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K P Datla

Publications and source records attributed to K P Datla.

7 recordsLinked to original sources
PubMed1992

Dopaminergic modulation of footshock induced aggression in paired rats.

Footshock induced aggression (FIA) was induced in weight matched paired rats and three paradigms of aggressive behaviour was recorded, namely, the latency to fight (LF), total period of physical contact (TPP) and cumulative aggression scores (CAS). Dopamine (DA), administered centrally, and peripherally administered L-dopa (with benserazide, a peripheral decarboxylase inhibitor), a DA precursor, and the postsynaptic D2 receptor agonists, apomorphine, N-n-propyl-norapomorphine (PNA), bromocriptine, lisuride and pergolide, induced a dose-related facilitation of FIA characterized by decrease in LF and increase in TPP and CAS. However, the DA presynaptic receptor agonist, BHT-920, induced a biphasic effect with inhibition of FIA being induced by a lower dose and facilitation of the aggressive behaviour produced by a higher dose. The postsynaptic D2 receptor antagonists, haloperidol, spiperone and pimozide, induced a dose-related attenuation of FIA, an effect not seen with domperidone, a peripheral DA receptor antagonist. The results indicate that central dopaminergic postsynaptic D2 receptors have a modulatory facilitative effect on FIA, while the presynaptic DA autoreceptors mitigate aggressive behaviour. However, the presynaptic DA receptor agonist, BHT-920, appears to lose its receptor specificity on dose increment. Long term administration of haloperidol, followed by withdrawal, or desipramine, induced per se augmentation of FIA and potentiated the aggression-facilitative effects of L-dopa, apomorphine and PNA. Since both these treatments are known to induce supersensitivity of central postsynaptic dopamine D2 receptors, the effects are likely to be related to augmented function of dopamine neurones. The findings, in conjunction with a recent report from this laboratory indicating an increase in rat brain DA levels in FIA, support the contention that the central DA system has a facilitative effect on FIA.

Aggression↗
PubMed1991

Effects of tianeptine on stress-induced behavioural deficits and 5-HT dependent behaviour.

The novel tricyclic antidepressant drug tianeptine had an antidepressant-like effect on a rat model of depression based on the deficit in open field activity observed on the day after 2 h restraint. Thus, when tianeptine (10 mg/kg IP) was given 2 h after the end of the restraint to either untreated rats or to animals previously given 10 mg/kg of the drug per day for 13 days, then the deficit was opposed. Tianeptine, given acutely but not chronically, moderately enhanced the 5-HT1C receptor-dependent hypolocomotor effect of m-chlorophenylpiperazine (mCPP) but did not alter other 5-HT1 receptor subtype-dependent behaviour. Acute but not chronic tianeptine also decreased 5-HT2 receptor-dependent body shakes induced by 5-hydroxytryptophan. Shakes induced by the 5-HT2 agonist 1-(2,5-dimethoxy-4-iodophenyl)-2 aminopropane (DOI) were unaffected. The results are discussed in relation to the possible mechanism of antidepressant action of tianeptine.

Animals↗
PubMed1991

Serotonergic modulation of footshock induced aggression in paired rats.

Footshock induced aggression (FIA) was induced in paired rats and three paradigms of aggressive behaviour were recorded, namely, latency to fight (LF), total period of physical contact (TPP) and cumulative aggression scores (CAS). The effects of increasing or decreasing central serotonergic activity, by using a number of pharmacological agents with well defined effects on rat brain serotonin, were investigated on FIA and on FIA augmented by apomorphine, a dopamine receptor agonist. The results show that centrally administered serotonin, the serotonin precursor, 5-hydroxytryptophan administered with clorgyline, a selective MAO A inhibitor, quipazine, a serotonin receptor agonist, and fluoxetine, a selective inhibitor of neuronal re-uptake of serotonin, attenuated all paradigms of FIA and apomorphine induced potentiation of FIA. On the contrary, the other re-uptake inhibitor used, citalopram, appeared to have a dual effect and decreased LF and CAS, while increasing TPP. The serotonin synthesis inhibitor, p-chlorophenylalanine and the selective serotonin receptor (5-HT2) antagonist, ketanserin, augmented all paradigms of FIA per se and apomorphine induced augmentation of FIA. However, the other serotonin receptor antagonist used, metergoline, which blocks both 5-HT1 and 5-HT2 receptor subtypes, attenuated FIA per se but decreased only CAS in apomorphine induced increase in FIA. The data confirm the inhibitory effect of the central serotonergic system on aggressive behaviour and the inverse relationship existing between it and the central dopaminergic system in the modulation of FIA, as has also been confirmed in earlier biochemical investigations from this laboratory. The data has been discussed in the light of existing knowledge on serotonin receptor subtypes and the presence of modulatory serotonergic heteroreceptors on central dopaminergic neurones.

5-Hydroxytryptophan↗
PubMed1990

Brain monoamines during footshock-induced aggression in paired rats.

Regional brain monoamine concentrations were investigated following footshock induced fighting behaviour in paired rats, by a spectrophotofluorometric method. The dopamine (DA) levels of the diencephalon-midbrain (DM), and that of the caudate nucleus (CN), were significantly augmented as compared to unshocked but paired rats, the increase being substantially more in DM. Noradrenaline (NA) concentrations of both DM and pons-medulla (PM) increased to almost similar extents, though the data remained statistically insignificant in comparison to controls. The 5-hydroxytryptamine (5HT) of both DM and PM, however, recorded a decrease, which was statistically significant in the latter brain area. The biochemical data are consonant with the reported facilitatory effect of central DA, and the inhibitory role of central 5HT, in experimental aggression. The observed changes in NA levels, for which a role in experimental aggression remains equivocal, may be due to the stress of footshock kept minimal due to the coping factor of fighting in response to the shock.

Aggression↗
PubMed1990

Effect of selective monoamine oxidase A and B inhibitors on footshock induced aggression in paired rats.

Effects of a selective monoamine oxidase (MAO)--A inhibitor, clorgyline, a selective MAO-B inhibitor, deprenyl, and a non-selective MAO inhibitor, nialamide, were investigated on footshock-induced aggression (FIA) in paired rats. The doses and pretreatment times of the inhibitors used were based on an earlier reported in vivo dose-response and time-course study. In addition, apomorphine, a dopaminergic receptor agonist, and beta-phenylethylamine, a preferred substrate for MAO-B, were also used to garner corroborative evidence. The results of the study indicate that selective MAO-A inhibitors are likely to attenuate FIA by augmenting central serotonergic activity, while selective MAO-B inhibitors accentuate the behaviour by facilitating dopaminergic activity. A permissive role for noradrenaline could not be delineated by the available data.

Aggression↗
PubMed1988

Clonidine-induced automutilation in mice as a laboratory model for clinical self-injurious behaviour.

Clonidine-induced automutilation in mice was investigated as a putative experimental model for human self-injurious behaviour. Clonidine (20, 50 and 100 mg/kg, ip) produced dose-related self-biting, causing severe automutilation in mice which had been isolated and food-deprived for 24 h. This clonidine-induced behaviour was significantly attenuated by pharmacological treatments which selectively augment central serotonergic or reduce central dopaminergic activity. Conversely, the clonidine effect was potentiated by pharmacological agents which selectively reduce or enhance central serotonergic and dopaminergic activity, respectively. Drug-induced alterations in central noradrenergic or cholinergic activity had no significant effect on the self-mutilatory behaviour induced by clonidine. The automutilation induced by clonidine in mice appears to be a good experimental model for human self-injurious behaviour, since the latter has been postulated to result from serotonin deficiency and/or facilitation of central dopaminergic activity.

Acetylcholine↗