Locomotor sensitization is expressed by ghrelin and D1 dopamine receptor agonist in the nucleus accumbens core in amphetamine pre‐exposed rat

Jang, Ji Sung; Kim, Wha Young; Cho, Bo Ram; Lee, Jung Won; Kim, Jeong-Hoon

doi:10.1111/adb.12533

Cited by 13 publications

(9 citation statements)

References 33 publications

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“…The protein encoded by the ghrelin gene is the ligand for the growth hormone secretagogue receptor, which mainly regulates the concentration of growth hormone in the body and affects some of the body’s functions through affecting the release of growth hormone, such as regulating growth and development, affecting sugar, lipid and protein metabolism, and relaxing the cardiovascular system [ 16 , 17 ]. It has been proved that the ghrelin gene polymorphisms can affect the occurrence and susceptibility to a variety of diseases, such as polycystic ovary syndrome [ 18 ], chronic hepatitis C [ 19 ], and type 2 diabetes mellitus [ 20 ].…”

Section: Discussionmentioning

confidence: 99%

Association Between Ghrelin Gene Polymorphism and Cerebral Infarction

et al. 2020

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Section: Discussionmentioning

confidence: 99%

Association Between Ghrelin Gene Polymorphism and Cerebral Infarction

et al. 2020

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“…The relationship of dopaminergic activity and locomotor behavior is mainly modulated in NAcc. Therefore, when exposed to the animal in a novel environment or at the beginning of the closed‐field motor activity test, dopamine levels increase in NAcc (Alquicer, Morales‐Medina, Quirion, & Flores, ; Muñoz‐Villegas, Rodríguez, Giordano, & Juárez, ), consequently, animals show an increase in locomotor activity (Bringas, Carvajal‐Flores, López‐Ramírez, Atzori, & Flores, ; Jang, Kim, Cho, Lee, & Kim, ; Silva‐Gómez, Rojas, Juárez, & Flores, ). Our results reveal that treatment with N‐PEP‐12 in elderly animals does not modify motor behavior compared with the vehicle group.…”

Section: Discussionmentioning

confidence: 99%

The neuropeptide‐12 improves recognition memory and neuronal plasticity of the limbic system in old rats

Hernández-Hernández

Hernandez

Vázquez-Roque

et al. 2018

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Aging is a stage of life where cognitive and motor functions are impaired. This is because oxidative and inflammatory processes exacerbate neurodegeneration, which affects dendritic morphology and neuronal communication of limbic regions with memory loss. Recently, the use of trophic substances has been proposed to prevent neuronal deterioration. The neuropeptide-12 (N-PEP-12) has been evaluated in elderly patients with dementia, showing improvements in cognitive tasks due to acts as a neurotrophic factor. In the present work, we evaluated the effect of N-PEP-12 on motor activity and recognition memory, as well as its effects on dendritic morphology and the immunoreactivity of GFAP, Synaptophysin (SYP), and BDNF in neurons of the prefrontal cortex (PFC), dorsal hippocampus (DH) and nucleus accumbens (NAcc) of aged rats. The results show that N-PEP-12 improved the recognition memory, but the motor activity was not modified compared to the control animals. N-PEP-12 increases the density of dendritic spines and the total dendritic length in neurons of the PFC (layers 3 and 5) and in DH (CA1 and CA3). Interestingly NAcc neurons showed a reduction in the number of dendritic spines. In the N-PEP-12 animals, when evaluating the immunoreactivity for SYP and BDNF, there was an increase in the three brain regions, while the mark for GFAP decreased significantly. Our results suggest that N-PEP-12 promotes neuronal plasticity in the limbic system of aged animals, which contributes to improving recognition memory. In this sense, N-PEP-12 can be considered as a pharmacological alternative to prevent or delay brain aging and control senile dementias.

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“…Rats in each group were pre‐exposed to saline or AMPH (1.0 mg/kg, IP) with a total of four injections 2‐3 days apart. This regimen of drug injection and the doses of the drugs used were previously shown to induce behavioral sensitization (Jang, Kim, Cho, Lee, & Kim, 2018; Kim, Perugini, Austin, & Vezina, 2001). Two weeks after the last pre‐exposure injection, each group of rats was further arbitrarily divided into two subgroups, followed by a challenge injection with saline or AMPH (1.0 mg/kg, IP).…”

Section: Methodsmentioning

confidence: 99%

“…Once they recovered from the surgery, each group of rats was further arbitrarily divided into two subgroups, without specific randomization methods, and pre‐exposed to saline or AMPH (1.0 mg/kg, IP) with a total of four injections 2‐3 days apart. This regimen of drug injection is known to produce enduring sensitization of the locomotor response to amphetamine (Jang et al, 2018; Kim et al, 2001). To avoid any confounding effects of conditioning, rats were administered AMPH in different places (i.e., in the activity boxes for the first and the fourth injections and in their home cages for the other injections).…”

Section: Methodsmentioning

confidence: 99%

Disruption of amphetamine sensitization by alteration of dendritic thin spines in the nucleus accumbens core

Cai

Kim

Kwak

et al. 2022

Journal of Neurochemistry

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Repeated injections of psychomotor stimulants like amphetamine (AMPH) to rodents can induce behavioral sensitization, which represents a long‐lasting craving that is usually observed in human addicts. Behavioral sensitization is characteristically maintained for a long duration, accompanied by structural plasticity in some brain areas involved in reward circuitry. For example, it increased dendritic spine densities in the nucleus accumbens (NAcc), which is considered to reflect neurophysiological changes at this site, leading to addictive behaviors. The ezrin, radixin, and moesin (ERM) proteins regulate spine maturity by modifying their phosphorylation at the C‐terminal region. We previously showed that ERM phosphorylation is reduced by AMPH in the NAcc core, suggesting that ERM‐mediated spine changes at this site might be associated with AMPH sensitization. To test this hypothesis, we administered AMPH to rats according to a sensitization development schedule, with lentivirus encoding a phosphomimetic pseudo‐active mutant of radixin (Rdx T564D) in the NAcc core, and examined dendritic spines at this site. We found that compared to acute AMPH, AMPH sensitization increased thin spine density with a similar ratio of filopodia‐like to mature thin spines. However, with Rdx T564D, the density of thin spines increased, with augmented filopodia‐like thin spines, resulting in no AMPH sensitization. These results indicate that Rdx T564D forces thin spines to immaturity and thereby inhibits AMPH sensitization, for which an increase in mature thin spines is normally necessary. These findings provide significant clues to our understanding of the role of dendritic spines in mediating the development of psychomotor stimulant addiction.

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Locomotor sensitization is expressed by ghrelin and D1 dopamine receptor agonist in the nucleus accumbens core in amphetamine pre‐exposed rat

Cited by 13 publications

References 33 publications

Association Between Ghrelin Gene Polymorphism and Cerebral Infarction

Association Between Ghrelin Gene Polymorphism and Cerebral Infarction

The neuropeptide‐12 improves recognition memory and neuronal plasticity of the limbic system in old rats

Disruption of amphetamine sensitization by alteration of dendritic thin spines in the nucleus accumbens core

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