Histofluorescent identification of indoleamine-concentrating brain loci associated with intraspecies, reflexive biting and locomotor behavior in olfactory-bulbectomized mice

Garris, David R.; Chamberlain, J.; DaVanzo, John P.

doi:10.1016/0006-8993(84)91056-4

Cited by 14 publications

(3 citation statements)

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“…Surprisingly, there are virtually no studies that have examined the dynamics of 5-HT neurotransmission during the actual performance of offensive aggressive behavior. There are a number of observations in the literature together with some recent findings from our own laboratory that would favor our hypothesis that the anti-aggressive effects of 5-HT 1A receptor agonists are exerted via 5-HT 1A autoreceptors in the raphe nuclei to transiently decrease intruder-activated serotonergic activity: 1) several reports indicate that the performance of spontaneous or ethanol-enhanced aggressive behavior is associated with marked increases in serotonergic activity in selected brain regions as estimated by 5HIAA/ 5HT ratios (Daruna and Kent 1976;Garris et al 1984;Broderick et al 1984;Haney et al 1990;Cadogan et al 1994), and increased 5-HT neuronal c-fos expression in the raphe nuclei (own unpublished results); and 2) local dorsal raphe administration of eltoprazine and 8-OH-DPAT in low dosages selectively inhibit offensive and maternal aggression (Mos et al 1993;De Almeida and Lucion 1997). Recent observations (not yet published) in our own laboratory show selective anti-aggressive effects of local dorsal raphe injections of alnespirone and S-15535 as well.…”

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confidence: 88%

Somatodendritic 5-HT1A Autoreceptors Mediate the Anti-Aggressive Actions of 5-HT1A Receptor Agonists in Rats An Ethopharmacological Study with S-15535, Alnespirone, and WAY-100635

Boer

Lesourd

Mocaër

et al. 2000

Neuropsychopharmacology

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Serotonin; Hypothermia; Rat A dysregulation of brain serotoninergic (5-HT) transmission, particularly at 5-HT 1A receptors, is implicated in the pathophysiology of anxiety, depression, and impulsive states like violent aggression (i.e., Coplan et al. 1995;Maes and Meltzer 1995;Berman et al. 1997). CorFrom the Department of Animal Physiology (SFB, JMK), University of Groningen, The Netherlands; and the Institut de Recherches Internationales Servier (ML, EM), Courbevoie Cedex, France.Address correspondence to: Dr. Sietse F. de Boer, Department of Animal Physiology, University of Groningen, PO Box 14, 9750 AA Haren, The Netherlands.Received January 13, 1999; revised August 5, 1999; accepted January 4, 2000. N EUROPSYCHOPHARMACOLOGY 2000 -VOL . 23 , NO . 1 Somatodendritic 5-HT 1A Autoreceptors and Aggression 21 respondingly, various 5-HT 1A receptor agonists exert potent anxiolytic, antidepressant, and anti-aggressive properties in experimental models (see for reviews, De Vry 1995;Broekkamp et al. 1995;Miczek et al. 1995;Olivier et al. 1995) and in man (Stahl 1994;Mann 1995;Ratey et al. 1991).Brain 5-HT 1A receptors are located postsynaptically, on various neurons in the limbic system and cortex, and presynaptically, as somatodendritic autoreceptors on the perikarya of serotoninergic neurons in the dorsal and median raphé (Palacios et al. 1987(Palacios et al. , 1990. Actions at both pre-and postsynaptic 5-HT 1A receptors appears to play a role in the therapeutic properties of 5-HT 1A receptor ligands, although their relative contribution remains to be clarified more precisely. To date, the anxiolytic-like effects of 5-HT 1A receptor agonists are generally ascribed to a selective stimulation of somatodendritic 5-HT 1A autoreceptors, thereby inhibiting the firing activity of 5-HT neurons consequently leading to a transient decrease in (anxiety-enhanced) 5-HT neurotransmission in limbic brain areas (Kidd et al. 1993;Schreiber and De Vry 1993;Millan et al. 1997). On the other hand, the rapid (i.e., immediately after drug administration) antidepressant-like effects of the same drugs mainly involve the acute stimulation of certain forebrain populations of postsynaptic 5-HT 1A receptors (Martin et al. 1990). Whereas a net increase in the tonic activation of these postsynaptic receptors is thought to underlie the therapeutic effects of several classes of antidepressants for long-term treatment Haddjeri et al. 1998).Concerning the potent anti-aggressive properties of 5-HT 1A receptor agonists, evidence on whether this occurs via a pre-or postsynaptic receptor mechanisms is conflicting. (e.g., McMillen et al. 1988;Sijbesma et al. 1991;Mos et al. 1993;Millan et al. 1997;De Almeida and Lucion 1997;Sanchez and Hyttel 1994). However, all these studies investigating the role of pre-and/or postsynaptic receptors in the anti-aggressive actions of 5-HT 1A receptor agonists have relied on 5-HT lesion/depletion or intracranial microinjection techniques, and it must be realized that both experimental approaches have limitati...

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confidence: 88%

Somatodendritic 5-HT1A Autoreceptors Mediate the Anti-Aggressive Actions of 5-HT1A Receptor Agonists in Rats An Ethopharmacological Study with S-15535, Alnespirone, and WAY-100635

Boer

Lesourd

Mocaër

et al. 2000

Neuropsychopharmacology

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“…The perturbation of the glutamatergic input from olfactory bulbs directly downregulates the function of these areas (Ho et al, 2001;Kelly et al, 1997). Despite the growing body of pharmacological evidence on reversion of BX effects with antidepressant agents, the evidence of neurochemical modification following olfactory bulbectomy is rather scarce, confined to quantitation of choline acetyltransferase (Bobkova et al, 2001), serotonin (Garris et al, 1984;Wrynn et al, 2000), neuropeptide Y (Holmes et al, 1998), and NMDA glutamatergic receptors, often with conflicting results (Robichaud et al, 2001;Webster et al, 2000). Also, neurochemical changes after destruction of the olfactory mucosa are rarely reported (Harding et al, 1978;Mucignat-Caretta and Caretta, 2001), and little is known on such changes in human psychiatric diseases.…”

Section: Hypotheses On the Neurobiological Substrates Of Behavioral M...mentioning

confidence: 99%

Animal models of depression: olfactory lesions affect amygdala, subventricular zone, and aggression

Mucignat‐Caretta

Bondı̀

Caretta

2004

Neurobiology of Disease

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“…The reinnervation of projection fields after the selective destruction of 5‐HT effer‐ences is a rather slow process and may even lead to a 5‐HT hyperinnervation of certain regions (Bjorklund et al , 1973; Zhou et al , 1995). Early histofluorescent studies of indolea‐mine accumulation in different brain regions revealed an increased indoleamine fluorescence in the olfactory tubercle and the piriform cortex 5 weeks after olfactory bulbectomy in mice (Garris et al , 1984). This finding, together with our recent observation of a simultaneous increase of the density of 5‐HT transporters and of tryptophan hydroxylase apoenzyme concentrations in the frontal cortex of bulbectomized rats (Zhou et al , 1997), suggests that one of the slow, secondary events associated with the reorganization of neuronal circuits is a compensatory 5‐HT hyperinnervation of anterior cortical regions.…”

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confidence: 99%

Influence of olfactory bulbectomy and subsequent imipramine treatment on 5‐hydroxytryptaminergic presynapses in the rat frontal cortex: behavioural correlates

Grecksch

Zhou

Franke

et al. 1997

British J Pharmacology

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1 Alterations of 5-hydroxytryptaminergic mechanisms are thought to play a special role in the pathogenesis of depression and antidepressant treatments are assumed to restore these changes. 2 We have used one of the most reliable models of depression, the olfactory bulbectomized rat to study the long term consequences of this manipulation and of subchronic imipramine treatment on two parameters of 5-hydroxytryptaminergic presynapses, 5-hydroxytryptamine (5-HT) transporter density and tryptophan hydroxylase apoenzyme concentration, in the frontal cortex as well as on active avoidance learning several weeks after bulbectomy. 3 The B max value of [ 3 H]-paroxetine binding and the concentration of the 5-HT synthesizing enzyme were both signi®cantly elevated in the frontal cortex of bulbectomized rats compared to sham-operated controls. 4 Imipramine treatment, either by daily injections or by subcutaneous implantation of slow release imipramine-containing polymers reduced the elevated tryptophan hydroxylase apoenzyme levels in the frontal cortex of bulbectomized, but not of sham-operated control rats and restored the de®cient learning performance of bulbectomized rats. 5 Both e ects were more pronounced after continuous drug administration by imipramine-releasing polymers compared to daily i.p. injections. 6 These ®ndings indicate that bulbectomy leads to a compensatory 5-hydroxytryptaminergic hyperinnervation of the frontal cortex. Chronic antidepressant treatment seems to attenuate the increased output of the 5-hydroxytryptaminergic projections in the frontal cortex through the destabilization of the rate limiting enzyme of 5-HT synthesis of the 5-hydroxytryptaminergic nerve endings in this brain region.

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Histofluorescent identification of indoleamine-concentrating brain loci associated with intraspecies, reflexive biting and locomotor behavior in olfactory-bulbectomized mice

Cited by 14 publications

References 14 publications

Somatodendritic 5-HT1A Autoreceptors Mediate the Anti-Aggressive Actions of 5-HT1A Receptor Agonists in Rats An Ethopharmacological Study with S-15535, Alnespirone, and WAY-100635

Somatodendritic 5-HT1A Autoreceptors Mediate the Anti-Aggressive Actions of 5-HT1A Receptor Agonists in Rats An Ethopharmacological Study with S-15535, Alnespirone, and WAY-100635

Animal models of depression: olfactory lesions affect amygdala, subventricular zone, and aggression

Influence of olfactory bulbectomy and subsequent imipramine treatment on 5‐hydroxytryptaminergic presynapses in the rat frontal cortex: behavioural correlates

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