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.
Datla
K P
KP
Department of Pharmacology, Banaras Hindu University, Varanasi, India.
Mitra
S K
SK
Bhattacharya
S K
SK
D006916:5-Hydroxytryptophan / Q000494:pharmacology; D000374:Aggression / Q000187:drug effects / Q000502:physiology*; D000378:Agonistic Behavior / Q000187:drug effects / Q000502:physiology; D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D015283:Citalopram / Q000494:pharmacology; D003010:Clorgyline / Q000494:pharmacology; D004347:Drug Interactions; D004597:Electroshock; D005260:Female; D010134:Fenclonine / Q000031:analogs & derivatives / Q000494:pharmacology; D005473:Fluoxetine / Q000494:pharmacology; D005528:Foot; D007650:Ketanserin / Q000494:pharmacology; D008297:Male; D008711:Metergoline / Q000494:pharmacology; D011814:Quipazine / Q000494:pharmacology; D051381:Rats / Q000502:physiology; D011919:Rats, Inbred Strains; D011954:Receptors, Dopamine / Q000187:drug effects* / Q000502:physiology; D011985:Receptors, Serotonin / Q000145:classification / Q000187:drug effects* / Q000502:physiology; D012701:Serotonin / Q000494:pharmacology / Q000502:physiology*; D012702:Serotonin Antagonists / Q000494:pharmacology*
D011954:Receptors, Dopamine; D011985:Receptors, Serotonin; D012702:Serotonin Antagonists; D005473:Fluoxetine; D015283:Citalopram; D008711:Metergoline; C020261:4-chlorophenylalanine methyl ester; D012701:Serotonin; D011814:Quipazine; D007650:Ketanserin; D006916:5-Hydroxytryptophan; D003010:Clorgyline; D001058:Apomorphine; D010134:Fenclonine