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To reproduce some of the observed alterations in patients, different developed animale models mimic some of the symptoms, constituting a valid approach to study the etiopathology of this disorder. The perinatal injection of N-methyl-d-aspartate receptor antagonists and the postweaning social isolation rearing are some of the most used models. Lister Hooded rats have been subjected to a single injection of MK at postnatal day 7 and have been socially isolated from postweaning during 8 weeks.
The new animal model, presented increased body weight gain and volume reductions in their medial prefrontal cortex mPFC and hippocampus. They also showed an increased number of activated pyramidal neurons and alterations in the numbers of parvalbumin and calbindin expressing interneurons in the mPFC. The mRNA level of calbindin was increased, while that of calretinin was decreased in the mPFC without changes in the hippocampus.
Furthermore the model showed no apoptosis in the studied areas, but the number of immature neurons was altered in the dentate gyrus. All these structural and neurochemical alterations, specially in cortical inhibitory circuits, are similar to those found in schizophrenic patients and are more numerous than in each of the single models. Schizophrenia SZ may involve a fundamental disruption in the intrinsic dynamics at the cortical microcircuit level giving rise to global deficits in perceptual and cognitive processing, yet such dynamics have so far been accessed mostly with indirect electrophysiological EEG, LFPs or anatomical assays.
We reasoned that examining cortical circuits at this level in a rodent model of SZ could yield key new insights on the neural substrate of psychotic states. We estimated spike rates for single cells and quantified population-state similarity across time. At rest KET mice displayed i a decrease in population activity-state dimensionality possibly reflecting highly stereotyped attractor states and impaired flexibility within the cortical network.
While viewing moving gratings, KET mice displayed ii stim-evoked activity comprised of population level patterns which were inconsistent across presentations of the same stimulus or hyperconsistent across all stimuli iii in the context of reduced orientation selectivity at the single cell level. The current study presents a novel depiction of disordered sensory cortical function in a mouse model of psychosis involving rigid default states and disordered externally driven states.
These findings could provide a crucial foundation for understanding the biopathphysiological cascade from putative SZ risk genotypes and their molecular consequences to clinically measurable deviations in behavior and noninvasively acquired electrophysiology. Deficits in the glutathione GSH antioxidant system have been implicated in the pathophysiology of several neuropsychiatric disorders, including schizophrenia. Synaptic NMDAR hypofunction is deleterious to developing forebrain neurons, and is associate with oxidative stress, but mechanisms are poorly understood Methods: Biochemical and live cell imaging measures of glutathione and glutathione pathway enzymes were performed, as were gene expression analyses of glutathione pathway genes and neuronal viability assays.
Glutathione pathway enzyme activities were perturbed by siRNA and pharmacological inhibitors. We found that synaptic activity is coupled, via the NMDAR, to transcriptional control of the glutathione antioxidant system, tuning its capacity to reflect the elevated needs of an active neuron and maintaining the correct redox balance in the brain. This control is mediated via a coordinated program of gene expression changes that boosts the synthesis, recycling and utilization of glutathione, which together facilitate rapid ROS detoxification in neurons which otherwise triggers Puma-dependent apoptosis.
Of particular importance to the developing brain is the direct NMDAR-dependent transcriptional control of glutathione biosynthesis. We find that the deleterious effects of NMDAR hypoactivity in vivo are due to this control being lost.
This study, coupled with previous published work shows that developmental NMDAR hypofunction and glutathione system deficits, separately implicated in several neurodevelopmental disorders, are mechanistically linked in a reciprocal manner. Emerging evidence from human epidemiology, genetics, and biomarker studies implicate neuroinflammation in both the pathogenesis and pathophysiology of some neuropsychiatric disorders.
However, the function of neuroinflammation in neuropsychiatric disorders is still debated because supporting evidence is indirect and no molecular mediators are identified. Next, we used the maternal immune activation MIA mouse model to investigate the inflammatory and pathway changes in a mouse model relevant to psychosis. We evaluated the rodent behavior, microglia inflammatory activation, microglia responsiveness to angiotensin treatment, and expression of angiotensin pathway components.
To test these finding, we used the MIA mouse model. After MIA, the male mice exhibit hyperlocomotion to amphetamine challenge and deficits in social memory in the three-chamber social interaction paradigm.
Next, we investigated the inflammatory potential of these mice. We isolated microglia from late embryonic E We found MIA microglia were hypo-responsive to inflammatory stimulation and angiotensin treatment, further supporting a role for microglia dysfunction, inflammation, and the ACE pathway in pathology. Finally, we found microglia after MIA had decreased angiotensin receptor expression.
Altogether, the human and animal data suggest a common cellular deficit in psychosis and the MIA mouse model through the ACE pathway. Our future direction is to investigate the relationship between the ACE pathway and inflammation using human cells and the MIA mouse model. If the ACE pathway can modulate inflammatory alterations observed in pathology, it may provide a novel therapeutic target for neuropsychiatric disorders with inflammatory underpinnings.
Cyclic nucleotide phosphodiesterases-4 PDE4 are a class of enzymes that regulate cellular signaling pathways involved in inflammation. The PDE4 inhibitors roflumilast and apremilast have been approved for the treatment of peripheral inflammatory disorders, however these drugs do not penetrate the brain. Neuroinflammation is also thought to contribute to the etiology of schizophrenia, with reports of elevated peripheral cytokines, and signs of central inflammation e.
In light of these data, studies were run to test the ability of the novel brain penetrant PDE4 inhibitor, ABI-4, to modulate the effects of lipopolysaccharide LPS in the periphery and brain.
To assess in vitro anti-inflammatory effects, primary blood monocytes PBMCs were isolated from human blood. Mice were co-dosed with LPS 0. Brain and plasma samples were collected 4h after the final dose for measurement of cytokines and brain TSPO binding.
These data demonstrate that ABI-4 is a potent inhibitor of the in vitro effects of LPS in human monocytes and in vivo effects in mouse plasma and brain. These data suggest that the anti-inflammatory properties of ABI-4, together with the antipsychotic properties of this molecule make this an interesting potential treatment for schizophrenia.
Strong evidence corroborates involvement of oligodendrocyte OLG dysfunction in the pathophysiology of schizophrenia SZ. We previously showed that the forebrain-restricted expression of mutant human DISC1 hDISC1 exerts a significant influence on oligodendrogenesis during early development and in adult hDISC1 mice, evidenced by premature OLG differentiation and increased proliferation of their progenitors in forebrain regions.
Concurrent reduction of OLG progenitor markers in hindbrain regions during fetal stage suggested expansion of hindbrain glial progenitors into the forebrain of hDISC1 mice.
Dislocation of OLG lineage cells as a result of their abnormal migration and premature differentiation may affect cortical organization of the brain. Given the critical role of DISC1 in migration of neuronal and glial progenitors during brain development, our results provide new clues for the developmental mechanisms contributing to oligodendrocyte dysfunction in SZ.
Parvalbumin PV positive GABA interneurons are particularly susceptible to adolescent exposure to drugs of abuse such as cocaine. Here we examined the effect of adolescent exposure to the selective dopamine reuptake inhibitor GBR on oxidative stress markers, PV-interneurons, and behavior relevant to schizophrenia.
We also examined whether two oxidative stress events at two sensitive periods of cortical development would exacerbate the effects on cortical PV-expressing interneurons by combining perinatal ketamine and adolescent GBR exposures. Mice were then tested for locomotor and investigatory behavior and probabilistic reversal learning. Immunohistochemical analysis of PV-neurons in medial prefrontal cortex but not in hippocampus also showed decrease in PV-expression in GBR treated mice. Behaviorally, adolescent GBR increased exploratory and investigatory behavior and slowed learning in the between-session probabilistic learning task, indicating a potential learning deficit in this model.
Hence GBRinduced oxidative stress in adolescence resulted in cognitive deficits and neurochemical changes particularly in PV-expressing neuron.
Our results also indicate that adolescent exposure to GBR in perinatal ketamine-exposed mice may exert long-lasting effects on impulsive behavior. Clozapine CZP is an atypical antipsychotic agent used in the treatment of psychotic disorders including schizophrenia and bipolar disorder. Accumulating evidence suggests that neuroinflammation is closely associated with the pathogenesis of schizophrenia as well as bipolar disorders. In this study, we investigated the effect of CZP on anti-inflammatory activity in lipopolysaccharide LPS -stimulated microglia.
Systemic injections of MK, a selective NMDA receptor antagonist, into neonatal rats induce long-term neurochemical and behavioral changes. It has been suggested that these changes form the neurodevelopmental basis for schizophrenia-like behavior in rats. In this study, postnatal 7-day PN7 rats were treated with MK, and their frontal cortices at PN60 were examined to investigate the long-term effects on the molecules in signal pathway of protein translation.
At PN60, the rats treated with MK at PN7 showed increased locomotor activity and deficits in prepulse inhibition, as reported previously. In summary, long-term behavioral changes induced by neonatal MK treatment was accompanied with the increased phosphorylation of S6 in the brain, which were recovered by ECS treatments. These findings may suggest an important role of aberrant long-term activation of protein translation machinery in the MK neurodevelopmental animal model of schizophrenia.
The most severe form of schizophrenia is clozapine-resistant schizophrenia CRShowever, there is no validated model of CRS which can allow investigation of drug resistance and development of novel treatments. We used a selective breeding methodology in which we selected the most extreme non-responders and responders. Response was based on the elevation of the time spent with the novel mice following clozapine treatment. Males and females were mated to produce the trans-generational experiments.
We replicated the selection process on each generation G2-G4. We analyzed selected biochemical parameters of brain tissues from the hippocampus of mice from G3 and G4 of the responsive mice line. The average score of the male group of the resistant G2 represented resistance to clozapine while females of the same group and the whole responsive group showed response on average. This finding is in concordance with the clinical observation of a more severe form of the disorder in male patients, manifesting with earlier age of onset and poor prognosis.
The apparent deficit in social abilities of resistant G2 male line has resulted in a very low fecundity that did not allow us to continue to G3 with the resistant colony.
The responsive colony, however, was proliferative and allowed us to preform further behavioral and biochemical analysis to brain tissues. We observed an increase of the proportion of clozapine responders, on G2, G3 and G4, both on male and female groups of the responsive line.
In this pioneer study we aimed to establish a valid clozapine-resistant and clozapine responsive animal model through selective breeding of these traits in mice.
Behavioral response to clozapine treatment in the SP task is augmented with generations, both in the resistant and the responsive mice lines. The clozapine responsive mice line showed increment of response rate through generation on both genders.
There was also a gender difference in the trans-generational levels of neurotropic factors. In the future we wish to enhance these mice lines to gather a putative mechanism for response and resistance to clozapine. Several neurodevelopmental animal models address the impact of a genetic manipulation or an environmental insult on developmental brain trajectories.
Frontal cortex, striatum and hippocampus were micro-dissected, flash frozen, and RNA was extracted. Both models showed reductions in BDNF transcripts in striatum.
As schizophrenia is not a purely genetic or environmental disorder, these data suggest that models based on such singular events can replicate some of the molecular changes observed in schizophrenia, but a combination of multiple factors may be necessary to replicate the broad range of behavioral, cognitive, and neural alterations that comprise the disorder.
Schizophrenia is an illness of unknown pathophysiology.
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The adolescent use of cannabis is repeatedly implicated as a risk factor for this disease. In the mouse model, exposure to cannabinoids during adolescence has persistent behavioral consequences including schizophrenia-like behaviors. We conducted a series of experiments to examine the long-term consequences of adolescent cannabinoid exposure on receptors involved in endocannabinoid signaling. Behavioral tests and molecular studies were carried out.
These behavioral deficits were not observed in mice treated with the CB1 agonist at later developmental time points. Group I metabotropic glutamate receptor mGluR activation drives endocannabinoid synthesis and release and we previously reported changes in CB1 and mGluR5 expression patterns in the hippocampus.
Here, we extend those studies, examining endocannabinoid genes in the frontal cortex and striatum in mice and a human post mortem tissue cohort of control and schizophrenia cases divided into individuals with and without a significant adolescent cannabis use history. There is a significant upregulation of CB1 in both the frontal cortex and striatum while mGluR5 protein levels demonstrated a bidirectional expression pattern with significantly increases in the frontal cortex and strong trend to reduction in the striatum.
Parallel human post mortem studies using prefrontal cortex BA9 tissue from control and schizophrenia cases with prior adolescent cannabis use history are being analyzed. Immunohistoflourescence experiments to localize cell type distribution of CB1 and mGluR5 are ongoing. These data suggest that adolescent cannabinoid administration leads to regionally specific persistent changes in receptors involved with endocannabinoid signaling. These data may be relevant to understanding the long term sequelae of significant adolescent cannabis use and may be of particular importance in understanding mechanisms by which adolescent cannabinoid exposure leads to molecular changes predisposing to schizophrenia.
Clozapine provides improved efficacy in treatment with schizophrenia, especially on the treatment-refractions and also their emotional symptoms. For the purpose, amygdala dopamine in response to an aversive conditioned cue was measured as a biochemical marker of the emotional cognitive processing.
Previously we had developed a stress vulnerability model which was treated with chronic administration of methamphetamine followed conditioned to an auditory cue with aversive electrical stimulation.
Using the model, we studied how clozapine influence basal dopamine release and phasic dopamine release in response to the aversive conditioned cue stimulation CS. Extracellular dopamine was taken from the amygdala of freely moving rats by in-vivo microdialysis and analyzed by high-performance liquid chromatography HPLC. The changing ratio of dopamine from the basal level after drug treatment and CS was analyzed. Dopamine release in response to a CS was greater for methamphetamine-sensitized rats than non-sensitized rats.
Haloperidol treatment increased basal level of dopamine both in non-sensitized and methamphetamine-sensitized rats. However, clozapine treatment did not elicit the increasing basal level in methamphetamine-sensitized rats at all while the drug increased basal level in non-sensitized rats, which was greater than haloperidol.
Both clozapine and haloperidol attenuated the phasic dopamine release in response to a CS both in non-sensitized and methamphetamine-sensitized rats.
The extent of the attenuation was greater for clozapine than for haloperidol both in non-sensitized and methamphetamine-sensitized rats. The results suggest that a stabilization of dopamine release in the amygdala during emotional processing is a common therapeutic mechanism of antipsychotics. The dopaminergic-state dependent action of clozapine suggests that some receptors bound with clozapine may functionally regulate due to hyper-dopaminergic conditions and which may lead to superior effect of clozapine on broadly varied conditions of patients with schizophrenia ID: Various immune and infectious factors contribute to the pathogenesis of schizophrenia via complex interactions with genetic risk factors in susceptible individuals.
C at embryonic day 9; 2 exposed to vehicle or T. We evaluated the neurobehavioral, immune and molecular changes in control and mutant DISC1, exposed and unexposed mice at postnatal day Only mutant DISC1 mice exposed to MIA demonstrated the brain and behavioral alterations consistent with aspects of affective disorders. These behaviors were associated with decreased volumes of the amygdala and periaqueductal gray matter and density of spines on dendrites of granule cells of the hippocampus.
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The brain and behavior effects of chronic T. Importantly, some behavioral effects of T. Our results suggest that mutant DISC1 and MIA interact to produce a range of behavioral, brain and molecular changes consistent with mood disorders in humans.
Our studies with T. Schizophrenia SZa catastrophic psychiatric disorder, results from a combination of genetic and environmental factors. Upon termination of the treatment, all rats were fed normal rodent chow until the animals were evaluated in adulthood [postnatal days 56—80].
This prenatal treatment causes increases in hippocampal KYNA and hippocampus-dependent cognitive dysfunctions in adulthood Pocivavsek et al. Microdialysis in the hippocampus of unanesthetized adult rats revealed that basal extracellular KYNA levels were modestly but significantly elevated in EKyn rats ECon: In contrast, extracellular glutamate was decreased ECon: In separate adult EKyn rats, we confirmed contextual memory deficits, evidenced as decreased avoidance latency during the retention trial of the passive avoidance paradigm ECon: Collectively, our results demonstrate that acute inhibition of KAT II in adulthood may be sufficient to overcome contextual memory deficits that arise as a consequence of elevated brain KYNA in early brain development.
Schizophrenia is associated with high susceptibility to substance abuse. Recent research suggests that dysregulation of NMDA receptor function via availability of receptor co-agonists, which bind at the allosteric glycine modulatory site GMSmay play a role in the pathopyhsiology of both schizophrenia and drug addiction.
Our laboratory has developed two transgenic mouse lines to test the validity of this hypothesis. The first line is a constitutive knockout of the synthetic enzyme that produces D-serine, serine racemase SR.
The second line is a constitutive knockdown of glycine transporter 1 GlyT1which regulates synaptic glycine, another NMDA receptor co-agonist. These results further elucidate the role of NMDA receptor co-agonists in cocaine-induced CPP and locomotor sensitization and may shed light on the neural mechanisms underlying co-morbid schizophrenia and substance abuse.
Also, these findings may indicate that D-serine could be an effective treatment for cocaine abuse. The past 25 years have seen well over a dozen circuit- or pathophysiology-based non-D2 mechanisms tested in schizophrenia yet no novel treatments have advanced into routine clinical use.
Although patient selection, trial design and clinical endpoints are receiving increased attention as contributors to this disappointing record, it is also important to consider how these prior efforts can inform future drug development programs. PF, a selective inhibitor of phosphodiesteraseA PDE10Awas recently reported to be ineffective as a monotherapy in acute exacerbation of schizophrenia.