Neurodevelopment and the Origins of Brain Disorders

doi:10.1038/npp.2014.237

Cited by 47 publications

(45 citation statements)

References 16 publications

(12 reference statements)

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“…Notably, these results differ from Jedynak et al (13), who noted that the same cocaine conditioning paradigm enhanced AMPAR function in the NAc core as assessed by electrically-evoked AMPAR/NMDAR and miniature EPSC (mEPSC) amplitude. These discrepancies may be explained by technical differences, biology, or both.…”

Section: Discussioncontrasting

confidence: 99%

“…The output neurons of the NAc, medium spiny neurons (MSNs), are largely distinguished by expression of dopamine receptor subtype 1 or 2 (D1 or D2). While both D1 (4; 7; 9–13) and D2 (10; 11; 14) NAc MSN subtypes have been shown to undergo drug-induced changes in AMPAR function, these changes occur in an experience-, subregion-, and input-specific manner. In contrast to AMPARs, drug-induced changes in NAc N-methyl-D-aspartate receptor (NMDAR) function have been less well documented.…”

Section: Introductionmentioning

confidence: 99%

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Cocaine Experience Enhances Thalamo-Accumbens N-Methyl-D-Aspartate Receptor Function

Joffe

Grueter

2016

Biological Psychiatry

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BACKGROUND Excitatory synaptic transmission in the nucleus accumbens (NAc) is a key biological substrate underlying behavioral responses to psychostimulants and susceptibility to relapse. Recent studies have demonstrated that cocaine induces changes in glutamatergic signaling at distinct inputs to the NAc. However, consequences of cocaine experience on synaptic transmission from the midline nuclei of the thalamus (mThal) to the NAc have yet to be reported. METHODS To examine synapses from specific NAc core inputs, we recorded light-evoked excitatory postsynaptic currents (EPSCs) following viral-mediated expression of channelrhodopsin-2 in the mThal, prefrontal cortex (PFC), or basolateral amygdala (BLA) from acute brain slices. To identify NAc medium spiny neuron (MSN) subtypes we utilized mice expressing tdTomato driven by the promoter for the dopamine receptor subtype 1 (D1). We recorded N-methyl-D-aspartate receptor (NMDAR) and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) properties to evaluate synaptic adaptations induced by cocaine experience, a 5-day cocaine exposure followed by 2-weeks of abstinence. RESULTS We determine that excitatory inputs to the NAc core display differential NMDAR properties and cocaine experience uniquely alters AMPAR and NMDAR properties at mThal-D1(+), mThal-D1(−), and PFC-D1(+) synapses, but not PFC-D1(−) synapses. Finally, at mThal-D1(+) synapses, we demonstrate that cocaine enhances GluN2C/D function and NMDAR-dependent synaptic plasticity. CONCLUSIONS Our results identify contrasting cocaine-induced AMPAR and NMDAR modifications at mThal- and PFC-NAc core synapses. These changes include an enhancement of NMDAR function and plasticity at mThal-D1(+) synapses. Incorporation of GluN2C/D-containing NMDARs most likely underlies these phenomena and represents a potential therapeutic target for psychostimulant use disorders.

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Section: Discussioncontrasting

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Cocaine Experience Enhances Thalamo-Accumbens N-Methyl-D-Aspartate Receptor Function

Joffe

Grueter

2016

Biological Psychiatry

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“…Identifying regions that exhibited significant activation within one group of participants and using them as inclusive masks for correcting multiple comparisons in between-group analyses in the same sample is a commonly used procedure in multiple domains of research (e.g. Labuschagne, et al, 2010; Rizio & Dennis, 2014; Williams et al, 2015), and allows us to examine BI-group differences in task-related executive control regions.…”

Section: Methodsmentioning

confidence: 99%

Frontolimbic functioning during threat-related attention: Relations to early behavioral inhibition and anxiety in children

Taber-Thomas

Pérez‐Edgar

2017

Biological Psychology

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Children with behavioral inhibition (BI), a temperament characterized by biologically-based hyper-vigilance to novelty, display threat-related attention biases (AB) that shape developmental trajectories of risk for anxiety. Here we explore the relations between BI, neural function, and anxiety. Fifty-six 9–12-year-olds (23 behaviorally inhibited) performed the dot-probe task while undergoing fMRI. AB scores were not associated with BI group or parent-rated anxiety symptoms. Trials requiring attention orienting away from threat engaged an executive and threat-attention network (dlPFC, vlPFC, mPFC, and amygdala). Within that network, behaviorally inhibited children showed greater activation in the right dlPFC. Heightened dlPFC activation related to increased anxiety, and BI levels accounted for the direct relation between dlPFC activation and anxiety. Behaviorally inhibited children may engage the executive attention system during threat-related processing as a compensatory mechanism. We provide preliminary evidence that the link between PFC functioning and anxiety might be attributed to early-emerging temperamental vulnerabilities present before the emergence of clinical anxiety.

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“…In studies measuring the rewarding effects of drugs using a conditioned place preference (CPP) paradigm, Taar 1−/− mice acquired methamphetamine-induced CPP earlier than wild-type mice and exhibited higher CPP score during extinction training sessions, which suggests that the conditioned rewarding effect of methamphetamine is greater in Taar 1−/− mice (Achat-Mendes et al, 2012). In Taar 1−/− mice, animals drank more methamphetamine and exhibited insensitivity to the aversive property of methamphetamine as compared to the wild-type mice (Harkness et al, 2015), suggesting that TAAR 1 function modulates methamphetamine consumption. Interestingly, there was no difference between those two genotypes of mice in morphine CPP (Achat-Mendes et al, 2012), suggesting an interesting differentiation between morphine and psychostimulants.…”

Section: Taar 1 Functionality: Lessons Learned From Genetically-momentioning

confidence: 99%

Trace amine-associated receptor 1: A promising target for the treatment of psychostimulant addiction

2015

European Journal of Pharmacology

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Abuse of and addiction to psychostimulants remains a challenging clinical issue, yet no effective pharmacotherapy is available. Trace amine associated receptor 1 (TAAR 1) is increasingly recognized as a novel drug target that participates in the modulation of drug abuse. This review analyzed existing preclinical evidence from electrophysiological, biochemical to behavioral aspects regarding the functional interactions between TAAR 1 and dopaminergic system. TAAR 1 knockout mice demonstrate increased sensitivity to dopaminergic activation while TAAR 1 agonists reduce the neurochemical effects of cocaine and amphetamines, attenuate abuse- and addiction-related behavioral effects of cocaine and methamphetamine. It is concluded that TAAR 1 activation functionally modulate the dopaminergic activity and TAAR 1 agonists appear to be promising pharmacotherapies against psychostimulant addiction.

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Neurodevelopment and the Origins of Brain Disorders

Cited by 47 publications

References 16 publications

Cocaine Experience Enhances Thalamo-Accumbens N-Methyl-D-Aspartate Receptor Function

Cocaine Experience Enhances Thalamo-Accumbens N-Methyl-D-Aspartate Receptor Function

Frontolimbic functioning during threat-related attention: Relations to early behavioral inhibition and anxiety in children

Trace amine-associated receptor 1: A promising target for the treatment of psychostimulant addiction

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