Female Oxytocin-Deficient Mice Display Enhanced Anxiety-Related Behavior

Mantella, Rose C.; Vollmer, Regis R.; Li, Xia; Amico, Janet A.

doi:10.1210/en.2002-0197

Cited by 164 publications

(120 citation statements)

References 27 publications

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“…[77][78][79] In addition, female OxtÀ/À mice have more, and male mice less, anxiety-like behavior than Oxt þ / þ mice. 77,80 Therefore, it may be that the deficits seen in PCP-disrupted PPI in OxtÀ/À mice are an extension of their overall deficits in cognitive functioning, perhaps reflecting a change in the glutamatergic system, beyond the CSPP.…”

Section: Discussionmentioning

confidence: 99%

Oxytocin as a natural antipsychotic: a study using oxytocin knockout mice

2008

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It has been previously suggested that oxytocin (Oxt) may act as a natural antipsychotic. To test this hypothesis, we investigated whether disruption of the oxytocin gene (OxtÀ/À) made mice more susceptible to the psychosis-related effects of amphetamine (Amp), apomorphine (Apo) and phencyclidine (PCP). We examined drug-induced changes in the prepulse inhibition (PPI) of the startle reflex, a measure of sensorimotor gating deficits characteristic of several psychiatric and neurological disorders, including schizophrenia. We found that treatment with Amp, Apo and PCP all had effects on PPI. However, in OxtÀ/À mice, but not Oxt þ / þ mice, PCP treatment resulted in large PPI deficits. As PCP is a noncompetitive N-methyl-D-aspartic acid receptor antagonist, these findings suggest that the absence of Oxt alters the glutamatergic component of the PPI.

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Section: Discussionmentioning

confidence: 99%

Oxytocin as a natural antipsychotic: a study using oxytocin knockout mice

2008

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“…Recent studies in oxytocin knockout mice have confirmed that these animals have abnormal autonomic and baroreflex control over heart rate (HR) and BP, and that female mice lacking oxytocin have increased anxiety-like behaviors (Mantella, Vollmer, Li, & Amico, 2003;Michelini, Marcelo, Amico, & Morris, 2003). Other recent research in both male and female animal models indicates that in addition to its production within the hypothalamus, oxytocin is produced and released in the heart and the vasculature, and that oxytocin specifically activates receptors that are present in both sites, leading to decreases in HR, contractile force and vascular resistance (Jankowski et al, 2000;Mukaddam-Daher, Yin, Roy, Gutkowska, & Cardinal, 2001;Thibonnier et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

Deficits in plasma oxytocin responses and increased negative affect, stress, and blood pressure in mothers with cocaine exposure during pregnancy

Light

Grewen

Amico

et al. 2004

Addictive Behaviors

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101

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In animals, oxytocin enhances maternal behavior and lowers blood pressure (BP) and negative affect, while parturitional cocaine disrupts oxytocin activity and increases maternal neglect and aggression. Thus, we compared oxytocin, BP, maternal behavior, and affect in mothers of infants who used cocaine (cocaine, n = 10) or did not (no drug, n = 25) during pregnancy. Laboratory BP and circulating oxytocin, catecholamines, and cortisol were examined before and during a speech stressor on 2 days, with vs. without prestress baby holding. Ambulatory monitoring assessed BP, urinary norepinephrine, and cortisol for 24 h at home. The cocaine group had lower oxytocin levels, greater hostility and depressed mood, less support from others and mastery over life events, higher BP during all events of testing without the baby, and higher ambulatory BP and urinary norepinephrine at home, while cortisol and epinephrine responses were blunted. Although they tended to hold their babies less often at home, baby holding in the laboratory led to decreased BP in cocaine mothers who then did not differ from no-drug mothers in BP or observed affect.

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“…after suspension in a minimal amount of Tween and made up to volume with distilled water. 8-Br-cAMP was prepared in artificial cerebrospinal fluid and injected into the right lateral ventricle (intracerebroventricularly) in a volume of 4 l at a rate of 1 l͞min as described (15). Cyclosporin A was prepared in 50% DMSO.…”

Section: Methodsmentioning

confidence: 99%

Lithium antagonizes dopamine-dependent behaviors mediated by an AKT/glycogen synthase kinase 3 signaling cascade

Beaulieu

Sotnikova

Yao

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

728

903

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Dopamine (DA) is a neurotransmitter involved in the control of locomotion, emotion, cognition, and reward. Administration of lithium salts is known to inhibit DA-associated behaviors in experimental animal models through unknown mechanisms. Here, we used a pharmacogenetic approach to show that DA can exert its behavioral effects by acting on a lithium-sensitive signaling cascade involving Akt͞PKB and glycogen synthase kinase 3 (GSK-3). In the mouse striatum, increased DA neurotransmission arising either from administration of amphetamine or from the lack of the DA transporter results in inactivation of Akt and concomitant activation of GSK-3␣ and GSK-3␤. These biochemical changes are not affected by activation of the cAMP pathway but are effectively reversed either by inhibition of DA synthesis, D2 receptor blockade, or administration of lithium salts. Furthermore, pharmacological or genetic inhibition of GSK-3 significantly reduces DA-dependent locomotor behaviors. These data support the involvement of GSK-3 as an important mediator of DA and lithium action in vivo and suggest that modulation of the Akt͞GSK-3 pathway might be relevant to DA-related disorders, such as attention deficit hyperactivity disorder and schizophrenia.

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Female Oxytocin-Deficient Mice Display Enhanced Anxiety-Related Behavior

Cited by 164 publications

References 27 publications

Oxytocin as a natural antipsychotic: a study using oxytocin knockout mice

Oxytocin as a natural antipsychotic: a study using oxytocin knockout mice

Deficits in plasma oxytocin responses and increased negative affect, stress, and blood pressure in mothers with cocaine exposure during pregnancy

Lithium antagonizes dopamine-dependent behaviors mediated by an AKT/glycogen synthase kinase 3 signaling cascade

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