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For example, psychostimulant-induced locomotion, the commonly utilised phenotype for positive symptoms in rodents, is heavily associated with dopaminergic activation in the limbic striatum. This anatomical misalignment has brought into question how we assess positive symptoms in animal models and represents an opportunity for improved translation between basic and clinical research.

The current review focuses on the role of subcortical dopamine dysfunction in psychosis and schizophrenia. We present and discuss alternative phenotypes that may provide a more translational approach to assess the neurobiology of positive symptoms in schizophrenia. Incorporation of recent clinical findings is essential if we are to develop meaningful translational animal models. Our knowledge of the neurobiology of schizophrenia, while still rudimentary, has advanced considerably in recent years.

However, these findings have not translated to better treatments for those with schizophrenia. The three primary symptom groups, positive, cognitive and negative Box 1 , have been associated with reports of abnormalities in virtually every neurotransmitter system 1 , 2 , 3 , 4 , 5. The onset of psychotic symptoms, which is strongly associated with alterations in dopamine function, is a key feature underpinning a clinical diagnosis 6 , 7. However, results from clinical research regarding the specific loci of dopamine dysfunction in schizophrenia 8 , 9 , 10 , have triggered a reappraisal of our perspective on the neurobiology of schizophrenia.

Currently there is a disparity between the tests for positive symptoms in animal models and recent clinical evidence for dopaminergic abnormalities in schizophrenia. Therefore, it is critical that this contemporary clinical knowledge actively influences the agenda in applied basic neuroscience. Psychiatric symptoms exist on continua from normal to pathological, meaning the threshold for diagnosis of schizophrenia in clinical practice can be challenging. The clinical diagnosis of schizophrenia relies heavily on the positive symptoms associated with a prolonged psychotic episode.

Psychotic symptoms are also not specific to a particular mental disorder The clinical efficacy of antipsychotic drugs is heavily correlated with their ability to block subcortical dopamine D2 receptors 17 , 18 , suggesting dopamine signalling is important. In spite of this, no consistent relationship between D2 receptors and the pathophysiology of schizophrenia has emerged 19 , In contrast, the clinical evidence points towards presynaptic dopamine dysfunction as a mediator of psychosis in schizophrenia For example, primates feature a more prominent substantia nigra and less distinctive ventral tegmental area than rodents.

However, more pertinent to the current review are homologous functional subdivisions of the striatum observed in both rodents and primates 21 , 22 , 23 , These include the limbic, associative and sensorimotor areas Fig. The associative striatum, defined by its dense connectivity from the frontal and parietal associative cortices, is key for goal-directed action and behavioural flexibility.

The limbic striatum, defined by connectivity to the hippocampus, amygdala and medial orbitofrontal cortex, is involved in reward and motivation. The sensorimotor striatum, defined by connectivity to sensory and motor cortices, is critical for habit formation. These functional subdivisions are also interconnected by feedforward striato-nigro-striatal projections The heavy basis on behavioural outcomes in neuropsychiatry has made functional subdivisions such as these more relevant than ever.

Midbrain dopamine neurons are the source of dopamine projections to the striatum in primates left and rodents right. Important neuroanatomical differences exist, especially when considering functional subdivisions of the striatum.

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In the primate, the limbic system orange originates in the dorsal tier of the substantia nigra the ventral tegmental area equivalent. In the rodent, the limbic system originates in ventral tegmental area, which sits medially to the substantia nigra. The midbrain projections to the associative striatum yellow and sensorimotor striatum blue follow a dorsomedial-to-ventrolateral topology. In healthy individuals, dopamine stimulants such as amphetamine can induce psychotic symptoms 26 , 27 and people with schizophrenia are more sensitive to these effects 27 , Studies using positron emission tomography PET imaging have shown patients with schizophrenia show increases in subcortical synaptic dopamine content 29 , 30 , abnormally high dopamine release after amphetamine treatment 30 , 31 , 32 , 33 , 34 , 35 and increased basal dopamine synthesis capacity determined indirectly by increased radiolabelled L-DOPA uptake 19 , 36 , 37 compared with healthy controls.

Increased subcortical dopamine synthesis and release capacity are strongly associated with positive symptoms in patients 33 , 38 , and increased subcortical synaptic dopamine content is predictive of a positive treatment response It was widely anticipated that the limbic striatum would be confirmed as the subdivision where these alterations in dopamine function would be localised in patients. The basis for this prediction was the belief that reward systems were aberrant in schizophrenia However, as PET imaging resolution improved it was found that increases in synaptic dopamine content 9 , 10 and synthesis capacity 8 were localised, or more pronounced 37 , in the associative striatum Fig.

Furthermore, alterations in dopamine function within the associative striatum likely contribute to the misappropriate attribution of salience to certain stimuli, a key aspect of delusions and psychosis Clinical studies have confirmed that dopamine abnormalities are also present prior to the onset of psychosis in schizophrenia and thus are not a consequence of psychotic episodes or antipsychotic exposure. Similar to what has been observed in patients with schizophrenia, ultra-high risk UHR subjects show increased subcortical synaptic dopamine content 41 and basal dopamine synthesis capacity 8 , 42 , 43 , Importantly, alterations in dopamine synthesis capacity in UHR subjects progress over time 45 and are greater in subjects who transition to psychosis compared with those who do not Furthermore, higher baseline synaptic dopamine levels in UHR subjects predicts a greater reduction in positive symptoms after dopamine depletion Overall, these findings in UHR subjects are congruent with those observed in schizophrenia and provide evidence indicating that presynaptic dopaminergic abnormalities are present prior to the onset of psychosis.

Several avenues have been proposed to explain a selective increase in associative striatal dopamine function, such as alterations in hippocampal control of dopamine projections 47 , 48 , alterations in cortical inputs to midbrain dopamine systems 2 , 49 and, although little direct evidence has been observed, developmental alterations in dopamine neurons themselves 50 , We propose a network model whereby dysfunction in a central circuit, including the associative striatum, prefrontal cortex and thalamus, is critical for the expression of psychotic symptoms in schizophrenia.

This model would suggest that dysfunction in auxiliary circuits both limbic and cortical contribute to psychotic symptoms by feeding into this primary network. Ascertaining the role of dopaminergic dysfunction, in the context of networks important for psychotic symptoms in schizophrenia, will provide a better base for constructing objective readouts in basic and clinical research. Psychosis is a condition that features a range of behavioural alterations that relate to a loss of contact with reality and a loss of insight.

People with psychosis experience hallucinations primarily auditory in schizophrenia 53 and delusions. In schizophrenia, auditory hallucinations have been associated with altered connectivity between the hippocampus and thalamus During hallucinations, increased activation of the thalamus, striatum and hippocampus have also been observed In contrast, delusions in people with schizophrenia have been associated with overactivation of the prefrontal cortex PFC and diminished deactivation of striatal and thalamic networks Thus, the complexity of psychotic symptoms is congruent with the highly connected nature of implicated brain regions.

Although we still know little about the underlying neurobiology of psychosis, focal brain lesions allow for a better understanding of the networks involved without the confounds of medication and unrelated neuropathology. Generally speaking, lesions that induce hallucinations are often in the brain networks associated with the stimulus of the hallucination i. Visual hallucinations have been associated with dysfunction of the occipital lobe, striatum and thalamus, whereas auditory hallucinations are associated with dysfunction of the temporal lobe, hippocampus, amygdala and thalamus Insight is generally maintained after focal brain lesions that produce hallucinations and subcortical dopamine function is normal 59 , unlike what is observed in schizophrenia In contrast, a loss of insight which can manifest as delusionary beliefs is associated with alterations in cortico-striatal networks.

For example, people with basal ganglia or caudate lesions can present with both hallucinations and delusions 60 , Furthermore, a case study of religious delusions in a patient with temporal lobe epilepsy was associated with overactivity of the PFC 62 , and there are multiple lines of evidence suggesting that the PFC is integral for delusionary beliefs Therefore, while impairing networks specific to certain sensory modalities can lead to hallucinations, dysfunctional integration of PFC input to the associative striatum may be especially important for delusional symptoms in schizophrenia.

Central to the networks involved in psychosis and schizophrenia, the thalamus acts as a relay for most information going to the cortex Brain imaging studies have demonstrated that medication-naive patients with schizophrenia have significantly reduced thalamic and caudate volumes relative to healthy controls and medicated patients Moreover, reduced thalamic volumes has also been observed in UHR subjects A simplified schematic of the networks that may be especially relevant to psychotic symptoms in schizophrenia is presented in Fig. The thalamus forms a circuit with the associative striatum and PFC whereby impairments in any of these regions can impair the functionality of the network as a whole.

In addition, the hippocampus and amygdala, which are both involved in sensory perception and emotional regulation, can affect this network via their connectivity with the thalamus but other indirect pathways also exist. Dysfunction in a variety of brain regions can elicit psychotic symptoms.

Basic Clinical Neuroscience

A primary circuit involved in psychosis includes the thalamus and prefrontal cortex yellow feeding into the associative striatum. Alterations in the thalamus and prefrontal cortex are involved in hallucinations and also insight for delusional symptoms. Expression of psychotic symptoms in most cases requires increased activity in the associative striatum and specifically excessive D2 receptor stimulation red. Other limbic regions such as the hippocampus and amygdala green can feed into this circuit contributing to altered sensory perception and emotional context.

This raises important questions as to how antipsychotic drugs exert their effects. In most individuals with schizophrenia, antipsychotic treatment is effective in reducing positive symptoms 67 ; therefore, excessive D2 signalling in the associative striatum appears to be critical. Stimulation of D2 and D1 receptor expressing medium spiny neurons which are largely segregated 68 in the associative striatum feedback indirectly to the thalamus, completing a loop that allows for feedforward-based and feedback-based signalling. The basal ganglia acts as a gateway for, or mediator of, cortical inputs 69 , 70 , 71 and may represent a common pathway through which psychotic symptoms present.

Therefore, excessive dopamine signalling in the associative striatum may directly lead to psychotic symptoms by compromising the integration of cortical inputs. In treatment-responsive patients, antipsychotics may attenuate the expression of psychotic symptoms by normalising excessive D2 signalling 29 to restore the balance between D1 and D2 receptor pathways Because they act downstream to schizophrenia-related presynaptic abnormalities, they fail to improve indices of cortical function i.

Alternatively, impaired cortical input to the associative striatum via the thalamus, PFC or other regions could dysregulate this system independently of, or in addition to, associative striatal dopamine dysfunction. In this case, D2 receptor blockade may be insufficient to restore normal function, which is one explanation for why some individuals are treatment refractory. For example, increases in subcortical synaptic dopamine content 29 and increases in presynaptic striatal dopamine function 52 are both associated with increased treatment efficacy.

Thus, in treatment-resistant subjects, there is little evidence of abnormal dopaminergic function 29 , Medicated persons with schizophrenia, who remain symptomatic with auditory hallucinations, show increased thalamic, striatal and hippocampal activation Moreover, treatment-refractory patients who respond positively to clozapine treatment show alterations in cerebral blood flow in fronto-striato-thalamic circuitry, suggesting clozapine is restoring a functional imbalance in these systems Taken together, this evidence suggests that psychosis is the result of a network dysfunction that includes a variety of brain regions and multiple neurotransmitter-specific pathways , of which impairment at any level could precipitate psychotic symptoms.

Although increased positive symptom severity has been associated with impaired cognitive flexibility 74 , there is a little evidence for subcortical hyperdopaminergia playing a direct role in the cognitive impairments observed in schizophrenia. There is a mounting evidence that cognitive symptoms may present prior to positive symptoms in schizophrenia Given brain networks involved in hallucinations and delusions all involve cortical regions, the underlying pathology causing cognitive symptoms may also contribute to psychotic symptoms.

Thus, in some cases psychosis may represent the summation of broad cognitive impairments inducing local network dysfunction Fig. Regardless, positive symptoms are relatively distinct in the clinical setting but the presence and severity of symptoms are determined interactively with interviews and questionnaires. The inability to do the same in other species means the best avenue for assessing animal models may be to identify outcomes that are sensitive to the underlying neurobiology observed in schizophrenia and psychosis. This schematic representation highlights the potential for cognitive symptoms to feed into psychosis networks and create positive feedback loops that spiral to psychosis.

Non-specific and heterogeneous deficits in auxiliary neurocircuitry in the context of psychosis lead to broad cognitive impairments unique to each individual. These systems feed into the primary psychosis networks leading to destabilisation of associative striatal dysfunction and further cognitive impairment. In most individuals with schizophrenia, excessive dopamine signalling in the associative striatum leads to positive symptoms. Antipsychotics antagonise downstream D2 receptor signalling to blunt the expression of symptoms.

In treatment-refractory patients those who do not respond to first-line antipsychotics blocking D2 receptors is insufficient to blunt positive symptoms suggesting further upstream dysfunction in the associative striatum or psychosis networks.

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Clozapine may lead to improvement in some of these individuals by stabilising function throughout these networks in addition to D2 receptor antagonism. Positive symptoms in treatment-refractory patients who fail to respond to clozapine may be the result of severe impairment throughout psychosis networks and the associative striatum that are independent of dopamine dysfunction. Thus, our current treatments for positive symptoms act downstream of the source of cognitive impairments, hence their ineffectiveness in treating cognitive symptoms.

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While the expression of psychotic symptoms may be a discrete outcome, separate to impairments in cognitive function, the upstream cause of these symptoms may share common neuropathology. Potentially, the most useful avenue for animal models to assist in schizophrenia research will be identifying convergent aetiological pathways Understanding which neurotransmitter systems and brain regions are most involved may help to identify the core neurobiological features of schizophrenia.

For example, changes in dopaminergic systems are observed in animal models after manipulation of factors based on schizophrenia epidemiology 50 , 51 , genetics 78 , pharmacology 79 and related hypotheses These include changes in early dopamine specification factors 50 , 51 , sensitivities to psychostimulants 50 , 51 , 78 , 80 and alterations in dopamine neurochemistry 50 , 51 , 78 , Evidence of subcortical dopaminergic hyperactivity or sensitivity in animal models is proposed to represent the face validity i.


The most commonly used behavioural assessments of positive symptoms in animal models include enhanced amphetamine-induced locomotion and deficits in prepulse inhibition PPI These tests are widely used because they are relatively simple to perform. However, we propose that given current knowledge of the neurobiology in schizophrenia, they have outlived their usefulness as measures of positive symptoms. Amphetamine increases dopamine release in striatal brain regions of both humans 38 and rats Amphetamine-related behaviours in rodents are also strongly linked to activity in striatal brain regions 82 , Thus, an increased locomotor response to amphetamine and other psychostimulants, which face similar criticisms is considered a simple test to reflect the subcortical hyperdopaminergia underlying the psychotic symptoms in schizophrenia.

Most animal models of schizophrenia report increased locomotor activation after psychostimulants However, the recent clinical evidence described above suggests that current assessments of animal models does not reflect contemporaneous knowledge of dopamine activity in those with schizophrenia. The relative contribution of specific dopamine pathways to amphetamine-induced locomotion provides a good example of why a paradigm shift is required for research using animal models for positive symptoms in schizophrenia.

For example, amphetamine-induced locomotion is largely driven by limbic dopamine release. Local administration of amphetamine 84 , 85 , 86 , 87 or dopamine 84 , 88 , 89 into the nucleus accumbens induces locomotion. Furthermore, blocking dopamine signalling in the nucleus accumbens attenuates amphetamine-induced locomotion Specifically activating limbic dopamine projections using chemogenetic tools robustly increases locomotion, but activating associative dopamine projections does not Thus, there is an anatomical misalignment between the primary behavioural outcome deemed important for positive symptoms in animal models of schizophrenia i.

Furthermore, clinical studies directly comparing activity levels in patients with schizophrenia and bipolar disorder suggest that hyperactivity may be a core feature of bipolar disorder rather than schizophrenia One argument for amphetamine-induced locomotion is that it is predictive of antipsychotic efficacy, but this is merely a serendipitous side effect. Systemically administered amphetamine increases dopamine function in both the limbic striatum locomotion and associative striatum positive symptoms.

Systemically administered antipsychotics antagonise D2 receptors throughout the brain. Therefore, amphetamine-induced locomotion acts serendipitously to predict antipsychotic effectiveness via dopamine release in a parallel circuit limbic vs. Optimally, antipsychotics that diminish dopamine signalling preferentially in the associative, rather than the limbic, striatum need to be developed.

Obviously, amphetamine-induced locomotion would not be predictive for the latter treatment options. One of the most consistently observed neurological impairments in schizophrenia is impaired sensorimotor gating in the form of decreased PPI 93 , Deficits in PPI may reflect an inability to gate out irrelevant information. PPI deficits also respond to antipsychotics but are not specific to schizophrenia 93 , Thus, PPI deficits do not represent a specific or diagnostic trait of schizophrenia.

Intact cortical and striatal function are critical for PPI 95 and, therefore, deficits in PPI also reflect an interface between positive and cognitive symptom groups PPI is assessed almost identically in rodents and humans and, therefore, is one of the most widely studied deficits in schizophrenia. In rodents, the contribution of limbic dopamine projections to PPI are well-known 95 , though the associative striatum has also been implicated 96 , Thus, PPI deficits clearly lack specificity concerning the hyperdopaminergia observed in schizophrenia.

Therefore, when assessing rodent models, PPI impairments alone are insufficient for determining positive symptom phenotypes and their predictive validity suffers from the same criticism as that of amphetamine-induced locomotion parallel blockade of limbic D2 receptors. This does not invalidate our current rodent models; it just emphasises that, in light of the recent compelling PET evidence in patients, we need to review their relevance to the positive symptoms of schizophrenia.

However, we can, and should, aim to establish more translationally relevant tests for the underlying neurobiology of psychosis. Ultimately, we need better behavioural tests for positive symptoms in animal models that will lead to therapies efficacious for both positive and cognitive symptoms in patients. We contend that tests aimed at understanding associative striatal function are imperative.

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We propose that a combination of cognitive behavioural tasks, that can be tested similarly in humans and rodents Fig. It is important to consider that neither task alone is a reliable indicator of positive symptom neurobiology as these tasks assess cognitive function and outcomes are therefore relevant to cognitive symptoms ; however, in combination they can help isolate associative striatal function. Humans and rodents can both perform cognitive tasks that feature actions to obtain rewards a The primary differences in testing are that humans can receive monetary rewards whereas rodents tend to be given food rewards.

Furthermore, rodents require more initial training to learn the action i. One of these rewards is then devalued through an aversive video cockroaches on the food item for humans or feeding to satiety in rodents. Healthy controls will demonstrate outcome-specific devaluation by biasing their response towards the food reward that was not devalued. Serial reversal learning c requires the subject to learn a simple discrimination between two choices of which one is associated with a reward.

Once certain criteria are met, the contingencies are reversed so that the non-rewarded stimulus is now rewarded and the previously rewarded stimulus does not attain a reward. This is classified as the first reversal. Once the criteria are met for the new contingencies, the rewarding stimulus is switched again back to the original pairings for the second reversal. This switching back and forth continues until completion of the test. Goal-directed behaviour is critical for understanding the relationship between actions and their consequences in both humans and rodents.

Moreover, goal-directed action heavily depends on the function of the associative striatum 21 , 24 , 98 , 99 , and can be assessed using near identical behavioural paradigms in both humans and rodents Fig. To test impairments in the learning of action-outcome associations in humans and rodents the sensitivity to outcome-specific devaluation can be determined. Outcome-specific devaluation is useful way of establishing that an action is goal-directed and that the correct action—outcome associations have been formed. In order to test this, after training to associate actions with specific outcomes action—outcome association , one of the outcomes is devalued.

After devaluation, when the subject is given the choice between the two action-outcome pairs, healthy controls respond more for the outcome that was not devalued. This demonstrates the ability to establish action-outcome associations correctly and adapt actions based on newly acquired information. The specific neurocircuitry involved in goal-directed behaviour is based on years of associative learning research Sensitivity to outcome devaluation is dependent on the PFC and associative striatum Fig.

Impairments in goal-directed action in schizophrenia have been associated with altered caudate function and disorganised thought Importantly, the insensitivity to outcome devaluation observed in persons with schizophrenia was not due to impairments in reward sensitivity after devaluation i. The associative system red , including the PFC and ACC, is required for the acquisition and expression of goal-directed action, which is sensitive to outcome devaluation. In contrast, the limbic system green is critical for the formation of associations between reward predictive stimuli and action.

Habitual behaviours rely on the sensorimotor system purple. The associative striatum is the only common region required for goal-directed action that is sensitive to outcome devaluation and serial reversal learning. One limitation of outcome-specific devaluation is that it does not allow for the delineation of functional deficits in the PFC vs. We will send you an email with instructions on how to reset your password.

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    Add To Cart. Buy from another retailer. Promocode will not apply for this product. Succeed in your course and on the boards with Basic Clinical Neuroscience, 3e. This clinically oriented, student-friendly book provides the anatomic and pathophysiologic basis for understanding neurologic abnormalities through concise descriptions of functional systems.

    Student users have consistently praised the book for its exceptionally clear explanations of concepts. Updated throughout to reflect recent advances in the field, the book emphasizes the localization of specific medically important anatomic structures and clinically important pathways, using anatomy-enhancing, full color 3-D illustrations, as well as schematic illustrations of lesions, pathways, and tracts. Chapter-opening cases apply chapter concepts to clinical practice. Clinical Connection boxes inserted near relevant anatomical structure or pathway discussions prepare you for the boards and clinical practice.

    A complete chapter that focuses on locating lesions helps you hone your knowledge and skills.

    Chapter-ending review questions allow you to assess your understanding as you move through the book. Unique, hand-drawn, full color artwork clarifies key structures. An end-of-the-book glossary of key terms is ideal for self-testing and review. An Atlas of Myelin-Stained Sections helps you identify lesions and anatomical structures. An online Question Bank makes it easy to prepare for course and board exams. Louis University School of Medicine, St. Louis, MO.

    A new full-color design enhances illustrations and images and makes the material more engaging and easier to understand. Additional clinical images, case studies, review questions, and clinical correlations have been added to help students master the subject matter.

    Basic Clinical Neuroscience

    Chapter-opening cases apply concepts to clinical practice, allowing students to see the real world relevance of what they are learning. Clinical Connection boxes inserted near relevant anatomical structure or pathway discussions prepare students for the boards and clinical practice. A complete chapter focuses on locating lesions. Chapter-ending review questions allow students to assess their understanding as they move through the book.