Rodent models of psychiatric disorders—practical considerations

Gass, Peter; Wotjak, Carsten T.

doi:10.1007/s00441-013-1706-7

Cited by 9 publications

(6 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, the estrus cycle in rodents is not equivalent to the menstrual cycle in humans 59 . That being said, NMS nonetheless meets key criteria expected from an animal model, including time-dependent and sex-specific effects on respiration 20 , 71 . The results reported here, therefore, offer valuable insights into the basic mechanism in this neurological disorder affecting female rats.…”

Section: Limitations and Conclusionmentioning

confidence: 93%

Disruption of estradiol regulation of orexin neurons: a novel mechanism in excessive ventilatory response to CO2 inhalation in a female rat model of panic disorder

et al. 2020

View full text Add to dashboard Cite

Panic disorder (PD) is ~2 times more frequent in women. An excessive ventilatory response to CO2 inhalation is more likely during the premenstrual phase. While ovarian hormones appear important in the pathophysiology of PD, their role remains poorly understood as female animals are rarely used in pre-clinical studies. Using neonatal maternal separation (NMS) to induce a “PD-like” respiratory phenotype, we tested the hypothesis that NMS disrupts hormonal regulation of the ventilatory response to CO2 in female rats. We then determined whether NMS attenuates the inhibitory actions of 17-β estradiol (E2) on orexin neurons (ORX). Pups were exposed to NMS (3 h/day; postnatal day 3–12). The ventilatory response to CO2-inhalation was tested before puberty, across the estrus cycle, and following ovariectomy. Plasma E2 and hypothalamic ORXA were measured. The effect of an ORX1 antagonist (SB334867; 15 mg/kg) on the CO2 response was tested. Excitatory postsynaptic currents (EPSCs) were recorded from ORX neurons using whole-cell patch-clamp. NMS-related increase in the CO2 response was observed only when ovaries were functional; the largest ventilation was observed during proestrus. SB334867 blocked this effect. NMS augmented levels of ORXA in hypothalamus extracts. EPSC frequency varied according to basal plasma E2 levels across the estrus cycle in controls but not NMS. NMS reproduces developmental and cyclic changes of respiratory manifestations of PD. NMS disrupts the inhibitory actions of E2 on the respiratory network. Impaired E2-related inhibition of ORX neurons during proestrus is a novel mechanism in respiratory manifestations of PD in females.

show abstract

Section: Limitations and Conclusionmentioning

confidence: 93%

Disruption of estradiol regulation of orexin neurons: a novel mechanism in excessive ventilatory response to CO2 inhalation in a female rat model of panic disorder

et al. 2020

View full text Add to dashboard Cite

show abstract

“…2 Modeling psychiatric disorders in animals is obviously challenging. 3 However, several characteristics of schizophrenia have correlates in mice such as abnormal social behavior, impaired working memory, and defective prepulse inhibition (PPI). [4][5][6] Positive symptoms are traditionally modeled in mice by studying dopamine-related behavior such as locomotor activity.…”

Section: Introductionmentioning

confidence: 99%

AMIGO-Kv2.1 Potassium Channel Complex is Associated With Schizophrenia-Related Phenotypes

Peltola

Kuja-Panula

Liuhanen

et al. 2015

SCHBUL

View full text Add to dashboard Cite

The enormous variability in electrical properties of neurons is largely affected by a multitude of potassium channel subunits. Kv2.1 is a widely expressed voltage-dependent potassium channel and an important regulator of neuronal excitability. The Kv2.1 auxiliary subunit AMIGO constitutes an integral part of the Kv2.1 channel complex in brain and regulates the activity of the channel. AMIGO and Kv2.1 localize to the distinct somatodendritic clusters at the neuronal plasma membrane. Here we have created and characterized a mouse line lacking the AMIGO gene. Absence of AMIGO clearly reduced the amount of the Kv2.1 channel protein in mouse brain and altered the electrophysiological properties of neurons. These changes were accompanied by behavioral and pharmacological abnormalities reminiscent of those identified in schizophrenia. Concomitantly, we have detected an association of a rare, population-specific polymorphism of KV2.1 (KCNB1) with human schizophrenia in a genetic isolate enriched with schizophrenia. Our study demonstrates the involvement of AMIGO-Kv2.1 channel complex in schizophrenia-related behavioral domains in mice and identifies KV2.1 (KCNB1) as a strong susceptibility gene for schizophrenia spectrum disorders in humans.

show abstract

“…The specific involvement of the dopaminergic structures in the neurotoxicity of arsenic is further supported by our observation that rearing (vertical activity), the OF activity form most sensitive to dopaminergic impairment (Sedelis et al 2001), was still significantly affected after 6 weeks without arsenic exposure (Table 3). Further, rats in groups As and As+F spent significantly more time in the corner zones of the OF box, indicating (according to Archer 1973) that they tended less to exploration and more to anxiety, the latter being linked to dopaminergic hypofunction both in rats and in humans (Chaudhuri & Schapira 2009;Gass & Wotjak 2013). Fluoride had no effect on OF motility.…”

Section: Discussionmentioning

confidence: 84%

Behavioral and general effects of subacute oral arsenic exposure in rats with and without fluoride

Sárközi

Horváth

Vezér

et al. 2014

International Journal of Environmental Health Research

View full text Add to dashboard Cite

Consequences of oral arsenic and fluoride exposure on motor behavior and general toxicity were modeled in young adult male rats which received sodium (meta)arsenite (10 mg/kg b.w.), sodium fluoride (5 mg/kg b.w.), and their combination by gavage, once daily, 5 days a week for 6 weeks. After 6 weeks, 6 animals per group were dissected, while the other 6 were kept for 6 more weeks untreated. Body weight, together with food and water consumption, was measured daily. Arsenic, alone or along with fluoride, caused significant decrease in rearing, and increase in immobility and local activity in the open field in the 3rd and 6th week. By the 12th week, these changes mostly diminished. Weight gain, and food and water consumption were significantly reduced by arsenic but normalized post treatment. Fluoride had no own effect and mostly no influence on effects of arsenic. Massive deposition of arsenic in the rats' blood, cerebral cortex, and liver by the 6th week, and partial elimination by the 12th week, was seen. The results underline the risk of neuro-functional damage by arsenic and call for further investigations.

show abstract

Rodent models of psychiatric disorders—practical considerations

Cited by 9 publications

References 36 publications

Disruption of estradiol regulation of orexin neurons: a novel mechanism in excessive ventilatory response to CO2 inhalation in a female rat model of panic disorder

Disruption of estradiol regulation of orexin neurons: a novel mechanism in excessive ventilatory response to CO2 inhalation in a female rat model of panic disorder

AMIGO-Kv2.1 Potassium Channel Complex is Associated With Schizophrenia-Related Phenotypes

Behavioral and general effects of subacute oral arsenic exposure in rats with and without fluoride

Contact Info

Product

Resources

About