N‐methyl‐<scp>d</scp>‐aspartate receptor dysfunction in the prefrontal cortex of stroke‐prone spontaneously hypertensive rat/Ezo as a rat model of attention deficit/hyperactivity disorder

Shikanai, Hiroki; Oshima, Naoya; Kawashima, Hidekazu; Kimura, Shin-ichi; Hiraide, Sachiko; Togashi, Hiroko; Iizuka, Kenji; Ohkura, Kazuhiro; Izumi, Tohru

doi:10.1002/npr2.12007

Cited by 10 publications

(2 citation statements)

References 34 publications

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“…NMDA-stimulated calcium uptake into prefrontal cortex slices has been shown to be significantly lower in SHRs than in WKY rats. This suggests impaired NMDAR function in the prefrontal cortex of SHRs, possibly leading to impaired cognition and an inability to sustain attention [33, 35]. However, the effects of NMDA on blood flow in the parietal cortex in SHRs have yet to be elucidated.…”

Section: Discussionmentioning

confidence: 99%

Methyl Palmitate Modulated NMDA-Induced Cerebral Hyperemia in Hypertensive Rats

Hsu

Chang²,

Lim

et al. 2023

J Vasc Res

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N-methyl-D-aspartate (NMDA) receptors were found to be dysfunctional in hypertensive rats. Methyl palmitate (MP) has been shown to diminish the nicotine-induced increase in blood flow in the brainstem. The aim of this study was to determine how MP modulated NMDA-induced increased regional cerebral blood flow (rCBF) in normotensive (WKY), spontaneously hypertensive (SHR), and renovascular hypertensive (RHR) rats. The increase in rCBF after the topical application of experimental drugs was measured using laser Doppler flowmetry. Topical NMDA application induced an MK-801-sensitive increase in rCBF in anesthetized WKY rats, which was inhibited by MP pretreatments. This inhibition was prevented by pretreatment with chelerythrine (a PKC inhibitor). The NMDA-induced increase in rCBF was also inhibited by the PKC activator in a concentration-dependent manner. Neither MP nor MK-801 affected the increase in rCBF induced by the topical application of acetylcholine or sodium nitroprusside. Topical application of MP to the parietal cortex of SHRs, on the other hand, increased basal rCBF slightly but significantly. MP enhanced the NMDA-induced increase in rCBF in SHRs and RHRs. These results suggested that MP had a dual effect on the modulation of rCBF. MP appears to play a significant physiological role in CBF regulation.

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Section: Discussionmentioning

confidence: 99%

Methyl Palmitate Modulated NMDA-Induced Cerebral Hyperemia in Hypertensive Rats

Hsu

Chang²,

Lim

et al. 2023

J Vasc Res

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“…For this reason, this review paper is aimed to focus on the role of NMDAR dysregulation in ADHD pathophysiology, which to date has not been studied extensively and is not well-understood. NMDAR dysfunction is one of the suggested mechanisms underlying ADHD pathogenesis in humans [ 31 ], as the role of NMDAR dysregulation has been well-established in a rat model of ADHD [ 32 , 33 ]. The most direct evidence is possibly from patients with a rare autoimmune disorder, anti-NMDAR encephalitis, in which autoantibodies against NMDAR cause NMDAR hypofunction.…”

Section: Introductionmentioning

confidence: 99%

Molecular Mechanisms Underlying NMDARs Dysfunction and Their Role in ADHD Pathogenesis

Kuś,

Saramowicz,

Czerniawska

et al. 2023

IJMS

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Attention deficit hyperactivity disorder (ADHD) is one of the most common neurodevelopmental disorders, although the aetiology of ADHD is not yet understood. One proposed theory for developing ADHD is N-methyl-D-aspartate receptors (NMDARs) dysfunction. NMDARs are involved in regulating synaptic plasticity and memory function in the brain. Abnormal expression or polymorphism of some genes associated with ADHD results in NMDAR dysfunction. Correspondingly, NMDAR malfunction in animal models results in ADHD-like symptoms, such as impulsivity and hyperactivity. Currently, there are no drugs for ADHD that specifically target NMDARs. However, NMDAR-stabilizing drugs have shown promise in improving ADHD symptoms with fewer side effects than the currently most widely used psychostimulant in ADHD treatment, methylphenidate. In this review, we outline the molecular and genetic basis of NMDAR malfunction and how it affects the course of ADHD. We also present new therapeutic options related to treating ADHD by targeting NMDAR.

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N‐methyl‐d‐aspartate receptor dysfunction in the prefrontal cortex of stroke‐prone spontaneously hypertensive rat/Ezo as a rat model of attention deficit/hyperactivity disorder

Shikanai

Oshima

Kawashima

et al. 2018

Neuropsychopharm Rep

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N‐methyl‐d‐aspartate receptor dysfunction in the prefrontal cortex of stroke‐prone spontaneously hypertensive rat/Ezo as a rat model of attention deficit/hyperactivity disorder

Abstract: These results suggest that the AD/HD animal model SHRSP/Ezo has NMDA receptor dysfunction in the PFC.

Cited by 10 publications

References 34 publications

Methyl Palmitate Modulated NMDA-Induced Cerebral Hyperemia in Hypertensive Rats

Methyl Palmitate Modulated NMDA-Induced Cerebral Hyperemia in Hypertensive Rats

Molecular Mechanisms Underlying NMDARs Dysfunction and Their Role in ADHD Pathogenesis

N‐methyl‐d‐aspartate receptor dysfunction in the prefrontal cortex of stroke‐prone spontaneously hypertensive rat/Ezo as a rat model of attention deficit/hyperactivity disorder

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