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Yukiori Goto

Publications and source records attributed to Yukiori Goto.

7 recordsLinked to original sources
PubMed2006

Alterations in medial prefrontal cortical activity and plasticity in rats with disruption of cortical development.

BACKGROUND: Psychiatric disorders such as schizophrenia are believed to emerge from an interaction of several factors. Thus, a genetic predisposition can lead to developmental compromises that may leave the system more susceptible to deficits induced by subsequent environmental variables such as stress. METHODS: The impact of neurodevelopmental interruption induced by exposure of rats prenatally to a compound methylazoxymethanol acetate (MAM) that disrupts neuronal proliferation was investigated using in vivo electrophysiologic recordings from the prefrontal cortex of adult rats. RESULTS: Prenatal exposure to MAM resulted in alterations in the medial prefrontal cortex indicative of a compromise in information processing. Specifically, we observed a disruption in activity patterns consistent with deficits in neuronal synchronization and abnormal augmentation of synaptic plasticity that was more severely disrupted by stress exposure than in normal animals. Furthermore, these deficits could be reversed by manipulating the mesocortical dopamine system. CONCLUSIONS: These results suggest that disruption of early cortical development causes impairments in medial prefrontal cortical function at adulthood that are more vulnerable to disruptive influences, despite the presence of only subtle structural alterations in the brain.

Action Potentials↗
PubMed2005

Dopamine-dependent interactions between limbic and prefrontal cortical plasticity in the nucleus accumbens: disruption by cocaine sensitization.

The prefrontal cortex and the hippocampus exhibit converging projections to the nucleus accumbens and have functional reciprocal connections via indirect pathways. As a result, information processing between these structures is likely to be bidirectional. Using evoked potential measures, we examined the interactions of these inputs on synaptic plasticity within the accumbens. Our results show that the direction of information flow between the prefrontal cortex and limbic structures determines the synaptic plasticity that these inputs exhibit within the accumbens. Moreover, this synaptic plasticity at hippocampal and prefrontal inputs selectively involves dopamine D1 and D2 activation or inactivation, respectively. Repeated cocaine administration disrupted this synaptic plasticity at hippocampal and prefrontal cortical inputs and goal-directed behavior in the spatial maze task. Thus, interactions of limbic-prefrontal cortical synaptic plasticity and its dysfunction within the accumbens could underlie complex information processing deficits observed in individuals following psychostimulant administration.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed2005

Dopaminergic modulation of limbic and cortical drive of nucleus accumbens in goal-directed behavior.

Goal-directed behavior is believed to involve interactions of prefrontal cortical and limbic inputs in the nucleus accumbens (NAcc), and their modulation by mesolimbic dopamine (DA) seems to be of primary importance in NAcc function. Using in vivo electrophysiological recordings simultaneously with DA system manipulation in rats, we show that tonic and phasic DA release selectively modulates hippocampal and prefrontal cortical inputs through D1 and D2 receptors, respectively. In addition, we also found that D1 activation and D2 inactivation in the NAcc produced behaviorally selective effects (learning versus set shifting of response strategy) that correspond to specific afferents. These results suggest that the dynamics of DA release regulate the balance between limbic and cortical drive through activation and inactivation of DA receptor subtypes in the accumbens, and this regulates goal-directed behavior.

Animals↗
PubMed2004

Prefrontal lesion reverses abnormal mesoaccumbens response in an animal model of schizophrenia.

BACKGROUND: A neonatal hippocampal lesion induces postpubertal behavioral alterations resembling phenomena observed in schizophrenia. We have recently reported that nucleus accumbens neurons exhibit altered response to ventral tegmental area activation, but only when animals with this lesion reach adulthood. Because a prefrontal cortical lesion eliminates postpubertal abnormal behaviors in these animals, we investigated whether altered accumbens responses were reversed with this manipulation. METHODS: In vivo intracellular recordings were conducted in accumbens neurons in rats that had received neonatal hippocampal lesions combined with either adult prefrontal cortical lesion or sham treatment. Accumbens response to mesolimbic pathway activation was recorded in these animals. RESULTS: Accumbens neurons from animals with a neonatal hippocampal lesion and an adult prefrontal sham operation still showed altered accumbens response to mesolimbic stimulation. On the other hand, most animals with combined neonatal hippocampal and adult prefrontal lesions exhibited responses similar to those of naïve animals. CONCLUSIONS: This result suggests that abnormal behaviors in these animals might be related to excessive prefrontal drive of accumbens neurons upon dopamine activation.

Animals↗
PubMed2002

Delayed mesolimbic system alteration in a developmental animal model of schizophrenia.

Pharmacological and imaging studies indicate that the prefrontal cortex and nucleus accumbens and their dopamine innervation are central elements of the pathophysiology of schizophrenia. Although symptoms typically appear in young adults, a developmental component has been suggested, primarily in the hippocampus. A neonatal hippocampal lesion in rats and monkeys produces changes resembling schizophrenia symptoms only after the animals reach adulthood, indicating that this procedure could be used as a developmental animal model of this disorder. Here, we explored whether the dopamine projection to the nucleus accumbens becomes functionally altered in these animals. In vivo intracellular recordings revealed abnormal responses in accumbens neurons to activation of their dopamine afferents in adult but not prepubertal animals with a neonatal lesion. This alteration was absent after antipsychotic drug treatment. These results indicate that neonatal hippocampal damage can result in delayed functional deficits in the mesolimbic system, providing a link between the developmental hippocampal deficit and altered dopamine systems postulated to occur in schizophrenia.

Administration, Oral↗
PubMed2002

Timing-dependent limbic-motor synaptic integration in the nucleus accumbens.

The nucleus accumbens is a brain region in which limbic and motor inputs converge. How these information modalities shape accumbens output is not clearly understood. Here, we report that synaptic inputs from the prefrontal cortex and limbic structures interact differently depending on their timing. Coincident inputs may result in enhancing information flow through the nucleus accumbens. Responses to asynchronous inputs are affected by their relative order of arrival, with limbic inputs allowing subsequent prefrontal responses, and prefrontal inputs dampening limbic responses. These mechanisms allow for both coincidence detection and input selection in this integrative brain region.

Animals↗