (Experiment 1) or; 2) SENK having aversive consequences (Experiment 2). In Experiment 1, the effects of intraventricular injections of SENK (200 ng) on taste reactivity responses to 0.5 M NaCl and 0.1 M sucrose were measured in sodium deficient rats. Intraoral infusions of 0.5 M NaCl elicited fewer ingestive taste reactivity responses following SENK than injections of isotonic saline in sodium deficient rats. Sucrose continued to elicit the same high number of ingestive taste reactivity responses following intraventricular injections of isotonic saline and SENK. Thus, SENK did not cause a general decrease in ingestive responding. A conditioned taste aversion test was employed in Experiment 2 to determine if SENK had aversive consequences. Rats were given 30 min access to alanine (0.3 M) and were then administered either lithium chloride (LiCl) or intraventricular injections of SENK (200 ng) on three consecutive days. Rats avoided alanine that was paired with LiCl, but those rats that had alanine paired with SENK showed no avoidance of the taste even after three pairings. These results replicate findings that intraventricular injections of the NK3 agonist SENK decreases the palatability of NaCl (as measured by taste reactivity) and suggest that its effect on NaCl-elicited taste reactivity is not due to the treatment causing a motor impairment or malaise.

Animals↗
PubMed1986

The effects of the cholecystokinin antagonist, proglumide, on gonadotropin release in the rat.

Since cholecystokinin had manifest effects on anterior pituitary hormone secretion following its intraventricular injection in ovariectomized rats, we have evaluated the effects of the cholecystokinin antagonist, proglumide, to assess the physiologic significance of CCK in the control of gonadotropin secretion. Conscious rats of either sex were used following implantation of third ventricular and/or intravenous cannulae for the administration of proglumide. Blood samples were drawn from conscious animals at various times after the injection of the compound. In castrate female rats proglumide produced a small but significant increase in plasma LH whether administered by the intravenous or intraventricular route at the lower dose of 10 or 2 micrograms, respectively. The higher doses of 10 micrograms injected intraventricularly or 100 micrograms, injected intravenously failed to affect LH levels in these animals. In contrast there was a much larger increase in plasma LH in castrate males following intraventricular or intravenous injection of the lower doses of proglumide. Even after the higher doses, there was a slight increase in levels of LH by either route of injection. The results indicate that in the castrate animal proglumide can elevate LH levels by either route of injection but that the response is greater in castrate males than females. The reduction in response with the higher doses may reflect an agonist activity of proglumide. By contrast proglumide had no effect on plasma FSH except for a slight elevation observed following the intravenous or intraventricular injection of the lower doses of the compound in castrate males. The results favor a physiologically significant role of CCK in control of LH release in the rat.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Reproductive functions in the adult male rats after prolonged intraventricular administration of corticotropin-releasing factor (CRF).

The effect of intraventricular injection of synthetic oCRF on reproductive functions in the male rats were studied and changes were compared with intact and control rats (daily intraventricular injections of 10 microliter of 0.1% albumin solution in PBS). The long-term administration of oCRF into lateral ventricle of freely moving rats caused a significant increase in relative weights of adrenals, pituitary glands and a decrease in body weight. Plasma LH and testosterone levels were significantly depressed after 8 days of oCRF administration, while there were no alteration in studied parameters in the control rats. Control i.v.c. injections of 0.1% albumin solution in PBS were without effect on levels of any of the hormones or weights of testes, epidydimis, seminal vesicles and prostate. Obtained results indicate a central inhibitory action of oCRF on LH and subsequent testosterone release.

Adrenal Glands↗
PubMed1968

The reversal of the central effects of noradrenaline by antidepressant drugs in mice.

1. Noradrenaline given directly into the lateral cerebral ventricles induced hypothermia in mice. This hypothermia was antagonized and eventually reversed to a hyperthermia by imipramine-like antidepressant drugs.2. The mechanism of action involved in this effect of antidepressant drugs has been studied using nortriptyline as a typical representative of antidepressant drugs.3. Nortriptyline pretreatment did not modify either the uptake, subcellular distribution, or the metabolism of (3)H-noradrenaline injected into the lateral cerebral ventricles.4. Nortriptyline had the same order of activity in reversing the hypothermia produced by the intraventricular injection of noradrenaline irrespective of whether it was given directly into the lateral cerebral ventricles or subcutaneously.5. Noradrenaline given subcutaneously caused hyperthermia in mice which antagonized and reversed the hypothermia induced by noradrenaline given directly into the lateral ventricles.6. The antagonism by both noradrenaline given subcutaneously and nortriptyline was reduced to the same degree by alpha- and beta-adrenoceptive receptor blocking agents.7. Nortriptyline, at dose levels required to antagonize and reverse the hypothermia induced by intraventricular injections of noradrenaline, potentiated the hyperthermia caused by noradrenaline given subcutaneously in conscious mice and the pressor responses to noradrenaline given either intravenously or into the lateral ventricles in anaesthetized mice.8. It is suggested that imipramine-like antidepressant drugs antagonize the hypothermia produced by intraventricular injections of noradrenaline by potentiating the hyperthermic effects of that part of the centrally administered noradrenaline that passes to the periphery rather than a direct central antagonism of the effects of noradrenaline.

Animals↗
PubMed1969

Behavioural and somatic effects of bradykinin injected into the cerebral ventricles of unanaesthetized rabbits.

1. The effects of bradykinin (1-5 mug) injected into the cannulated lateral cerebral ventricles were studied in unanaesthetized rabbits before and after intravenous atropine, diphemanil and morphine.2. The intraventricular injections of bradykinin produced a short-lasting phase of behavioural excitation with vocalization followed by sedation. The behavioural excitation was associated with desynchronization in the electrocorticogram (e.co.g.), bradycardia and hypotension followed by tachycardia and hypertension. Tachypnoea was also observed. The subsequent phase of sedation was more prolonged and associated with synchronization of the e.co.g. and signs of catalepsy. Intense miosis was present during both phases.3. With repeated intraventricular injections of bradykinin, excitation, miosis, cardiovascular responses and tachypnoea diminished and eventually disappeared but the sedation did not exhibit tachyphylaxis.4. Atropine abolished the e.co.g. desynchronization, vocalization and bradycardia, reduced the duration of the excitatory and sedatory phase, diminished the tachycardia and hypotension, enhanced the hypertension, but did not affect the miosis and tachypnoea.5. Diphemanil affected only the cardiovascular effects produced by intraventricular bradykinin. They were affected in the same way as by atropine.6. Morphine did not affect the excitatory phase, but enhanced the cardiovascular effects produced by intraventricular bradykinin.7. The intraventricular injection of bradykinin (50 mug) caused a reduction in the amount of noradrenaline but not of 5-hydroxytryptamine (5-HT) in the brain stem; the amount of dopamine in the caudate nuclei was not affected.8. It is suggested that central cholinergic and adrenergic systems are activated by intraventricular bradykinin.

Animals↗
PubMed2002

Brain vasopressin and sodium appetite.

Intraventricular injections of vasopressin (VP) and antagonists with varying degrees of specificity for the VP receptors were used to identify the action of endogenous brain VP on 0.3 M NaCl intake by sodium-deficient rats. Lateral ventricular injections of 100 ng and 1 microg VP caused barrel rotations and a dramatic decrease in NaCl intake by sodium-deficient rats and suppressed sucrose intake. Intraventricular injection of the V(1)/V(2) receptor antagonist [d(CH(2))(5)(1),O-Et-Tyr(2),Val(4), Arg(8)]VP and the V(1) receptor antagonist [d(CH(2))(5)(1),O-Me-Tyr(2),Arg(8)]VP (MeT-AVP) significantly suppressed NaCl intake by sodium-deficient rats without causing motor disturbances. MeT-AVP had no effect on sucrose intake (0.1 M). In contrast, the selective V(2) receptor antagonist had no significant effect on NaCl intake. Last, injections of 100 ng MeT-AVP decreased mean arterial blood pressure (MAP), whereas 100 ng VP elevated MAP and pretreatment with MeT-AVP blocked the pressor effect of VP. These results indicate that the effects produced by 100 ng MeT-AVP represent receptor antagonistic activity. These findings suggest that the effect of exogenous VP on salt intake is secondary to motor disruptions and that endogenous brain VP neurotransmission acting at V(1) receptors plays a role in the arousal of salt appetite.

Animals↗
PubMedDate not supplied

The pharmacology of endorphin modulation of chick distress vocalization.

Intraventricular injections of beta-endorphin, gamma-endorphin and alpha-endorphin were demonstrated to reduce isolation-induced distress vocalization on 2-4 day old chicks in a dose response manner at doses as small as 12.5 picomoles (pmol). beta-Endorphin was more potent than the other peptides and morphine, while Met-enkephalin was without effect. However, the D-Ala2 substituted form of Met-enkephalin was as potent as morphine. None of the opioid peptides was effective when injected peripherally in doses of 400 pmol/g body weight. Extension of the interval between injection and behavioral observation from 4 minutes eliminated the ability of alpha- and gamma-endorphin to reduce the peeps. Specificity of the opioid effect was determined by testing intraventricular injections (200 pmol) of 9 other endogenously found peptides. Somatostatin, vasoactive intestinal peptide, and human pancreatic peptide reduced the vocalizations modestly, while alpha-MSH reliably increased them.

Animals↗
PubMed1980

Kynurenines and audiogenic excitement in mice.

Adult male and female albino mice (SHR strain) responded to sound by locomotor excitement (73-81%), running fits (33-47%), clonic convulsions (15-25%), tonic extension (10-22%) and lethality (7-17%). Intraperitoneal injection of metabolites of tryptophan on the kynurenine pathway (Kynurenines): DL- and L-kynurenine sulfate, 3-hydroxyanthranilic, anthranilic, quinolinic, picolinic, nicotinic and xanthurenic acids (in doses of 200 and 400 mg/kg) decreased audiogenic excitement. Intraventricular injection of kynurenines (1-50 mcg), even in stimulating and convulsive doses, had no effect. Intraventricular injection did not induce an audiogenic response in C57 BL/6 and CC57BR mice which are not normally susceptible to sound. Pentylenetetrazol and strychnine injected intraventricularly in up to lethal dosages did not modify audiogenic excitement. Decrease of audiogenic excitement by kynurenines is suggested to be partially related to lowering of body temperature.

Acoustic Stimulation↗
PubMed1978

[Sisomicine in the lumbar and ventricular cerebrospinal fluid. Concentration after intramuscular or intrathecal injection. Study in 14 subjects-therapeutic implications (author's transl)].

Following intramuscular injection sisomicine, in common with other aminosides, shows poor intrathecal diffusion (less than 10% of serum levels) even during the initial phase of purulent meningitis. Following the intraspinal or intraventricular injection of 0.5 mg/kg, high levels are obtained which persist up to 48th hour. This dose is very well tolerated and no accumulation phenomena were demonstrated after repeated injections. In cases of meningitis due to organisms resistant to diffusible antibiotics, sisomicine sulphate may be used by lumbar intraspinal or sometimes intraventricular injection in severe forms, in a dose of 0.5 mg/kg every 48 hours (or even 24 hours). In combination with systemic treatment. The duration of treatment cannot be precisely defined.

Adolescent↗
PubMed1992

Effects of L-threo- and erythro-3,4-dihydroxyphenylserine on learning performance and concentrations of brain noradrenaline and its metabolites in rats.

Effects of L-threo and L-erythro-3,4-dihydroxyphenylserine [DOPS, precursor amino acids for noradrenaline (NA)] on the learning performance in a maze paradigm designed to model on the water maze paradigm using a multicomputerized behavioral analysis system were studied. A marked facilitation of learning performance was observed in rats after an intraventricular injection of 5 micrograms L-threo-DOPS (the s-NA precursor), and this effect was inhibited by a simultaneous administration of 1 or 2 micrograms propranolol (a beta-adrenergic antagonist). As concentrations of brain NA, 3-methoxy-4-hydroxyphenylglycol, and normethanephrine were increased by the injection of 5 micrograms L-threo-DOPS, the effect seemed to be derived from activation of beta-adrenoceptors in the CNS by the formed s-NA. On the other hand, an intraventricular injection of 5 micrograms L-erythro-DOPS (the r-NA precursor) attenuated the learning performance, and this effect was probably caused by the formed r-NA from L-erythro-DOPS.

Animals↗