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J J Braszko

Publications and source records attributed to J J Braszko.

At least 37 records · Page 2Linked to original sources
PubMed1991

The 3-7 fragment of angiotensin II is probably responsible for its psychoactive properties.

The abilities of angiotensin II-(3-7)-pentapeptide (A-II-(3-7), 1 nmol) and angiotensin II (A-II, 1 nmol) to influence rat's psychomotor and cognitive behaviours were compared. Both peptides, given intracerebroventricularly (i.c.v.), 15 min before the experiment, increased number of crossings, rearings and bar approaches in the open field. A-II-(3-7) as well as A-II, at the same doses and routes, significantly intensified stereotypy produced by apomorphine (1 mg/kg) and amphetamine (6.5 mg/kg), both given intraperitoneally. The 3-7 fragment of A-II and A-II in equimolar doses (1 nmol, i.c.v.) were similarly effective in improving learning of conditioned avoidance responses and recall of a passive avoidance behaviour. Taken together, these data and our previous findings indicate that, in rats, the 3-7 fragment of A-II is responsible for the psychoactive properties of angiotensins.

Analysis of Variance↗
PubMed1990

Some behavioural effects of captopril in rats.

1. Effects of inhibition of angiotensin converting enzyme (ACE, EC 3.4.15.1) in brain on psychomotor, exploratory, stereotyped and cognitive behaviour in rats were investigated. To inhibit brain ACE captopril (D-3-mercaptopropanoyl-L-proline) was given orally (p.o., 50 mg/kg) or intracerebroventricularly (i.c.v., 5 micrograms/rat). 3. Captopril given p.o. but not i.c.v. significantly enhanced stereotypy, overall number of conditioned avoidance responses, and decreased blood pressure. 4. No statistically significant influence of captopril given by either route on the number of crossings, rearings and bar approaches in the open field, performance of passive avoidance and number of correct choices as well as the speed of running for food in the T-maze was observed. 5. In conclusion, a small decrease of the activity of nigrostriatal dopaminergic system caused by the decrease of AII and/or increase of bradykinin, substance P, enkephalins and neurotensin in brain resulting from ACE inhibition is postulated.

Administration, Oral↗
PubMed1990

Alpha 1 and alpha 2-adrenergic receptor blockade influences angiotensin II facilitation of avoidance behavior and stereotypy in rats.

Pretreatment of rats with prazosin (PRA), an alpha 1-adrenergic receptor blocker, abolished the increased rate of learning of conditioned avoidance responses stimulated by intracerebroventricular angiotensin II (AII) administration. Yohimbine (YOH), an alpha 2-receptor blocker, reversed the effect of AII. PRA did not affect, and YOH abolished, the improvement of recall of a passive avoidance behavior caused by AII. The stereotypies produced by apomorphine (APO) and amphetamine (AMP) were enhanced by AII. PRA changed neither stereotypy, but it abolished the AII effect in both cases. YOH did not alter APO stereotypy and abolished the enhancement of that behavior caused by AII. YOH increased AMP stereotypy and had an additive effect with AII. No significant changes of exploratory motor activity were caused by PRA, YOH, or their combination, with AII. These findings indicate that functioning alpha 1- and alpha 2-adrenergic receptors are necessary for the facilitation of learning by AII, while only alpha 2-receptors appear to be involved in AII improvement of recall. The central dopaminergic system may in part be responsible for the modulation by PRA and YOH of the effects of AII on learning and recall.

Angiotensin II↗
PubMed1989

Psychotropic activity of angiotensin II and its fragments Val-Tyr-Ile-NH2 and Val-Tyr-Ile-His-NH2.

Angiotensin II (A II) significantly enhanced the motor activity of rats in the open field as measured by forward locomotion, rearings and bar approaches while the tripeptide [A II(3-5)] and the tetrapeptide [A II(3-6)] were ineffective in this test. Also, the stereotyped behavior produced by apomorphine (2 mg/kg) or amphetamine (6.5 mg/kg), both given intraperitoneally, was significantly more intense in rats receiving an icv injection of A II but not A II(3-5) or A II(3-6). A II significantly increased the rate of acquisition of active avoidance while AII(3-5) and AII(3-6) were ineffective. Finally, a remarkable improvement of performance in the passive avoidance situation was caused by AII, and none by AII(3-5) and AII(3-6). These results show that 3-5 and 3-6 fragments of AII are not responsible for the psychotropic activity of their parent octapeptide and suggest that AII(3-7) pentapeptide should be the fragment in question.

Amino Acid Sequence↗
PubMed1988

Behavioral effects of angiotensin II and angiotensin II-(4-8)-pentapeptide in rats.

One nM of angiotensin II (AII) or angiotensin II-(4-8)-pentapeptide [AII(4-8)] given intracerebroventricularly did not affect locomotor and exploratory behavior of rats in open field. AII significantly increased and AII(4-8) did not affect vertical activity of animals in electromagnetic motimeter. Neither of the peptides influenced horizontal activity in the motimeter. Both peptides intensified stereotypy produced by apomorphine and amphetamine. AII significantly improved, while AII(4-8) did not affect, consolidation of memory of the correct way to food in T-maze. Similarly, AII increased and AII(4-8) did not change the rate of acquisition of conditioned avoidance responses in a shuttle-box. Of the two examined peptides only AII significantly improved retrieval of memory of the passive avoidance behavior. The results show that AII(4-8) influences central dopaminergic system but, unlike its parent peptide AII, has no apparent effect on memory.

Angiotensins↗
PubMed1988

Angiotensin II-(3-8)-hexapeptide affects motor activity, performance of passive avoidance and a conditioned avoidance response in rats.

Angiotensin II-(3-8)-hexapeptide, at the dose of 1 nmol given intracerebroventricularly, only slightly less than angiotensin II (the same dose and route) stimulated exploratory locomotor behaviour in an open field and electromagnetic motimeter. Both peptides considerably enhanced stereotyped behaviour produced by apomorphine and amphetamine. Angiotensin II-(3-8)-hexapeptide improved recall in a passive avoidance situation as well as angiotensin II. The 3-8 C-terminus of angiotensin II enhanced acquisition of active avoidance nearly as effectively as the complete peptide. The results indicate that the effectiveness of equimolar doses of angiotensin II-(3-8)-hexapeptide and angiotensin II in improving processes related to learning and memory in rats is almost identical and thus must be independent of specific angiotensin receptors in brain to which the hexapeptide binds with about 1000 times lower affinity than angiotensin II. The stimulation of stereotypy, a dopamine-controlled behaviour, by the peptides points to the possibility of dopaminergic mediation of their psychotropic effects.

Angiotensin II↗
PubMed1987

Psychotropic effects of angiotensin II and III in rats: locomotor and exploratory vs cognitive behaviour.

One nmol of angiotensin II (AII) or angiotensin III (AIII) given intracerebroventricularly (i.c.v.) increased locomotor and exploratory activity in an open field apparatus but not in the electromagnetic field motimeter. Both peptides significantly enhanced stereotyped behaviour produced by apomorphine (2 mg/kg) and amphetamine (6.5 mg/kg) given intraperitoneally. Also, AII and AIII improved consolidation but not retrieval of memory for an appetitively reinforced spatial discrimination task in a T-maze. AII as well as AIII, given prior to the learning session on day 1, increased rate of acquisition of conditioned avoidance responses in a shuttle-box over the next 7 days. Both angiotensins, injected i.c.v. 15 min before the retention testing, remarkably (5-fold) prolonged re-entry latencies in the passive avoidance situation, suggesting facilitation of the retrieval of memory for an aversively motivated behaviour.

Amphetamines↗
PubMed1985

Effect of angiotensin II on some behavioral and neurochemical measures of the central serotonine system.

The effects of angiotensin II (AII) given intracerebroventricularly (icv.) on behaviors controlled by central serotonine (5-HT) and on some neurochemical measures of central 5-HT function have been investigated in rats. AII (0.1 and 0.5 micrograms) increased the 5-HT (20 micrograms, icv.) and L-tryptophan (200 mg/kg, ip.) induced hyposensitivity to painful electric stimuli delivered to the animals feet. Also AII (0.5 micrograms) intensified yawning, a 5-HT dependent behavior. This effect was decreased or abolished, respectively, by mianserin (3 mg/kg, i.p.) or cyproheptadine (1 mg/kg, i.p.), the 5-HT receptors blockers. AII, however, influenced neither the slight hyposensitivity of rats to electric current caused by 5-hydroxytryptophane (5-HTP, 12.5 and 25 mg/kg, ip.) nor the number of 'Wet-Dog' shakes evoked by 5-HTP (100 mg/kg, i.p.). Also, the peptide did change the rate of 5-HTP accumulation in brain measured after pretreatment of the animals with L-tryptophan (200 and 500 mg/kg, i.p.) preceded by the inhibition of central aromatic amino acid decarboxylase. In vitro AII (10(-5) - 10(-9) mol/l) did not affect release and only slightly increased uptake of 3H-5-HT by blood platelets. The data indicate that AII stimulates central 5-HT neurotransmission and that this action does not result from the peptide interference with the synthesis, release and uptake of 5-HT.

5-Hydroxytryptophan↗
PubMed1983

Effect of angiotensin II and vasopressin on acquisition and extinction of conditioned avoidance in rats.

The effect of angiotensin II on the acquisition and extinction of a conditioned avoidance response was examined in rats. Angiotensin II, 1 and 2 micrograms, given intracerebroventricularly facilitated acquisition of the conditioned avoidance response but did not influence extinction. [Sar1, Ile8]-angiotensin II (1 microgram), a specific antagonist of angiotensin II receptors, unexpectedly produced an effect quite similar to that of angiotensin II. Vasopressin (1 microgram) did not influence the rate of acquisition of the conditioned avoidance response but it markedly delayed its extinction. The data are discussed in terms of learning and memory facilitating properties of angiotensin II. This action seems to be independent of an interaction of angiotensin II with its known receptors or of release of vasopressin caused by the peptide.

Angiotensin II↗
PubMed1981

Intrastriatal kainic acid: acute effects on electrophysiological and biochemical measures of nigrostriatal dopaminergic activity.

The acute effects of intrastriatal kainic acid injection in nigrostriatal dopamine cell activity were assessed using electrophysiological and biochemical techniques. One hour after kainic acid injection, dopamine cell firing rates were significantly increased, as were striatal dopamine synthesis (dopa accumulation) and dopamine metabolism (3,4-dihydroxyphenylacetic acid levels). Twelve hours postkainic acid administration, cell firing rate had returned to control levels, as had dopa accumulation and DOPAC levels, but the number of dopamine cells firing had significantly decreased. Action potentials were elicited from the "silent" dopamine cells by iontophoretic application of gamma-aminobutyric acid but not glutamate. Conversely, 48 hr after kainic acid, the number of dopamine cells firing was significantly increased, as were 3,4-dihydroxyphenylacetic acid levels. Both cell firing rate and dopa accumulation, however, matched control values. The results are discussed in terms of the role of strionigral pathways in mediating the acute effects of kainic acid on the nigrostriatal dopaminergic system and are interpreted in light of the recently described phenomenon of presumed dopamine cell depolarization inactivation.

Animals↗
PubMedDate not supplied

Losartan influences behavioural effects of angiotensin II in rats.

The role of the angiotensin AT1 receptors in certain behavioural effects of angiotensin II (Ang II), using their selective antagonist losartan (DuP 753), was assessed. Ang II, given intracerebroventricularly (ICV) at the dose of 1 nmole, significantly improved object recognition, learning of conditioned avoidance responses (CARs), and recall of a passive avoidance behaviour. Losartan alone (1 microgram) was ineffective in any test except for the elevated 'plus' maze measuring anxiety which was diminished by the drug, both in peptide treated and in control rats. Losartan, given 5 min before Ang II, abolished improved after the peptide recall of the passive avoidance and object recognition. Losartan did not influence increased after Ang II rate of CARs acquisition. None of the treatments significantly changed behaviour of rats in the open field. The results point to the considerable involvement of the AT1 angiotensin receptors in the cognition improving effects of Ang II. However, unspecific psychoactivity of losartan should also be taken into account.

Angiotensin II↗
PubMedDate not supplied

Effect of angiotensin II and saralasin on motor activity and the passive avoidance behavior of rats.

One nmole of angiotensin II (ANG II) or saralasin, given intracerebroventricularly, failed to alter the motor activity of rats in open field. A combined injection of both peptides caused a significant decrease of the number of crossings and rearings. In the electromagnetic motimeter horizontal activity of animals was changed by neither of the peptides while the vertical activity was increased by ANG II. Again, a combined injection of saralasin and ANG II inhibited both horizontal and vertical activity. Stereotypies evoked by both apomorphine (2 mg/kg) and amphetamine (6.5 mg/kg), given intraperitoneally, were markedly intensified by ANG II and saralasin. A five-fold increase of the re-entry latencies in the passive avoidance situation was observed after pre-test administration of ANG II or saralasin but not the two in combination. These results suggest that ANG II and saralasin may improve processes related to learning and memory through an unspecific mechanism involving central dopamine systems.

Angiotensin II↗
PubMedDate not supplied

Moclobemide enhances aversively motivated learning and memory in rats.

Moclobemide belongs to a new class of short-acting reversible monoamine oxidase type A inhibitors with antidepressant activity. Male Wistar rats (180-220 g) were administered single and multiple (14x, daily) intragastrical doses of 20 mg/kg of moclobemide. The effects of the drug on the acquisition of conditioned avoidance responses (CARs), retrieval of passive avoidance, recognition memory, psychomotor activity in open field, and level of anxiety in an elevated "plus" maze were assessed. Moclobemide, given repeatedly, increased rate of the CAR acquisition, retrieval of the passive avoidance and had some anxiolytic properties. The drug, however, did not influence rats' psychomotor activity tested in open field and their ability to discriminate between familiar and unfamiliar objects. The results show that moclobemide in rats, given chronically, enhances aversively motivated learning and does not influence recognition.

Animals↗
PubMedDate not supplied

Trandolapril attenuates acquisition of conditioned avoidance in rats.

We have previously shown that angiotensin II (Ang II) improves cognitive performance of rats. In this study, behavioral effects of trandolapril, a highly lipophilic antihypertensive drug efficiently inhibiting brain angiotensin converting enzyme (ACE), were examined in rats. Single (0.1, 0.5, 1.0 mg/kg) or repetitive (0.1 mg/kg daily for 14 days) doses of trandolapril were given orally. The medium dose of the drug administered acutely as well as the chronic treatment significantly attenuated acquisition of conditioned avoidance responses. None of the three doses of trandolapril changed consolidation of memory and recall of the passive avoidance behavior, object recognition, and locomotor exploratory activity in open field. These data point to the psychoactive properties of trandolapril and suggest that physiological levels of the endogenous Ang II may be required for effective learning.

Administration, Oral↗
PubMedDate not supplied

6-OHDA lesion to the entorhinal cortex does not abolish angiotensin II improvement of recall in rats.

Our recent studies have shown that facilitating effect of angiotensin II (AII) on recall is mediated by dopaminergic systems. In this study the influence of bilateral destruction of dopaminergic endings in the entorhinal cortex on improving recall intracerebroventricular injection of AII was tested. Since this lesion did not abolish the facilitating influence of AII, it may be suggested that the dopaminergic projection to the entorhinal cortex is not responsible for the facilitating effect of AII on recall in a passive avoidance situation.

Angiotensin II↗
PubMedDate not supplied

The significance of Na+ ions in angiotensin II stimulation of acquisition of active avoidance in rats.

Angiotensin II (1 microgram) dissolved in water and given intracerebroventricularly on day 1, 15 min before the first learning session, enhanced rate of learning of active avoidance in rats over the next 7 days. However, the peptide, dissolved in 0.25 M NaCl, and given at the same dose and route, stimulated learning significantly more than that dissolved in water. A possible involvement of Na+ ions in facilitating learning action of A II is discussed.

Angiotensin II↗