Displaying all 11 publications

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  1. Idris Z, Zakaria Z, Halim SA, Razak SA, Ghani ARI, Abdullah JM
    Childs Nerv Syst, 2021 05;37(5):1797-1802.
    PMID: 32949261 DOI: 10.1007/s00381-020-04893-z
    The neural basis for epilepsy and attention deficit hyperactivity disorder (ADHD) is currently incompletely known. We reported a young girl with both epilepsy and ADHD, who had a calcified lesion in the right basolateral amygdalo-hippocampal region extending to the ventral striatum. The child underwent disconnecting surgery and biopsy of the lesion. Fascinatingly, the child's behavior changed immediately after the surgery from inattentive and impulsive to nearly normal behavior experiencing no more breakthrough seizures since after 3 years of surgery. The Schaltenbrand Wahren Brain Atlas revealed alveus, cornu ammonis, amygdala superficialis, and medium as the disconnected region in this surgery.
    Matched MeSH terms: Amygdala/surgery
  2. Gopalsamy B, Sambasevam Y, Zulazmi NA, Chia JSM, Omar Farouk AA, Sulaiman MR, et al.
    Neurochem Res, 2019 Sep;44(9):2123-2138.
    PMID: 31376053 DOI: 10.1007/s11064-019-02850-0
    Number of ligations made in the chronic constriction injury (CCI) neuropathic pain model has raised serious concerns. We compared behavioural responses, nerve morphology and expression of pain marker, c-fos among CCI models developed with one, two, three and four ligations. The numbers of ligation(s) on sciatic nerve shows no significant difference in displaying mechanical and cold allodynia, and mechanical and thermal hyperalgesia throughout 84 days. All groups underwent similar levels of nerve degeneration post-surgery. Similar c-fos level in brain cingulate cortex, parafascicular nuclei and amygdala were observed in all CCI models compared to sham-operated group. Therefore, number of ligations does not impact intensity of pain symptoms, pathogenesis and neuronal activation. A single ligation is sufficient to develop neuropathic pain, in contrast to the established model of four ligations. This study dissects and characterises the CCI model, ascertaining a more uniform animal model to surrogate actual neuropathic pain condition.
    Matched MeSH terms: Amygdala/metabolism; Amygdala/pathology; Amygdala/physiopathology
  3. Ng, Sok Bee, Ahmad Nazlim Yusoff, Teng, Xin Ling, Aini Ismafairus Abd. Hamid
    MyJurnal
    Knowledge about the hemodynamic model that mediates synaptic activity and measured magnetic resonance signal is essential in understanding brain activation. Neural efficacy is a hemodynamic parameter that would change the evoked hemodynamic responses. In this work, brain activation and neural efficacy of the activated brain areas during simple addition task in two different backgrounds were studied using fMRI. The objectives were to determine the activated areas during the performance of arithmetic addition in quiet (AIQ) and noisy (AIN) background and to investigate the relationship between neural efficacy and height extent of activation for the respective areas. Eighteen healthy male participants performed simple arithmetic addition in quiet and in noise. Bilateral cerebellum, superior temporal gyrus (STG), temporal pole (TP) and supplementary motor area (SMA) were significantly (p < 0.05) activated during AIQ and AIN. Left middle frontal gyrus (L-MFG), right superior frontal gyrus (R-SFG), right superior orbital gyrus (R-SOG) and bilateral insula were more active in quiet as compared to in noise while the left middle cingulate cortex (L-MCC), left amygdala (L-AMG), right temporal pole (R-TP) and left cerebellum (L-CER) were more active in noise as compared to in quiet. The t value for most of the activated regions was found to be inversely proportional to the neural efficacy. Significant (p < 0.05) negative relationship between t value and neural efficacy were found for R-STG and bilateral cerebellum during AIQ, while for AIN, similar relationships were found in R-CER, R-STG and R-TP. This study suggests that while being significantly activated, the hemodynamic responses of these brain regions could have been suppressed by the stimulus resulting in an intensity decrease with increasing neural efficacy.
    Matched MeSH terms: Amygdala
  4. Hanim A, Mohamed IN, Mohamed RMP, Mokhtar MH, Makpol S, Naomi R, et al.
    Nutrients, 2023 Jul 05;15(13).
    PMID: 37447362 DOI: 10.3390/nu15133036
    Multiple alcohol use disorder (AUD)-related behavioral alterations are governed by protein kinase C epsilon (PKCε), particularly in the amygdala. Protein kinase C (PKC) is readily phosphorylated at Ser729 before activation by the mTORC2 protein complex. In keeping with this, the current study was conducted to assess the variations in mTORC2 and PKCε during different ethanol exposure stages. The following groups of rats were employed: control, acute, chronic, ethanol withdrawal (EW), and EW + ethanol (EtOH). Ethanol-containing and non-ethanol-containing modified liquid diets (MLDs) were administered for 27 days. On day 28, either saline or ethanol (2.5 g/kg, 20% v/v) was intraperitoneally administered, followed by bilateral amygdala extraction. PKCε mRNA levels were noticeably increased in the amygdala of the EW + EtOH and EW groups. Following chronic ethanol consumption, the stress-activated map kinase-interacting protein 1 (Sin1) gene expression was markedly decreased. In the EW, EW + EtOH, and chronic ethanol groups, there was a profound increase in the protein expression of mTOR, Sin1, PKCε, and phosphorylated PKCε (Ser729). The PKCε gene and protein expressions showed a statistically significant moderate association, according to a correlation analysis. Our results suggest that an elevated PKCε protein expression in the amygdala during EW and EW + EtOH occurred at the transcriptional level. However, an elevation in the PKCε protein expression, but not its mRNA, after chronic ethanol intake warrants further investigation to fully understand the signaling pathways during different episodes of AUD.
    Matched MeSH terms: Amygdala
  5. Cheah KH, Nisar H, Yap VV, Lee CY, Sinha GR
    J Healthc Eng, 2021;2021:5599615.
    PMID: 33859808 DOI: 10.1155/2021/5599615
    Emotion is a crucial aspect of human health, and emotion recognition systems serve important roles in the development of neurofeedback applications. Most of the emotion recognition methods proposed in previous research take predefined EEG features as input to the classification algorithms. This paper investigates the less studied method of using plain EEG signals as the classifier input, with the residual networks (ResNet) as the classifier of interest. ResNet having excelled in the automated hierarchical feature extraction in raw data domains with vast number of samples (e.g., image processing) is potentially promising in the future as the amount of publicly available EEG databases has been increasing. Architecture of the original ResNet designed for image processing is restructured for optimal performance on EEG signals. The arrangement of convolutional kernel dimension is demonstrated to largely affect the model's performance on EEG signal processing. The study is conducted on the Shanghai Jiao Tong University Emotion EEG Dataset (SEED), with our proposed ResNet18 architecture achieving 93.42% accuracy on the 3-class emotion classification, compared to the original ResNet18 at 87.06% accuracy. Our proposed ResNet18 architecture has also achieved a model parameter reduction of 52.22% from the original ResNet18. We have also compared the importance of different subsets of EEG channels from a total of 62 channels for emotion recognition. The channels placed near the anterior pole of the temporal lobes appeared to be most emotionally relevant. This agrees with the location of emotion-processing brain structures like the insular cortex and amygdala.
    Matched MeSH terms: Amygdala
  6. Asiff M, Sidi H, Masiran R, Kumar J, Das S, Hatta NH, et al.
    Curr Drug Targets, 2018;19(12):1391-1401.
    PMID: 28325146 DOI: 10.2174/1389450118666170321144931
    Hypersexuality refers to abnormally increased or extreme involvement in any sexual activity. It is clinically challenging, presents trans-diagnostically and there is extensive medical literature addressing the nosology, pathogenesis and neuropsychiatric aspects in this clinical syndrome. Classification includes deviant behaviours, diagnosable entities related to impulsivity, and obsessional phenomena. Some clinicians view an increase in sexual desire as 'normal' i.e. psychodynamic theorists consider it as egodefensive at times alleviating unconscious anxiety rooted in intrapsychic conflicts. We highlight hypersexuality as multi-dimensional involving an increase in sexual activity that is associated with distress and functional impairment. The aetiology of hypersexuality is multi-factorial with differential diagnoses that include major psychiatric disorders (e.g. bipolar disorder), adverse effects of treatments (e.g. levodopatreatment), substance-induced disorders (e.g. amphetamine substance use), neuropathological disorders (e.g. frontal lobe syndrome), among others. Numerous neurotransmitters are implicated in its pathogenesis, with dopamine and noradrenaline playing a crucial role in the neural reward pathways and emotionally- regulated limbic system neural circuits. The management of hypersexuality is determined by the principle of de causa effectu evanescent, if the causes are treated, the effect may disappear. We aim to review the role of pharmacological agents causing hypersexuality and centrally acting agents treating the associated underlying medical conditions. Bio-psycho-social determinants are pivotal in embracing the understanding and guiding management of this complex and multi-determined clinical syndrome.
    Matched MeSH terms: Amygdala/physiopathology
  7. Kumar J, Hapidin H, Get Bee YT, Ismail Z
    Alcohol, 2016 Feb;50:9-17.
    PMID: 26626323 DOI: 10.1016/j.alcohol.2015.10.001
    Withdrawal from long-term ethanol consumption results in overexcitation of glutamatergic neurotransmission in the amygdala, which induces an anxiety-like syndrome. Most alcoholics that suffer from such symptoms frequently depend on habitual drinking as self-medication to alleviate their symptoms. Metabotropic glutamate receptor subtype 5 (mGlu5) and protein kinase C (PKC) epsilon have been reported to mediate acute and chronic effects of ethanol. This study explores the changes in mGlu5 and PKC epsilon in the amygdala following acute administration of ethanol during ethanol withdrawal (EW) induced anxiety. Male Wistar rats were fed a modified liquid diet containing low-fat cow milk, sucrose, and maltodextrin, with a gradual introduction of 2.4%, 4.8% and 7.2% ethanol for 20 days. Six hours into EW, the rats were intraperitoneally injected with normal saline and ethanol (2.5 g/kg, 20% v/v), and exposed to open-field and elevated plus maze tests. Then, amygdala tissue was dissected from the rat brain for Western blot and gene expression studies. EW-induced anxiety was accompanied by a significant increase in mGlu5, total PKC epsilon, and phosphorylated PKC epsilon protein levels, and also of mRNA of mGlu5 (GRM5) in the amygdala. Acute administration of ethanol significantly attenuated EW-induced anxiety as well as an EW-induced increase in GRM5. The acute challenge of ethanol to EW rats had little effect on the phosphorylated and total protein levels of PKC epsilon in the amygdala. Our results demonstrate that amygdala PKC epsilon may not be directly involved in the development of anxiety following EW.
    Matched MeSH terms: Amygdala
  8. Nasser NS, Sharifat H, Rashid AA, Hamid SA, Rahim EA, Loh JL, et al.
    Front Psychol, 2020;11:556060.
    PMID: 33224051 DOI: 10.3389/fpsyg.2020.556060
    Background: Problematic Instagram use (PIGU), a specific type of internet addiction, is prevalent among adolescents and young adults. In certain instances, Instagram acts as a platform for exhibiting photos of risk-taking behavior that the subjects with PIGU upload to gain likes as a surrogate for gaining peer acceptance and popularity.

    Aims: The primary objective was to evaluate whether addiction-specific cues compared with neutral cues, i.e., negative emotional valence cues vs. positive emotional valence cues, would elicit activation of the dopaminergic reward network (i.e., precuneus, nucleus accumbens, and amygdala) and consecutive deactivation of the executive control network [i.e., medial prefrontal cortex (mPFC) and dorsolateral prefrontal cortex (dlPFC)], in the PIGU subjects.

    Method: An fMRI cue-induced reactivity study was performed using negative emotional valence, positive emotional valence, and truly neutral cues, using Instagram themes. Thirty subjects were divided into PIGU and healthy control (HC) groups, based on a set of diagnostic criteria using behavioral tests, including the Modified Instagram Addiction Test (IGAT), to assess the severity of PIGU. In-scanner recordings of the subjects' responses to the images and regional activity of the neural addiction pathways were recorded.

    Results: Negative emotional valence > positive emotional valence cues elicited increased activations in the precuneus in the PIGU group. A negative and moderate correlation was observed between PSC at the right mPFC with the IGAT scores of the PIGU subjects when corrected for multiple comparisons [r = -0.777, (p < 0.004, two-tailed)].

    Conclusion: Addiction-specific Instagram-themed cues identify the neurobiological underpinnings of Instagram addiction. Activations of the dopaminergic reward system and deactivation of the executive control network indicate converging neuropathological pathways between Instagram addiction and other types of addictions.

    Matched MeSH terms: Amygdala
  9. Wasli NS, Ridzwan IE, Azzubaidi MS, Kasmuri AR, Ahmed QU, Ming LC, et al.
    J Pharm Bioallied Sci, 2020 Nov;12(Suppl 2):S826-S830.
    PMID: 33828384 DOI: 10.4103/jpbs.JPBS_379_19
    Introduction: κ-opioid receptor (KOPr) system has been linked to relapse to many substances, especially opioids. Positive responses were recently reported in morphine and methamphetamine (polydrug)-dependent mice treated with buprenorphine and naltrexone, a functional κ antagonist.

    Objectives: This study aimed to determine the specific brain region that is responsive to KOPr treatment following polydrug dependence.

    Materials and Methods: The polydrug-dependent mice model was developed using conditioned place preference (CPP) method. Following successful withdrawal phase, the mice were treated with 0.3 mg/kg buprenorphine and 1.0 mg/kg naltrexone. Four brain regions (hippocampus, prefrontal cortex, amygdala, and striatum) were investigated using immunohistochemistry technique. This is to quantify the changes in KOPr expression in each major brain region that was primarily involved in addiction neurocircuits of many substances. Unpaired Student's t test was used to analyze all results, where P < 0.05 is considered significant.

    Results: The results showed that treatment with buprenorphine and naltrexone successfully attenuated relapse in 60% of mice (n = 14). A significant upregulation of KOPr was detected in striatum at the end of post-withdrawal phase (P < 0.01, n = 12). This treatment successfully suppressed KOPr in striatum (P < 0.001, n = 12), which supports the positive results seen in the CPP setting. No significant changes were observed in other brain regions studied.

    Conclusion: The hyperactivity of striatum suggests that the affected brain region following KOPr antagonist treatment is the region that primarily controls the drug rewarding activity, in which nucleus accumbens is located. This indicates that manipulation of KOPr system is one of the potential targets to treat morphine- or methamphetamine-dependence problem.

    Matched MeSH terms: Amygdala
  10. Ubuka T, Moriya S, Soga T, Parhar I
    PMID: 29643838 DOI: 10.3389/fendo.2018.00139
    Perinatal exposure of Bisphenol A (BPA) to rodents modifies their behavior in later life. To understand how BPA modifies their neurodevelopmental process, we first searched for BPA responsive genes from androgen and estrogen receptor signaling target genes by polymerase chain reaction array in the neonatal male rat brain. We used a transgenic strain of Wistar rats carrying enhanced green fluorescent protein tagged to gonadotropin-inhibitory hormone (GnIH) promoter to investigate the possible interaction of BPA responsive genes and GnIH neurons. We found upregulation of transmembrane protease serine 2 (Tmprss2), an androgen receptor signaling target gene, and downregulation of Forkhead box A1 (Foxa1), an ER signaling target gene, in the medial amygdala of male rats that were subcutaneously administered with BPA from day 1 to 3. Tmprss2-immunoreactive (ir) cells were distributed in the olfactory bulb, cerebral cortex, hippocampus, amygdala, and hypothalamus in 3 days old but not in 1-month-old male rats. Density of Tmprss2-ir cells in the medial amygdala was increased by daily administration of BPA from day 1 to 3. Tmprss2 immunoreactivity was observed in 26.5% of GnIH neurons clustered from the ventral region of the ventromedial hypothalamic nucleus to the dorsal region of the arcuate nucleus of 3-day-old male rat hypothalamus. However, Tmprss2 mRNA expression significantly decreased in the amygdala and hypothalamus of 1-month-old male rats. Foxa1 mRNA expression was higher in the hypothalamus than the amygdala in 3 days old male rats. Intense Foxa1-ir cells were only found in the peduncular part of lateral hypothalamus of 3-day-old male rats. Density of Foxa1-ir cells in the hypothalamus was decreased by daily administration of BPA from day 1 to 3. Foxa1 mRNA expression in the hypothalamus also significantly decreased at 1 month. These results suggest that BPA disturbs the neurodevelopmental process and behavior of rats later in their life by modifying Tmprss2 and Foxa1 expressions in the brain.
    Matched MeSH terms: Amygdala
  11. Singh, Darshan, Chye, Yann, Chao, Suo, Yücel, Murat, Grundmann, Oliver, Muhamad Zabidi Ahmad, et al.
    MyJurnal
    Mitragyna speciosa (Korth.) or kratom is a native medicinal plant of Southeast Asia. Commonly used by hard labours in harsh working environment, the ingestion of brewed kratom decoction is reported to produce dose-dependent stimulant and opioid-like effects. Kratom is also regularly consumed as a pain killer and as traditional cure for common maladies such as fever and cough. However, it remains unknown whether regular consumption of kratom decoction is associated with brain abnormalities in regular users in traditional settings. Methods: A total of 14 subjects (7 regular kratom users and 7 non-kratom users) voluntarily participated in this cross-sectional study. Face-to-face interviews were conducted with kratom users to determine history of kratom use and later these respondents underwent brain magnetic resonance imaging (MRI). Results: There were no significant differences (p>0.05) in the intracranial volume (ICV), cortical volumes (frontal, parietal, temporal, occipital, or cingulate lobe), or subcortical volumes (striatum, hippocampus, or amygdala), as well as in the diffusion tensor imaging (DTI) metrics, fractional anisotropy (FA) and mean diffusivity (MD) between kratom users and the controls. Conclusion: This preliminary study showed long-term consumption of kratom decoction is not significantly associated with altered brain structures in regular kratom users in traditional settings. However, further study is needed to establish more data for kratom use and its effects.
    Matched MeSH terms: Amygdala
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