ORCID Profile
0000-0002-9175-3854
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Psychology | Central Nervous System | Biological Psychology (Neuropsychology, Psychopharmacology, Physiological Psychology) | Animal Behaviour | Biological psychology | Condensed Matter Physics | Central nervous system | Decision making | Behavioural neuroscience | Condensed Matter Imaging |
Expanding Knowledge in Psychology and Cognitive Sciences | Scientific Instruments | Neurodegenerative Disorders Related to Ageing | Mental Health | Expanding Knowledge in the Biological Sciences | Expanding Knowledge in the Medical and Health Sciences
Publisher: Elsevier BV
Date: 08-2016
DOI: 10.1016/J.EJPHAR.2016.05.013
Abstract: The mechanistic target of rapamycin complex 1 (mTORC1) regulates synaptic protein synthesis and therefore synaptic function and plasticity. A role for mTORC1 has recently been demonstrated for addiction-related behaviors. For ex le, central or intra-accumbal injections of the mTORC1 inhibitor rapamycin attenuates several indices of cocaine-seeking including progressive ratio (PR) responding and reinstatement. These behavioral effects are associated with decreased mTORC1 activity and synaptic protein translation in the nucleus accumbens (NAC) and point to a possible therapeutic role for rapamycin in the treatment of addiction. Currently, it is unclear whether similar behavioral and biochemical effects can be achieved by administering rapamycin systemically, which represents a more clinically-appropriate route of administration. Here, we assessed the effects of repeated, systemic administration of rapamycin (10mg/kg, i.p.) on PR responding for cocaine. We also assessed whether systemic rapamycin was associated with changes in measures of mTORC1 activity and GluA1 expression in the ventral and dorsal striatum. We report that systemic rapamycin treatment reduced PR breakpoints to levels comparable to intra-NAC rapamycin. Systemic rapamycin treatment also reduced phosphorylated p70S6K and GluA1 AMPARs within the NAC but not dorsal striatum. Thus, systemic administration of rapamycin is as effective at reducing drug seeking behavior and measures of mTORC1 activity compared to direct accumbal application and may therefore represent a possible therapeutic option in the treatment of addiction. Possible caveats of this treatment approach are discussed.
Publisher: MDPI AG
Date: 15-03-2017
DOI: 10.3390/NU9030285
Publisher: Public Library of Science (PLoS)
Date: 30-05-2014
Publisher: American Psychological Association (APA)
Date: 04-2017
DOI: 10.1037/BNE0000185
Publisher: Elsevier BV
Date: 08-2019
Publisher: Bentham Science Publishers Ltd.
Date: 02-03-2015
DOI: 10.2174/1874609808666150122150850
Abstract: The dopaminergic neurons of the substantia nigra (SN), which constitute the origin of the nigrostriatal system, are vulnerable to age-related degenerative processes. For ex le, in humans there is a relatively small age-related loss of neurons but a marked decline of the dopaminergic phenotype associated with impaired voluntary motor control. However, the mechanisms responsible for the dysfunction and degeneration of SN dopamine neurons remain poorly understood. One potential contributor is mitochondrial dysfunction, resulting from an increased abundance of mitochondrial DNA (mtDNA) mutations such as deletions. Human studies have identified relatively high levels of mtDNA deletions in these cells in both aging and Parkinson's disease (>35%), with a higher abundance of deletions (>60%) in in idual neurons with mitochondrial dysfunction. However, it is unknown whether similar mtDNA mutations occur in other species such as the rat. In the present study, we quantified mtDNA deletion abundance in laser microdissected SN dopaminergic neurons from young and old F344 rats. Our results indicate that mtDNA deletions accumulated with age, with approximately 20% more mtDNA deletions in SN dopaminergic neurons from old compared to young animals. Thus, while rat SN dopaminergic neurons do accumulate mtDNA deletions with aging, this does not reflect the deletion burden in humans, and other mechanisms may be operating to compensate for age-related mtDNA damage in the rat SN dopaminergic neurons.
Publisher: Wiley
Date: 13-06-2017
DOI: 10.1111/ADB.12520
Abstract: MicroRNAs (miRNAs) within the ventral and dorsal striatum have been shown to regulate addiction-relevant behaviours. However, it is unclear how cocaine experience alone can alter the expression of addiction-relevant miRNAs within striatal subregions. Further, it is not known whether differential expression of miRNAs in the striatum contributes to in idual differences in addiction vulnerability. We first examined the effect of cocaine self-administration on the expression of miR-101b, miR-137, miR-212 and miR-132 in nucleus accumbens core and nucleus accumbens shell (NAcSh), as well as dorsomedial striatum and dorsolateral striatum (DLS). We then examined the expression of these same miRNAs in striatal subregions of animals identified as being 'addiction-prone', either immediately following self-administration training or following extinction and relapse testing. Cocaine self-administration was associated with changes in miRNA expression in a regionally discrete manner within the striatum, with the most marked changes occurring in the nucleus accumbens core. When we examined the miRNA profile of addiction-prone rats following self-administration, we observed increased levels of miR-212 in the dorsomedial striatum. After extinction and relapse testing, addiction-prone rats showed significant increases in the expression of miR-101b, miR-137, miR-212 and miR-132 in NAcSh, and miR-137 in the DLS. This study identifies temporally specific changes in miRNA expression consistent with the engagement of distinct striatal subregions across the course of the addiction cycle. Increased dysregulation of miRNA expression in NAcSh and DLS at late stages of the addiction cycle may underlie habitual drug seeking, and may therefore aid in the identification of targets designed to treat addiction.
Publisher: Elsevier BV
Date: 2019
DOI: 10.1016/J.YFRNE.2018.09.002
Abstract: The neuropeptide oxytocin has been associated with food intake and feeding behaviour. This systematic review aimed to investigate the impact of oxytocin on dietary intake and feeding behaviour in rodent studies. Six electronic databases were searched to identify published studies to April 2018. Preclinical studies in mice and rats were included if they reported: (1) a dietary measure (i.e. food or nutrient and/or behaviour (2) an oxytocin measure, and (3) relationship between the two measures. A total of 75 articles (n = 246 experiments) were included, and study quality appraised. The majority of studies were carried out in males (87%). The top three oxytocin outcomes assessed were: exogenous oxytocin administration (n = 126), oxytocin-receptor antagonist administration (n = 46) and oxytocin gene deletion (n = 29). Meta-analysis of exogenous studies in mice (3 studies, n = 43 comparisons) and rats (n = 8 studies, n = 82 comparisons) showed an overall decrease in food intake with maximum effect shown at 2 h post-administration.
Publisher: Cold Spring Harbor Laboratory
Date: 04-02-2023
DOI: 10.1101/2023.02.03.527084
Abstract: Impaired motivational drive is a key feature of depression. Chronic stress is a known antecedent to the development of depression in humans and depressive-like states in animals. Whilst there is a clear relationship between stress and motivational drive, the mechanisms underpinning this association remain unclear. One hypothesis is that the endocrine system, via corticotropin-releasing hormone (CRH) in the paraventricular nucleus of the hypothalamus (PVN PVN CRH ), initiates a hormonal cascade resulting in glucocorticoid release, and that excessive glucocorticoids change brain circuit function to produce depression-related symptoms. Another, mostly unexplored hypothesis is that the direct activity of PVN CRH neurons and their input to other stress- and reward-related brain regions drives these behaviours. To further understand the direct involvement of PVN CRH neurons in motivation, we used optogenetic stimulation to activate these neurons one hour/day for 5 consecutive days and showed increased acute stress-related behaviours and long-lasting deficits in the motivational drive for sucrose. This was associated with increased Fos-protein expression in the lateral hypothalamus (LH). Direct stimulation of the PVN CRH inputs in the LH produced a similar pattern of effects on sucrose motivation. Together, these data suggest that PVN CRH neuronal activity may be directly responsible for changes in motivational drive and that these behavioural changes may, in part, be driven by PVN CRH synaptic projections to the LH.
Publisher: Frontiers Media SA
Date: 2012
Publisher: Oxford University Press (OUP)
Date: 09-2011
Publisher: Hindawi Limited
Date: 2013
DOI: 10.1155/2013/747938
Abstract: The ability to microdissect in idual cells from the nervous system has enormous potential, as it can allow for the study of gene expression in phenotypically identified cells. However, if the resultant gene expression profiles are to be accurately ascribed, it is necessary to determine the extent of contamination by nontarget cells in the microdissected s le. Here, we show that midbrain dopamine neurons can be laser-microdissected to a high degree of enrichment and purity. The average enrichment for tyrosine hydroxylase (TH) gene expression in the microdissected s le relative to midbrain sections was approximately 200-fold. For the dopamine transporter (DAT) and the vesicular monoamine transporter type 2 (Vmat2), average enrichments were approximately 100- and 60-fold, respectively. Glutamic acid decarboxylase (Gad65) expression, a marker for GABAergic neurons, was several hundredfold lower than dopamine neuron-specific genes. Glial cell and glutamatergic neuron gene expression were not detected in microdissected s les. Additionally, SN and VTA dopamine neurons had significantly different expression levels of dopamine neuron-specific genes, which likely reflects functional differences between the two cell groups. This study demonstrates that it is possible to laser-microdissect dopamine neurons to a high degree of cell purity. Therefore gene expression profiles can be precisely attributed to the targeted microdissected cells.
Publisher: Springer International Publishing
Date: 2017
DOI: 10.1007/7854_2016_56
Abstract: Orexins (hypocretins) are critically involved in coordinating appropriate physiological and behavioral responses to aversive and threatening stimuli. Acute stressors engage orexin neurons via direct projections from stress-sensitive brain regions. Orexin neurons, in turn, facilitate adaptive behavior via reciprocal connections as well as via direct projections to the hypophysiotropic neurons that coordinate the hypothalamic-pituitary-adrenal (HPA) axis response to stress. Consequently, hyperactivity of the orexin system is associated with increased motivated arousal and anxiety, and is emerging as a key feature of panic disorder. Accordingly, there has been significant interest in the therapeutic potential of pharmacological agents that antagonize orexin signaling at their receptors for the treatment of anxiety disorders. In contrast, disorders characterized by inappropriately low levels of motivated arousal, such as depression, generally appear to be associated with hypoactivity of the orexin system. This includes narcolepsy with cataplexy, a disorder characterized by the progressive loss of orexin neurons and increased rates of moderate/severe depression symptomology. Here, we provide a comprehensive overview of both clinical and preclinical evidence highlighting the role of orexin signaling in stress reactivity, as well as how perturbations to this system can result in dysregulated behavioral phenotypes.
Publisher: Elsevier BV
Date: 07-2015
DOI: 10.1016/J.MAD.2015.06.002
Abstract: Ageing affects most, if not all, functional systems in the body. For ex le, the somatic motor nervous system, responsible for initiating and regulating motor output to skeletal musculature, is vulnerable to ageing. The nigrostriatal dopamine pathway is one component of this system, with deficits in dopamine signalling contributing to major motor dysfunction, as exemplified in Parkinson's disease (PD). However, while the dopamine deficit in PD is due to degeneration of substantia nigra (SN) dopamine (DA) neurons, it is unclear whether there is sufficient loss of SN DA neurons with ageing to explain observed motor impairments. Instead, evidence suggests that age-related loss of DA neuron function may be more important than frank cell loss. To further elucidate the mechanisms of functional decline, we have investigated age-related changes in gene expression specifically in laser microdissected SN DA neurons. There were significant age-related changes in the expression of genes associated with neurotrophic factor signalling and the regulation of tyrosine hydroxylase activity. Furthermore, reduced expression of the DA neuron-associated transcription factor, Nurr1, may contribute to these changes. Together, these results suggest that altered neurotrophic signalling and tyrosine hydroxylase activity may contribute to altered DA neuron signalling and motor nervous system regulation in ageing.
Publisher: Frontiers Media SA
Date: 21-12-2020
DOI: 10.3389/FPHYS.2020.560802
Abstract: The pain experience depends on the relay of nociceptive signals from the spinal cord dorsal horn to higher brain centers. This function is ultimately achieved by the output of a small population of highly specialized neurons called projection neurons (PNs). Like output neurons in other central nervous system (CNS) regions, PNs are invested with a substantial axon collateral system that ramifies extensively within local circuits. These axon collaterals are widely distributed within and between spinal cord segments. Anatomical data on PN axon collaterals have existed since the time of Cajal, however, their function in spinal pain signaling remains unclear and is absent from current models of spinal pain processing. Despite these omissions, some insight on the potential role of PN axon collaterals can be drawn from axon collateral systems of principal or output neurons in other CNS regions, such as the hippoc us, amygdala, olfactory cortex, and ventral horn of the spinal cord. The connectivity and actions of axon collaterals in these systems have been well-defined and used to confirm crucial roles in memory, fear, olfaction, and movement control, respectively. We review this information here and propose a framework for characterizing PN axon collateral function in the dorsal horn. We highlight that experimental approaches traditionally used to delineate axon collateral function in other CNS regions are not easily applied to PNs because of their scarcity relative to spinal interneurons (INs), and the lack of cellular organization in the dorsal horn. Finally, we emphasize how the rapid development of techniques such as viral expression of optogenetic or chemogenetic probes can overcome these challenges and allow characterization of PN axon collateral function. Obtaining detailed information of this type is a necessary first step for incorporation of PN collateral system function into models of spinal sensory processing.
Publisher: Elsevier BV
Date: 09-2016
DOI: 10.1016/J.NEUROBIOLAGING.2016.05.017
Abstract: The spinal cord is vital for the processing of sensorimotor information and for its propagation to and from both the brain and the periphery. Spinal cord function is affected by aging, however, the mechanisms involved are not well-understood. To characterize molecular mechanisms of spinal cord aging, microarray analyses of gene expression were performed on cervical spinal cords of aging rats. Of the metabolic and signaling pathways affected, cholesterol-associated pathways were the most comprehensively altered, including significant downregulation of cholesterol synthesis-related genes and upregulation of cholesterol transport and metabolism genes. Paradoxically, a significant increase in total cholesterol content was observed-likely associated with cholesterol ester accumulation. To investigate potential mechanisms for the perturbed cholesterol homeostasis, we quantified the expression of myelin and neuroinflammation-associated genes and proteins. Although there was minimal change in myelin-related expression, there was an increase in phagocytic microglial and astrogliosis markers, particularly in the white matter. Together, these results suggest that perturbed cholesterol homeostasis, possibly as a result of increased inflammatory activation in spinal cord white matter, may contribute to impaired spinal cord function with aging.
Publisher: Elsevier BV
Date: 07-2019
DOI: 10.1016/J.CMET.2019.04.001
Abstract: Neuropeptide Y (NPY) exerts a powerful orexigenic effect in the hypothalamus. However, extra-hypothalamic nuclei also produce NPY, but its influence on energy homeostasis is unclear. Here we uncover a previously unknown feeding stimulatory pathway that is activated under conditions of stress in combination with calorie-dense food NPY neurons in the central amygdala are responsible for an exacerbated response to a combined stress and high-fat-diet intervention. Central amygdala NPY neuron-specific Npy overexpression mimics the obese phenotype seen in a combined stress and high-fat-diet model, which is prevented by the selective ablation of Npy. Using food intake and energy expenditure as readouts, we demonstrate that selective activation of central amygdala NPY neurons results in increased food intake and decreased energy expenditure. Mechanistically, it is the diminished insulin signaling capacity on central amygdala NPY neurons under combined stress and high-fat-diet conditions that leads to the exaggerated development of obesity.
Publisher: Wiley
Date: 10-2001
DOI: 10.1046/J.0953-816X.2001.01733.X
Abstract: It has been hypothesized that the brain categorizes stressors and utilizes neural response pathways that vary in accordance with the assigned category. If this is true, stressors should elicit patterns of neuronal activation within the brain that are category-specific. Data from previous immediate-early gene expression mapping studies have hinted that this is the case, but interstudy differences in methodology render conclusions tenuous. In the present study, immunolabelling for the expression of c-fos was used as a marker of neuronal activity elicited in the rat brain by haemorrhage, immune challenge, noise, restraint and forced swim. All stressors elicited c-fos expression in 25-30% of hypothalamic paraventricular nucleus corticotrophin-releasing-factor cells, suggesting that these stimuli were of comparable strength, at least with regard to their ability to activate the hypothalamic-pituitary-adrenal axis. In the amygdala, haemorrhage and immune challenge both elicited c-fos expression in a large number of neurons in the central nucleus of the amygdala, whereas noise, restraint and forced swim primarily elicited recruitment of cells within the medial nucleus of the amygdala. In the medulla, all stressors recruited similar numbers of noradrenergic (A1 and A2) and adrenergic (C1 and C2) cells. However, haemorrhage and immune challenge elicited c-fos expression in subpopulations of A1 and A2 noradrenergic cells that were significantly more rostral than those recruited by noise, restraint or forced swim. The present data support the suggestion that the brain recognizes at least two major categories of stressor, which we have referred to as 'physical' and 'psychological'. Moreover, the present data suggest that the neural activation footprint that is left in the brain by stressors can be used to determine the category to which they have been assigned by the brain.
Publisher: S. Karger AG
Date: 2015
DOI: 10.1159/000369483
Publisher: Bentham Science Publishers Ltd.
Date: 31-12-2013
DOI: 10.2174/1874609806666131204153812
Abstract: The causes of ageing remain poorly understood, although a role for mitochondria is widely accepted. These unique organelles that are responsible for a cell's energy, rely on their own small genome and translational machinery to produce proteins that, together with nuclear genome encoded proteins, form the electron transport chain complexes necessary for ATP production. Various forms of mitochondrial genome mutation and rearrangements are thought to be involved in the ageing process, particularly in post-mitotic cells, such as those of the nervous system. In the present study, we have characterised mitochondrial DNA (mtDNA) deletion mutations in five central nervous system (CNS) regions of the young, middle-aged, and old Fischer 344 (F344) rats. DNA was extracted from the cerebral cortex, striatum, midbrain, cerebellum and spinal cord, and long-PCR was used to detect mtDNA with deletions in the minor and major arcs. This approach has the advantage that all deletions can be detected without a priori knowledge of breakpoints. In the minor arc, we found evidence for deletions in the striatum of five out of six old animals and in the spinal cords from two of six old animals. In contrast, mtDNA deletions in the major arc appeared markedly more abundant, both in terms of affected CNS regions and number of deleted mtDNA molecules. Furthermore, major arc deletions were apparent earlier with a number of CNS regions showing deletions in the middle-aged group. The cerebral cortex, striatum and spinal cord were the most affected regions, while the midbrain and cerebellum were relatively spared. These findings are remarkably consistent with previous human brain data and further underscore the value of the rat model for investigation of ageing-related changes in the mitochondrial genome.
Publisher: Elsevier BV
Date: 12-2011
DOI: 10.1016/J.NEUROSCIENCE.2011.09.047
Abstract: The thalamus is considered an important interface between the ventral striatopallidum and the dorsal striatum, and may therefore contribute to compulsive drug-seeking behaviour. Recent evidence suggests that the paraventricular thalamus (PVT), a dorsal midline thalamic nucleus, and the mediodorsal thalamus (MD) are involved in drug self-administration and respond to drug-associated cues. At present, however, the role of these thalamic regions in mediating cue-induced reinstatement of cocaine-seeking is unclear. Similarly, the habenula complex, part of the epithalamus, has been implicated in nicotine self-administration and cue-induced reinstatement of heroin seeking, but the role of this region in cocaine reinstatement behaviour has received little attention. Rats (n=20) were trained to self-administer cocaine in the presence of discriminative stimuli associated with drug availability (S⁺) or drug non-availability (S⁻). Once a stable level of responding was reached, lever pressing was extinguished. Animals were then tested for reinstatement and sacrificed immediately following the presentation of either the S⁻ or S⁺ discriminative stimuli, and Fos-protein expression was assessed in thalamic and epithalamic regions. Interestingly, significant variation was observed in reinstatement behaviour, allowing a comparison between high-reinstating (HR), low-reinstating (LR) and control animals. Compared with LR animals, HR animals exhibited increased Fos-protein expression in the PVT, intermediodorsal thalamus and the medial and lateral isions of the habenula. Our data provide evidence that activation of thalamic and epithalamic nuclei is associated with propensity to reinstate to cocaine-seeking elicited by drug-related cues. We also build upon existing data highlighting the importance of the PVT in reinstatement behaviour.
Publisher: Frontiers Media SA
Date: 10-03-2015
Publisher: Wiley
Date: 22-09-2017
DOI: 10.1111/EJN.13674
Abstract: Altered motivated behaviour is a cardinal feature of several neuropsychiatric conditions including mood disorders. One well-characterized antecedent to the development of mood disorders is exposure to early life stress (ELS). A key brain substrate controlling motivated behaviour is the lateral hypothalamus (LH). Here, we examined the effect of ELS on LH activation and the motivation to self-administer sucrose. We tested whether chemogenetic activation of LH circuits could modify sucrose responding in ELS rats and examined the impact on LH cell populations. Male rat pups were maternally separated for 0 or 3 h on postnatal days 2-14. During adolescence, rats received bilateral injections of hM3D(Gq), the excitatory designer receptor exclusively activated by designer drugs, into LH. In adulthood, rats were trained to self-administer sucrose and tested under a progressive ratio schedule to determine their motivation for reward following injection with either vehicle or 5 mg/kg clozapine-N-oxide. Brains were processed for Fos-protein immunohistochemistry. ELS significantly suppressed lever responding for sucrose, indicating a long-lasting impact of ELS on motivation circuits. hM3D(Gq) activation of LH increased responding, normalizing deficits in ELS rats, and increased Fos-positive orexin and MCH cell numbers within LH. Our findings indicate that despite being susceptible to environmental stressors, LH circuits retain the capacity to overcome ELS-induced deficits in motivated behaviour.
Publisher: eLife Sciences Publications, Ltd
Date: 12-11-2019
DOI: 10.7554/ELIFE.49190
Abstract: Nociceptive information is relayed through the spinal cord dorsal horn, a critical area in sensory processing. The neuronal circuits in this region that underpin sensory perception must be clarified to better understand how dysfunction can lead to pathological pain. This study used an optogenetic approach to selectively activate spinal interneurons that express the calcium-binding protein calretinin (CR). We show that these interneurons form an interconnected network that can initiate and sustain enhanced excitatory signaling, and directly relay signals to lamina I projection neurons. Photoactivation of CR interneurons in vivo resulted in a significant nocifensive behavior that was morphine sensitive, caused a conditioned place aversion, and was enhanced by spared nerve injury. Furthermore, halorhodopsin-mediated inhibition of these interneurons elevated sensory thresholds. Our results suggest that dorsal horn circuits that involve excitatory CR neurons are important for the generation and lification of pain and identify these interneurons as a future analgesic target.
Publisher: Oxford University Press (OUP)
Date: 22-07-2014
DOI: 10.1093/NAR/GKU594
Publisher: Cold Spring Harbor Laboratory
Date: 15-09-2021
DOI: 10.1101/2021.09.12.21263471
Abstract: Almost half of in iduals diagnosed with schizophrenia also present with a substance use disorder, however, little is known about potential molecular mechanisms underlying this comorbidity. We used genetic analyses to enhance our understanding of the molecular overlap between these conditions. Our analyses revealed a positive genetic correlation between schizophrenia and the following dependence phenotypes: alcohol ( r g = 0.3685, SE = 0.0768, P = 1.61 × 10 −06 ), cannabis use disorder ( r g = 0.309, SE = 0.0332, P = 1.19 × 10 −20 ) and nicotine dependence ( r g = 0.1177, SE = 0.0436, P = 7.0 × 10- 03 ), as well as lifetime cannabis use ( r g = 0.234, SE = 0.0298, P = 3.73 × 10 − 15) and drinks per week ( r g = 0.0688, SE = 0.0217, P = 1.5 × 10 −03 ). We further constructed latent causal variable (LCV) models to test for partial genetic causality and found evidence for a potential causal relationship between alcohol dependence and schizophrenia ( GCP = 0.6, SE = 0.22, P = 1.6 × 10 −03 ). This putative causal effect with schizophrenia was not seen using a continuous phenotype of drinks consumed per week, suggesting that distinct molecular mechanisms underlying dependence are involved in the relationship between alcohol and schizophrenia. To localise the specific genetic overlap between schizophrenia and substance use disorders, we conducted a gene-based and gene-set pairwise meta-analysis between schizophrenia and each of the four in idual substance dependence phenotypes in up to 790,806 in iduals. These bivariate meta-analyses identified 44 associations not observed in the in idual GWAS, including five shared genes that play a key role in early central nervous system development. These genes may play an important role in substance dependence in schizophrenia, and, as a result, could represent important targets for future treatment or early intervention, as comorbid substance dependence is associated with poor treatment adherence, greater chronicity and increased mortality.
Publisher: Frontiers Media SA
Date: 23-07-2014
Publisher: Oxford University Press (OUP)
Date: 09-03-2018
Abstract: Oxytocin plays an important hormonal role in the regulation of feeding and energy intake. The aims of this review were to 1) determine the effects of dietary intake/behaviors on endogenous oxytocin and 2) examine the effect of exogenous oxytocin on dietary intake/behaviors. Published studies up to December 2016 were identified through searches of 5 electronic databases. Eligible studies included those in adults that included a measure related to an in idual's diet and a measure of oxytocin and the relationship between the 2 outcomes. Twenty-six studies (n = 912 participants 77% female) were included. The most common dietary outcomes assessed were alcohol, caffeine, calcium, sodium, fat, and calorie intake. It was found that endogenous oxytocin (n = 13) in nonclinical s les did not change significantly (P > 0.05) through altered diet or behaviors (neutral effect) in contrast, significant (P < 0.05) differences (increases and decreases) were identified in clinical s les. Exogenous oxytocin studies (n = 13) found reduced indices of food intake (positive effect) in clinical and nonclinical s les. Overall, few studies included comprehensive investigation of dietary intakes through the use of validated assessment tools. Dietary intake and behaviors appear to have some influence on oxytocin, with more pronounced effects found with exogenously administered oxytocin.
Publisher: Frontiers Media SA
Date: 2014
Publisher: Oxford University Press (OUP)
Date: 06-2011
Publisher: Public Library of Science (PLoS)
Date: 23-09-2010
Publisher: Springer Science and Business Media LLC
Date: 28-01-2014
DOI: 10.1038/NPP.2014.16
Publisher: Elsevier BV
Date: 12-2019
DOI: 10.1016/J.PHYSBEH.2019.112684
Abstract: The neuropeptide oxytocin is best known for its role during parturition and the milk-let down reflex. Recent evidence identifies a role for oxytocin in eating behaviour. After oxytocin administration, caloric intake is reduced with stronger inhibitory effects in in iduals with obesity. Whether the experience of visual food cues affects secretion or circulating levels of oxytocin is unknown. This pilot study had three aims: 1) to measure fasting appetite hormones with a focus on plasma oxytocin concentrations 2) determine whether healthy vs. hyperpalatable visual food cues differentially altered plasma oxytocin and 3) assess whether appetite hormone responses to healthy vs. hyperpalatable food images depended on weight or food addiction status. Eighteen healthy women of varying weight status, with/without self-reported food addiction were recruited. Study participants completed a set of standardised questionnaires, including Yale Food Addiction Scale, and attended a one-off experimental session. Blood was collected before and after viewing two sets of food images (healthy and hyperpalatable foods). Participants were randomly allocated in a crossover design to view either healthy images or hyperpalatable foods first. A positive correlation between BMI and plasma oxytocin was found (r
Publisher: Wiley
Date: 31-07-2012
Publisher: eLife Sciences Publications, Ltd
Date: 12-01-2022
DOI: 10.7554/ELIFE.72668
Abstract: Agouti-related peptide (AgRP) neurons increase motivation for food, however, whether metabolic sensing of homeostatic state in AgRP neurons potentiates motivation by interacting with dopamine reward systems is unexplored. As a model of impaired metabolic-sensing, we used the AgRP-specific deletion of carnitine acetyltransferase ( Crat ) in mice. We hypothesised that metabolic sensing in AgRP neurons is required to increase motivation for food reward by modulating accumbal or striatal dopamine release. Studies confirmed that Crat deletion in AgRP neurons (KO) impaired ex vivo glucose-sensing, as well as in vivo responses to peripheral glucose injection or repeated palatable food presentation and consumption. Impaired metabolic-sensing in AgRP neurons reduced acute dopamine release (seconds) to palatable food consumption and during operant responding, as assessed by GRAB-DA photometry in the nucleus accumbens, but not the dorsal striatum. Impaired metabolic-sensing in AgRP neurons suppressed radiolabelled 18F-fDOPA accumulation after ~30 min in the dorsal striatum but not the nucleus accumbens. Impaired metabolic sensing in AgRP neurons suppressed motivated operant responding for sucrose rewards during fasting. Thus, metabolic-sensing in AgRP neurons is required for the appropriate temporal integration and transmission of homeostatic hunger-sensing to dopamine signalling in the striatum.
Publisher: MDPI AG
Date: 26-04-2021
DOI: 10.3390/BS11050060
Abstract: The symptoms of addictive eating are often debated, with some overlap in symptoms with substance addictions or other disorders such as binge eating disorder. This study explored the levels of agreement with symptoms of addictive eating among different health professions, the conditions they provide advice for, and the population group/s they work with. An online cross-sectional survey was conducted in February–April 2020 including 142 health professionals (87% female, 65% residing in Australia, 28% each working in private practice/hospital settings). Of these, 47% were dietitians, 20% psychologists sychotherapists/counsellors, 16% other health practitioners (e.g., social workers), 13% health researchers, and 5% medical professionals. Agreement with 11 statements relating to addictive eating symptoms was assessed on a scale of 1/strongly disagree to 5/strongly agree (e.g., certain foods produce physiological effects in the brain rewards system). Differences in agreement by health profession were assessed by one-way analysis of variance. There were significant differences in agreement with in idual statements between health professions. Psychologists, psychotherapists, and counsellors reported lower agreement to statements relating to physiological effects in the reward system, withdrawal symptoms, and over-eating to alleviate stress/anxiety, than other professions (p 0.05). Those providing advice for disordered eating only reported lower agreement across statements compared with those providing advice for overweight/obesity or both (p 0.001). There were minimal differences based on the population group/s that health professionals work with. There is some agreement among health professionals regarding addictive eating symptoms, however, this differs by profession and the conditions they treat. This study provides a novel perspective on health professionals’ views on addictive eating symptoms, and there is a need for more research to explore the concepts further.
Publisher: Elsevier BV
Date: 06-2020
Publisher: Springer Science and Business Media LLC
Date: 03-02-2015
DOI: 10.1038/TP.2014.144
Publisher: Frontiers Media SA
Date: 22-08-2014
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 22-02-2021
DOI: 10.1097/J.PAIN.0000000000002194
Abstract: Projection neurons in the spinal dorsal horn relay sensory information to higher brain centres. The activation of these populations is shaped by afferent input from the periphery, descending input from the brain, and input from local interneuron circuits. Much of our recent understanding of dorsal horn circuitry comes from studies in transgenic mice however, information on projection neurons is still based largely on studies in monkey, cat, and rat. We used viral labelling to identify and record from mouse parabrachial nucleus (PBN) projecting neurons located in the dorsal horn of spinal cord slices. Overall, mouse lamina I spinoparabrachial projection neurons (SPBNs) exhibit many electrophysiological and morphological features that overlap with rat. Unbiased cluster analysis distinguished 4 distinct subpopulations of lamina I SPBNs, based on their electrophysiological properties that may underlie different sensory signalling features in each group. We also provide novel information on SPBNs in the deeper lamina (III-V), which have not been previously studied by patch cl analysis. These neurons exhibited higher action potential discharge frequencies and received weaker excitatory synaptic input than lamina I SPBNs, suggesting this deeper population produces different sensory codes destined for the PBN. Mouse SPBNs from both regions (laminae I and III-V) were often seen to give off local axon collaterals, and we provide neuroanatomical evidence they contribute to excitatory input to dorsal horn circuits. These data provide novel information to implicate excitatory input from parabrachial projection neuron in dorsal horn circuit activity during processing of nociceptive information, as well as defining deep dorsal horn projection neurons that provide an alternative route by which sensory information can reach the PBN.
No related organisations have been discovered for Christopher Dayas.
Start Date: 05-2022
End Date: 05-2026
Amount: $750,006.00
Funder: Australian Research Council
View Funded ActivityStart Date: 11-2022
End Date: 11-2024
Amount: $420,347.00
Funder: Australian Research Council
View Funded ActivityStart Date: 03-2023
End Date: 03-2026
Amount: $649,942.00
Funder: Australian Research Council
View Funded ActivityStart Date: 2018
End Date: 12-2018
Amount: $414,570.00
Funder: Australian Research Council
View Funded Activity