citalopram escitalopram Lexapro
The effect of citalopram hydrobromide on 5-HT(2A) receptors in the impulsive-aggressive dog, as measured with (123)I-5-I-R91150 SPECT.

Peremans K, Audenaert K, Hoybergs Y, Otte A, Goethals I, Gielen I, Blankaert P, Vervaet M, van Heeringen C, Dierckx R.

Department of Medical Imaging, Faculty of Veterinary Medicine, Ghent University, Salisburylaan 133, 9820, Merelbeke, Belgium, kathelijne.peremans ugent.be.

PURPOSE: Involvement of the serotonergic system in impulsive aggression has been demonstrated in both human and animal studies. The purpose of the present study was to investigate the effect of citalopram hydrobromide (a selective serotonin re-uptake inhibitor) on the 5-HT(2A) receptor and brain perfusion in impulsive-aggressive dogs by means of single-photon emission computed tomography. METHODS: The binding index of the radioligand (123)I-5-I-R91150 was measured before and after treatment with citalopram hydrobromide in nine impulsive-aggressive dogs. Regional perfusion was measured with (99m)Tc-ethyl cysteinate dimer (ECD). Behaviour was assessed before treatment and again after 6 weeks of treatment. RESULTS: A correlation was found between decreased binding and behavioural improvement in eight out of nine dogs. The 5-HT(2A) receptor binding index was significantly reduced after citalopram hydrobromide treatment in all cortical regions but not in the subcortical area. None of the dogs displayed alterations in perfusion on the post-treatment scans. CONCLUSION: This study supports previous findings regarding the involvement of the serotonergic system in impulsive aggression in dogs in general. More specifically, the effect of treatment on the 5-HT(2A) receptor binding index could be demonstrated and the decreased binding index correlated with behavioural improvement.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15739093&dopt=Abstract citalopram escitalopram Lexapro



citalopram escitalopram Lexapro
Basal Prolactin Values Correlate with Response to Reboxetine Treatment in Major Depression, but Not with Response to Citalopram.

Moeller O, Hetzel G, Michael N, Rothermundt M, Arolt V, Erfurth A.

Affective Disorders Research Unit, Department of Psychiatry, University of Munster, Munster, Germany.

Little is known about variables that might predict outcome in major depression. Recently, basal prolactin values (BPV) have been suggested to predict response to treatment with tricyclic antidepressive drugs. In order to examine whether BPV predict response to selective mono-aminergic therapy, 24 in-patients with major depression were treated in a single-masked, randomised study using the most selective noradrenergic or serotonergic reuptake inhibitors available for antidepressant treatment, i.e. reboxetine and citalopram. A significant correlation between BPV and treatment response to reboxetine was found, but not between BPV and response to citalopram. As BPV are influenced by noradrenergic activity, it can be hypothesized that depressed patients with comparatively high BPV have a relatively high noradrenergic function. This might explain why in our study depressed patients with the highest BPV responded strongest to selective noradrenergic treatment with reboxetine. As measurement of BPV is simple, further studies are suggested to examine the possible clinical value of the link between prolactin, noradrenergic function in major depression and treatment response. Copyright (c) 2005 S. Karger AG, Basel.

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citalopram escitalopram Lexapro
Induction of Fos-like-immunoreactivity in the central extended amygdala by antidepressant drugs.

Morelli M, Pinna A, Ruiu S, Del Zompo M.

Department of Toxicology, University of Cagliari, Italy. morellim tin.it

The induction of the early gene c-fos was evaluated through Fos immunohistochemistry in areas belonging to the extended amygdala after acute administration of two antidepressants, citalopram and imipramine. Both citalopram and imipramine at the dose of 5 and 20 mg/kg, respectively, induced Fos-like immunoreactivity (FLI) in the central amygdaloid nucleus, lateral division of the bed nucleus of the stria terminalis (BSTL), and interstitial nucleus of the posterior limb of the anterior commissure (IPAC). The shell of the nucleus accumbens, which forms a continuum with the central extended amygdala, showed a decrease of FLI after administration of either citalopram or imipramine. The mechanism of action and the brain areas affected by antidepressants are still a matter of debate. By showing that the central extended amygdala is a common site of action for two different antidepressant types, these results provide new insight into the mechanism of action of antidepressants.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10025677&dopt=Abstract citalopram escitalopram Lexapro



citalopram escitalopram Lexapro
Alterations in serum and brain trace element levels after antidepressant treatment: part I. Zinc.

Nowak G, Schlegel-Zawadzka M.

Department of Pharmacology, Institute of Pharmacology, Polish Academy of Sciences, Krakow, Poland.

We have studied the effect of chronic treatment with imipramine, citalopram and electroconvulsive shock (ECS) on serum and brain zinc levels in rats. Chronic treatment with citalopram (but not with imipramine or ECS) significantly (approx 20%) increased the serum zinc level. Chronic treatment with both drugs slightly (by approx 10%) increase the zinc level in the hippocampus and slightly decreased it in the cortex, cerebellum and basal forebrain. Calculation of the ratio hippocampus/brain region within each group demonstrated a significantly (approx 20%) higher value after treatment with either imipramine or citalopram. Moreover, chronic ECS induced a significant increase (by 30%) in the zinc level in the hippocampus and also a slight increase (by 11-15%) in the other brain regions. Thus, these different antidepressant therapies induced an elevation of the hippocampal zinc concentration, which indicates a significant role of zinc in the mechanism of antidepressant therapy.

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citalopram escitalopram Lexapro
Behavioral sensitization to nicotine is associated with behavioral disinhibition; counteraction by citalopram.

Olausson P, Engel JA, Soderpalm B.

Department of Pharmacology, Institute of Physiology and Pharmacology, Goteborg University, Sweden. peter.olausson pharm.gu.se

This study investigated the effects of repeated nicotine treatment on locomotor activity and behavioral inhibition, and the influence of citalopram on the behavioral effects obtained. Male rats received daily subcutaneous injections of vehicle + vehicle (veh + veh), citalopram (5.0 mg/kg) + vehicle (cit + veh), vehicle + nicotine (1.0 mg/kg; veh + nic) or citalopram + nicotine (cit + nic). Acutely, nicotine stimulated locomotor activity, and repeated daily nicotine injections sensitized veh + nic rats to the nicotine-induced locomotor stimulation after 5, 10 and 15 treatment days, whereas in cit + nic rats, the enhancement of nicotine-induced locomotion was suppressed. However, when challenged with nicotine after citalopram withdrawal (-36 h), the cit + nic treated animals were also observed to be sensitized. In the elevated plus-maze, repeated nicotine treatment produced behavioral disinhibition, measured as an increase of time spent in and entries made into open arms (%), and chronic citalopram treatment attenuated the expression of behavioral disinhibition. Moreover, the degree of nicotine sensitization correlated to the behavioral disinhibition observed. In summary, these findings suggest that behavioral sensitization to nicotine is associated with behavioral disinhibition and that chronic citalopram treatment counteracts the expression of both phenomena. Since citalopram is a highly selective serotonin reuptake inhibitor, the effects of citalopram may be due to a facilitation of serotonin neurotransmission caused by the chronic citalopram treatment.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10102762&dopt=Abstract citalopram escitalopram Lexapro



citalopram escitalopram Lexapro
Oxytocin as a possible mediator of SSRI-induced antidepressant effects.

Uvnas-Moberg K, Bjokstrand E, Hillegaart V, Ahlenius S.

Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.

The nonapeptide oxytocin is released into systemic circulation in situations of psychosocial interaction, and has been shown to be involved in mechanisms of social bonding and social recognition in laboratory studies. In view of disturbances in psychosocial relationships being a triggering factor for depression and anxiety, it is interesting to note that experimental studies have shown oxytocin to possess antidepressant- and anxiolytic-like actions. Thus. in the present study we examined effects of the SSRI citalopram (20 mg/kg i.p.) on plasma oxytocin, acutely and upon repeated administration, in adult male Sprague-Dawley rats. Plasma oxytocin, and some functionally related peptides (CCK, gastrin, somatostatin and insulin), were measured by standard radioimmunoassay techniques. Acute citalopram administration produced a statistically significant increase in plasma oxytocin and CCK levels. Administration of citalopram for 14 days did not attenuate the oxytocin-releasing effect to a challenge dose of the SSRI zimeldine (20 mg/kg s.c.), whereas CCK levels were not increased after the subchronic citalopram treatment. Thus, the SSRI citalopram produces increased plasma oxytocin levels acutely, and there appears to be no or little tolerance to this effect upon repeated administration. There were no, or variable, effects on plasma levels of gastrin, somatostatin or insulin. It is suggested that oxytocin release is an important aspect of the pharmacological actions of SSRIs, and this could be an important contributory factor for the clinical profile of this group of antidepressants with particular efficacy in disorders of psychosocial origin.

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citalopram escitalopram Lexapro
5-HT2C receptors are involved in the discriminative stimulus effects of citalopram in rats.

Millan MJ, Girardon S, Dekeyne A.

Institut de Recherches Servier, Psychopharmacology Department, Paris, France.

Rats were trained on a fixed ratio 10, food-reinforced schedule to recognize a discriminative stimulus (DS) elicited by the selective serotonin (5-HT) reuptake inhibitor (SSRI), citalopram (2.5 mg/kg, IP). The preferential, high efficacy agonist at 5-HT2C receptors, Ro60-0175, dose-dependently generalized to citalopram with an ED50 of 0.3 mg/kg, IP. Further, the selective 5-HT2C receptor antagonist, SB242,084, dose-dependently (ED50=0.1 mg/kg, IP) blocked the citalopram DS. These data suggest that 5-HT2C receptors are involved in the DS properties of the SSRI, citalopram, in rats. They do not, however, exclude a potential role of other 5-HT receptor types.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10229070&dopt=Abstract citalopram escitalopram Lexapro