Spontaneously hypertensive rat (SHR) as an animal model for ADHD: a short overview

Meneses, Alfredo; Pérez-García, Georgina; Ponce-López, Teresa; Tellez, Ruth; Gallegos-Cari, Andrea; Castillo, Carlos

doi:10.1515/rns.2011.024

Cited by 66 publications

(40 citation statements)

References 74 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Both were similarly hypoactive compared to the SHR in the elevated plus maze and open field tests, consistent with many previous reports of the SHR being hyperactive when compared with WKYs[41]. This indicates that hypo-activity in the open field or other testing chambers is likely to be an inherited and strain-specific trait for WKY rats when compared with SHR.…”

Section: Discussionsupporting

confidence: 89%

Autism-related behavioral phenotypes in an inbred rat substrain

Zhang-James¹,

Li²,

Middleton³

et al. 2014

Behavioural Brain Research

View full text Add to dashboard Cite

Behavioral and genetic differences among Wistar-Kyoto (WKY) rats from different vendors and different breeders have long been observed, but generally overlooked. In our prior work, we found that two closely related WKY substrains, the WKY/NCrl and WKY/NHsd rats, differ in a small percentage of their genome which appeared to be highly enriched for autism risk genes. Although both substrains have been used widely in studies of hypertension, attention deficit/hyperactivity disorder (ADHD) and depression, they have not been tested for any autism-related behavioral phenotypes. Furthermore, these two substrains have often been used interchangeably in previous studies; no study has systematically examined the phenotypic differences that could be attributed by their small yet potentially meaningful genetic differences. In this paper we compared these two substrains on a battery of neurobehavioral tests. Although two substrains were similar in locomotor activity, WKY/NCrl rats were significantly different from WKY/NHsd rats in the elevated plus maze test, as well as measures of social interaction and ultrasonic vocalization. These strains were also compared with Sprague Dawley (SD) rats, a common outbred strain, and spontaneous hypertensive rats (SHR), an inbred rat model for ADHD and hypertension, which were derived from the same ancestor strain as the WKY strains. Our behavioral findings suggest that WKY/NCrl rats may be useful as a model autism spectrum disorders due to their lower social interest, lower ultrasonic vocalization and higher anxiety levels when WKY/NHsd rats are used as the control strain. Given the small genetic difference between the two inbred substrains, future studies to identify the exact gene and sequence variants that differ between the two may be useful for identifying the genetic mechanisms underlying these behaviors.

show abstract

Section: Discussionsupporting

confidence: 89%

Autism-related behavioral phenotypes in an inbred rat substrain

Zhang-James¹,

Li²,

Middleton³

et al. 2014

Behavioural Brain Research

View full text Add to dashboard Cite

show abstract

“…Impulsivity and hyperactivity have been measured with response-withholding tasks and the open field test [21][22][23]. The spontaneously hypertensive rat, an animal model of ADHD, has been validated using many of these behavioral tasks [1,24]. Recently, however, the homogeneity of spontaneously hypertensive rat behavior has been called into question [25].…”

Section: Introductionmentioning

confidence: 99%

Western-style diet induces insulin insensitivity and hyperactivity in adolescent male rats

Marwitz

Woodie

Blythe

2015

Physiology & Behavior

View full text Add to dashboard Cite

“…They also have disturbances in glutamate, DA, and NE functions, which in parallel demonstrate that ADHD patients have defects in the neuronal circuits required for reward-guided associative learning and memory formation [87] . Clearly, the SHR is a good model for the study of memory deficits in ADHD, primarily in the context of particular risk factors/ symptoms, responsiveness to specific drugs or other treatments or biomarkers for the diagnosis of ADHD, and for understanding the pathological mechanisms for the development of therapeutic approaches.…”

Section: N Ew Insights To Develop a Primate Model Of Adhdmentioning

confidence: 95%

Prefrontal cortical α2A-adrenoceptors and a possible primate model of attention deficit and hyperactivity disorder

Sun

Luo

et al. 2015

Neurosci. Bull.

View full text Add to dashboard Cite

Attention deficit and hyperactivity disorder (ADHD), a prevalent syndrome in children worldwide, is characterized by impulsivity, inappropriate inattention, and/or hyperactivity. It seriously afflicts cognitive development in childhood, and may lead to chronic under-achievement, academic failure, problematic peer relationships, and low self-esteem. There are at least three challenges for the treatment of ADHD. First, the neurobiological bases of its symptoms are still not clear. Second, the commonly prescribed medications, most showing short-term therapeutic efficacy but with a high risk of serious side-effects, are mainly based on a dopamine mechanism. Third, more novel and effi cient animal models, especially in nonhuman primates, are required to accelerate the development of new medications. In this article, we review research progress in the related fi elds, focusing on our previous studies showing that blockade of prefrontal cortical α 2A -adrenoceptors in monkeys produces almost all the typical behavioral symptoms of ADHD.Keywords: prefrontal cortex; α 2A -adrenoceptors; cognitive functions; attention defi cit and hyperactivity disorder; animal models ·Review· IntroductionAttention deficit and hyperactivity disorder (ADHD) is one of the most prevalent childhood neurodevelopmental conditions, affecting 3-5% of grade-school children worldwide [1] . It is characterized by i nappropriate levels of inattention, i mpulsivity, and/or hyperactivity [2][3][4] . These symptoms develop in childhood, and can persist into adolescence and adulthood [5] . ADHD seriously affects cognitive development [6][7][8] , and, without appropriate treatment, has consequences for the risk of anxiety, substance abuse, and depression in adulthood [ 2, 5, 9] .T he neurobiological bases o f ADHD symptoms are still not clear [10] . Clarifying them can help better understand the biological vulnerabilities that may underlie ADHD in a specifi c patient and how to modulate the responses to treatment, thereby contributing to better and more effective therapy.It has been suggested that the symptoms involve a dopaminergic mechanism in the prefrontal cortex (PFC) and striatum [11, 12] . Experimentally decreased dopamine (DA) release in the PFC results in ADHD-like symptoms [13, 14] .To date, DA dysregulation is thought to be central to the neurobiology of ADHD, and its pharmacological treatment, such as m ethylphenidate (MPH, i.e. Ritalin) [15][16][17] , levels the DA c oncentration in the synapse and extrasynaptic space in the PFC as a blocker of the DA transporter. MPH ameliorates inappropriate inattention [18][19][20] , decreases impulsivity [21] , and enhances inhibitory control [22] . However, as MPH is a prescription psychostimulant, there are strong concerns over drug dependence, paranoia, schizophrenia, and behavioral sensitization that might be caused by longterm therapy, similar to other stimulants [23][24][25].Converging evidence indicates that the pathophysiology of ADHD has multiple origins [26][27][28][29][30][31][32] ; for i...

show abstract

Spontaneously hypertensive rat (SHR) as an animal model for ADHD: a short overview

Cited by 66 publications

References 74 publications

Autism-related behavioral phenotypes in an inbred rat substrain

Autism-related behavioral phenotypes in an inbred rat substrain

Western-style diet induces insulin insensitivity and hyperactivity in adolescent male rats

Prefrontal cortical α2A-adrenoceptors and a possible primate model of attention deficit and hyperactivity disorder

Contact Info

Product

Resources

About