Opioid circuitry and the aetiology of equine oral stereotypy

2007 ◽  
Vol 2007 ◽  
pp. 172-172
Author(s):  
A. Hemmings ◽  
S.D McBride ◽  
C.E Hale

Stereotypic behaviour is generally attributed to a dysfunction of the basal ganglia, although confusion exists as to whether altered function stems from the dorsal (Caudatus and putamen) or ventral regions (nucleus accumbens). In rodents, imbalanced basal ganglia opioid physiology leads to enhanced efferent neural transmission from only the dorsal striatum to cortex. However, in horses performing oral stereotypy (crib-biting), neural alterations in dopamine receptor density have been recorded in both dorsal and ventral striatal regions (McBride and Hemmings, 2005) suggesting that both projections may be altered in the stereotypy phenotype. Indeed, if stereotypies are considered to stem from highly motivated appetitive behaviours, it seems probable that ventral elements of the basal ganglia ‘reward’ circuitry should also be involved If this is the case, then stereotypy performance has potentially rewarding consequences and could thus be employed as a coping strategy. To further address the issue of dorsal versus ventral striatum involvement in the equine oral stereotypy phenotype, comparisons of opioid receptor physiology between crib-biters and control horses were performed.

2004 ◽  
Vol 32 ◽  
pp. 67-78
Author(s):  
A J Hemmings ◽  
S D McBride ◽  
N C Smith

AbstractA review of physiology and behaviour–based studies on the function of stereotypic behaviour indicates contradiction and inconsistency within the literature. By considering appropriate neurochemical data alongside an existing model of motivation (Hughes and Duncan, 1988), a greater understanding of the function of stereotypy may be gained. The Hughes and Duncan model (1988), described stereotypies as highly motivated appetitive behaviours performed repeatedly in an environment where consummatory goals are denied. Moreover, appetitive behaviours activate reward circuitry such as the ventral tegmental area and nucleus accumbens and are thus considered to have a reward value associated with their performance (Carr, 2002; Jones et al., 1990). Stress induced sensitisation of reward circuitry may result in appetitive ‘stereotypies’ having increased reward value, perhaps becoming consummatory in their own right. In such a scenario, stereotypic behaviour could function as a coping tool, allowing the animal to counter the effects of an aversive environment.


2020 ◽  
Vol 19 (4) ◽  
pp. 47-54
Author(s):  
Valery N. Mukhin ◽  
Ivan R. Borovets ◽  
Vadim V. Sizov ◽  
Konstantin I. Pavlov ◽  
Victor M. Klimenko

Kinetics of the evoked dopamine release and subsequent uptake in the parts of the rat striatum has not been studied sufficiently. The aim of this study is to fill this gap and to investigate kinetics of dopamine release and uptake in vivo so that comparison can be made between the dorsal and the parts of the ventral striatum and with taking into account the overlapping electrochemical factors during the subsequent analysis of voltammetry recordings. Materials and methods. The evoked wave of dopamine release and uptake in the dorsal striatum, core, and shell of the nucleus accumbens in the different groups of rats was recorded by the fast-scan cyclic voltammetry. Voltammetry recordings were subjected to principal component analysis and only the components associated with dopamine were taken for further analysis. The values of the parameters of the curves of dopamine release and uptake were defined. Then factor and variance analyses of the parameters were carried out. Results. Factor analysis showed that the set of parameters of the dopamine wave can be reduced to the 4 factors that are comparable with the variables of the known from the literature mathematical model that describes the dopamine wave based on the MichaelisMenten equation. Two of the factors and the corresponding parameters of the dopamine curve differ within the dorsal and ventral striatum. Factor 1 is associated with the parameters HL, T80_20, T20_0, slope_T20T0, which are significantly larger in the core of the nucleus accumbens. Factor 3 is associated with the parameters T50_2, AUC, FWHH, T100_80 which are significantly less in the dorsal striatum. Conclusions. The parameters of the curve of dopamine release and uptake are determined by 4 factors. Among the dopamine curve parameters, the best measures of the factors are T50_1, DAC, T100_80 и T20_0. The kinetics of stimulated dopamine release and uptake varies within the dorsal and ventral striatum. The final phase of dopamine uptake is slowed in the core of the nucleus accumbens in comparison to the shell, and the dorsal striatum. The slope of initial phase of dopamine uptake in the dorsal striatum is steeper.


2021 ◽  
Author(s):  
Kristen Hirter ◽  
Elaine N. Miller ◽  
Cheryl D. Stimpson ◽  
Kimberley A. Phillips ◽  
William D. Hopkins ◽  
...  

Abstract Recent evidence suggests that increased dopaminergic signaling within the dorsal striatum played a central role in the evolution of the human brain. This increase has been linked to human pro-sociality and language in what has been described as a dopamine-dominated striatum personality style. Increased striatal dopamine is associated with an increase in ventral striatal activity and promotes externally-driven behaviors, including cooperation and social conformity. In contrast, decreased striatal dopamine is associated with increased dorsal striatal activity andfavors internally driven and goal-oriented behaviors. Previous comparative studies have focused on the dorsal striatum, measuring dopaminergic innervation in the dorsal and medial caudate nucleus and putamen. Here, we add to this knowledge by examining regions of the ventral striatum. We quantified the density of tyrosine hydroxylase-immunoreactive axons, as a measure of dopaminergic innervation, in the nucleus accumbens and ventral pallidum of humans, great apes, platyrrhine and cercopithecid monkeys. Our data show that humans have a significantly greater dopaminergic innervation in both structures, supporting the hypothesis that selection for a prosocial neurochemistry in the human basal ganglia may have contributed to the evolution of our uniquely social behavior profile.


Author(s):  
Lidia Bellés ◽  
Andrea Dimiziani ◽  
Stergios Tsartsalis ◽  
Philippe Millet ◽  
François R Herrmann ◽  
...  

Abstract Background Impulsivity and novelty preference are both associated with an increased propensity to develop addiction-like behaviors, but their relationship and respective underlying dopamine (DA) underpinnings are not fully elucidated. Methods We evaluated a large cohort (n = 49) of Roman high- and low-avoidance rats using single photon emission computed tomography to concurrently measure in vivo striatal D2/3 receptor (D2/3R) availability and amphetamine (AMPH)-induced DA release in relation to impulsivity and novelty preference using a within-subject design. To further examine the DA-dependent processes related to these traits, midbrain D2/3-autoreceptor levels were measured using ex vivo autoradiography in the same animals. Results We replicated a robust inverse relationship between impulsivity, as measured with the 5-choice serial reaction time task, and D2/3R availability in ventral striatum and extended this relationship to D2/3R levels measured in dorsal striatum. Novelty preference was positively related to impulsivity and showed inverse associations with D2/3R availability in dorsal striatum and ventral striatum. A high magnitude of AMPH-induced DA release in striatum predicted both impulsivity and novelty preference, perhaps owing to the diminished midbrain D2/3-autoreceptor availability measured in high-impulsive/novelty-preferring Roman high-avoidance animals that may amplify AMPH effect on DA transmission. Mediation analyses revealed that while D2/3R availability and AMPH-induced DA release in striatum are both significant predictors of impulsivity, the effect of striatal D2/3R availability on novelty preference is fully mediated by evoked striatal DA release. Conclusions Impulsivity and novelty preference are related but mediated by overlapping, yet dissociable, DA-dependent mechanisms in striatum that may interact to promote the emergence of an addiction-prone phenotype.


1987 ◽  
Vol 151 (3) ◽  
pp. 288-301 ◽  
Author(s):  
P. J. McKenna

The dopamine hypothesis of schizophrenia implies that positive schizophrenic symptoms should be understandable by reference to brain structures receiving a dopamine innervation, or in terms of the functional role of dopamine itself. The basal ganglia, ventral striatum, septo-hippocampal system, and prefrontal cortex, sites of mesotelencephalic dopamine innervation, are examined and it is argued that their dysfunction could form the basis of particular schizophrenic symptom classes. The postulated involvement of dopamine in reinforcement processes might further assist such interpretations. This type of analysis can be extended to other categories of schizophrenic psychopathology.


2020 ◽  
Author(s):  
Msema Msackyi ◽  
Yuanxin Chen ◽  
Wangchen Tsering ◽  
Ninghan Wang ◽  
Jingyu Zhao ◽  
...  

AbstractParkinson’s disease (PD) is the second most common neurodegenerative disease. Dopamine (DA) neurons in the substantia nigra par compacta with axonal projections to the dorsal striatum (dSTR) degenerate in PD while in contrast, DA neurons in the ventral tegmental area with axonal projections to the ventral striatum including the nucleus accumbens (NAcc) shell, are largely spared. To understand the pathogenesis of PD, it is important to study the neuroenergetics of DA neurons. This study aims to uncover the relative contribution of glycolysis and oxidative phosphorylation (OxPhos) to evoked DA release in the striatum. We measured evoked DA release in mouse striatal brain slices by fast-scan cyclic voltammetry every 2 minutes. Blocking OxPhos caused a greater reduction in evoked DA release in the dSTR compared to the NAcc shell, and blocking glycolysis caused a greater reduction in evoked DA release in the NAcc shell than in the dSTR. Furthermore, when glycolysis was bypassed in favor of direct OxPhos, evoked DA release in the NAcc shell was decreased by ∼50% over 40 minutes whereas evoked DA release in the dSTR was largely unaffected. These results demonstrated that the dSTR relies primarily on OxPhos for energy production to maintain evoked DA release whereas the NAcc shell relies more on glycolysis. Using two-photon imaging, we consistently found that the oxidation level of the DA terminals was higher in the dSTR than in the NAcc shell. Together, these findings partially explain the specific vulnerability of DA terminals in the dSTR to degeneration in PD.Significant statementThe neuroenergetics of dopaminergic neuron is important to understand Parkinson’s disease (PD), a neurodegenerative disorder associated with mitochondrial dysfunctions. However, the relative contributions of glycolysis and oxidative phosphorylation (OxPhos) to presynaptic energy demands in DA terminals are unclear. We addressed this question by measuring DA release in the dorsal striatum and nucleus accumbens (NAcc) shell of mouse brain using FSCV under reagents blocking different energy systems. We found that the NAcc shell relies on both glycolysis and OxPhos to maintain DA release while the dSTR relies heavily on OxPhos. We demonstrate the different neuroenergetics of DA terminals in these two brain areas, providing new fundamentally important insight into the specific vulnerability of DA terminals in the dSTR to degeneration in PD.


2019 ◽  
Vol 5 (1) ◽  
Author(s):  
Hirotaka Sekiguchi ◽  
Geoff Pavey ◽  
Brian Dean

AbstractThe dopamine hypothesis proposes that there is a hypodopaminergic state in the prefrontal cortex and a hyperdopaminergic state in the striatum of patients with schizophrenia. Evidence suggests the hyperdopaminergic state in the striatum is due to synaptic dopamine elevation, particularly in the dorsal striatum. However, the molecular mechanisms causing disrupted dopaminergic function in schizophrenia remains unclear. We postulated that the dopamine transporter (DAT), which regulates intra-synaptic dopamine concentrations by transporting dopamine from the synaptic cleft into the pre-synaptic neuron, could be involved in dopaminergic dysfunction in schizophrenia. Therefore, we measured levels of DAT in the cortex and striatum from patients with schizophrenia and controls using postmortem human brain tissue. Levels of desmethylimipramine-insensitive mazindol-sensitive [3H]mazindol binding to DAT were measured using in situ radioligand binding and autoradiography in gray matter from Brodmann’s area (BA) 10, BA 17, the dorsal striatum, and nucleus accumbens from 15 patients with schizophrenia and 15 controls. Levels of desmethylimipramine-insensitive mazindol-sensitive [3H]mazindol binding were significantly higher in BA 10 from patients with schizophrenia (p = 0.004) and significantly lower in the dorsal striatum (dorsal putamen p = 0.005; dorsal caudate p = 0.007) from those with the disorder. There were no differences in levels of desmethylimipramine-insensitive [3H]mazindol binding in BA 17 or nucleus accumbens. These data raise the possibility that high levels of DAT in BA 10 could be contributing to lower synaptic cortical dopamine, whereas lower levels of DAT could be contributing to a hyperdopaminergic state in the dorsal striatum.


NeuroImage ◽  
2015 ◽  
Vol 116 ◽  
pp. 68-79 ◽  
Author(s):  
Karsten Mueller ◽  
Thomas Fritz ◽  
Toralf Mildner ◽  
Maxi Richter ◽  
Katrin Schulze ◽  
...  

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