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Antonello Bonci - One of the best experts on this subject based on the ideXlab platform.

  • rescuing cocaine induced prefrontal Cortex hypoactivity prevents compulsive cocaine seeking
    Nature, 2013
    Co-Authors: Billy T Chen, Christina Hatch, Ikue Kusumotoyoshida, Woodward F Hopf, Antonello Bonci
    Abstract:

    A study of compulsive drug-seeking behaviour in rats reveals that prolonged cocaine self-administration decreases Prelimbic Cortex activity resulting in increased compulsive drug-seeking actions; conversely, increasing activity in the Prelimbic Cortex decreases drug-seeking behaviour, a finding relevant to addiction treatment. Antonello Bonci and colleagues use a rodent model for compulsive cocaine usage to show that in animals expressing the strongest drug-seeking behaviours, there is a prolonged reduction in activity in the deeper layers of the Prelimbic Cortex, part of the brain thought to be associated with compulsive drug seeking. Correcting this hypoactivity using optogenetic strategies prevents cocaine-seeking behaviours. In addition, optogenetic inhibition of Prelimbic activity was sufficient to drive compulsive drug seeking. This work identifies Prelimbic stimulation as a possible therapy in compulsive drug users. Loss of control over harmful drug seeking is one of the most intractable aspects of addiction, as human substance abusers continue to pursue drugs despite incurring significant negative consequences1. Human studies have suggested that deficits in prefrontal cortical function and consequential loss of inhibitory control2,3,4 could be crucial in promoting compulsive drug use. However, it remains unknown whether chronic drug use compromises cortical activity and, equally important, whether this deficit promotes compulsive cocaine seeking. Here we use a rat model of compulsive drug seeking5,6,7,8 in which cocaine seeking persists in a subgroup of rats despite delivery of noxious foot shocks. We show that prolonged cocaine self-administration decreases ex vivo intrinsic excitability of deep-layer pyramidal neurons in the Prelimbic Cortex, which was significantly more pronounced in compulsive drug-seeking animals. Furthermore, compensating for hypoactive Prelimbic Cortex neurons with in vivo optogenetic Prelimbic Cortex stimulation significantly prevented compulsive cocaine seeking, whereas optogenetic Prelimbic Cortex inhibition significantly increased compulsive cocaine seeking. Our results show a marked reduction in Prelimbic Cortex excitability in compulsive cocaine-seeking rats, and that in vivo optogenetic Prelimbic Cortex stimulation decreased compulsive drug-seeking behaviours. Thus, targeted stimulation of the prefrontal Cortex could serve as a promising therapy for treating compulsive drug use.

  • rescuing cocaine induced prefrontal Cortex hypoactivity prevents compulsive cocaine seeking
    Nature, 2013
    Co-Authors: Billy T Chen, Christina Hatch, Ikue Kusumotoyoshida, Woodward F Hopf, Antonello Bonci, Hau Jie Yau, Saemi L Cho
    Abstract:

    Loss of control over harmful drug seeking is one of the most intractable aspects of addiction, as human substance abusers continue to pursue drugs despite incurring significant negative consequences. Human studies have suggested that deficits in prefrontal cortical function and consequential loss of inhibitory control could be crucial in promoting compulsive drug use. However, it remains unknown whether chronic drug use compromises cortical activity and, equally important, whether this deficit promotes compulsive cocaine seeking. Here we use a rat model of compulsive drug seeking in which cocaine seeking persists in a subgroup of rats despite delivery of noxious foot shocks. We show that prolonged cocaine self-administration decreases ex vivo intrinsic excitability of deep-layer pyramidal neurons in the Prelimbic Cortex, which was significantly more pronounced in compulsive drug-seeking animals. Furthermore, compensating for hypoactive Prelimbic Cortex neurons with in vivo optogenetic Prelimbic Cortex stimulation significantly prevented compulsive cocaine seeking, whereas optogenetic Prelimbic Cortex inhibition significantly increased compulsive cocaine seeking. Our results show a marked reduction in Prelimbic Cortex excitability in compulsive cocaine-seeking rats, and that in vivo optogenetic Prelimbic Cortex stimulation decreased compulsive drug-seeking behaviours. Thus, targeted stimulation of the prefrontal Cortex could serve as a promising therapy for treating compulsive drug use.

Billy T Chen - One of the best experts on this subject based on the ideXlab platform.

  • rescuing cocaine induced prefrontal Cortex hypoactivity prevents compulsive cocaine seeking
    Nature, 2013
    Co-Authors: Billy T Chen, Christina Hatch, Ikue Kusumotoyoshida, Woodward F Hopf, Antonello Bonci
    Abstract:

    A study of compulsive drug-seeking behaviour in rats reveals that prolonged cocaine self-administration decreases Prelimbic Cortex activity resulting in increased compulsive drug-seeking actions; conversely, increasing activity in the Prelimbic Cortex decreases drug-seeking behaviour, a finding relevant to addiction treatment. Antonello Bonci and colleagues use a rodent model for compulsive cocaine usage to show that in animals expressing the strongest drug-seeking behaviours, there is a prolonged reduction in activity in the deeper layers of the Prelimbic Cortex, part of the brain thought to be associated with compulsive drug seeking. Correcting this hypoactivity using optogenetic strategies prevents cocaine-seeking behaviours. In addition, optogenetic inhibition of Prelimbic activity was sufficient to drive compulsive drug seeking. This work identifies Prelimbic stimulation as a possible therapy in compulsive drug users. Loss of control over harmful drug seeking is one of the most intractable aspects of addiction, as human substance abusers continue to pursue drugs despite incurring significant negative consequences1. Human studies have suggested that deficits in prefrontal cortical function and consequential loss of inhibitory control2,3,4 could be crucial in promoting compulsive drug use. However, it remains unknown whether chronic drug use compromises cortical activity and, equally important, whether this deficit promotes compulsive cocaine seeking. Here we use a rat model of compulsive drug seeking5,6,7,8 in which cocaine seeking persists in a subgroup of rats despite delivery of noxious foot shocks. We show that prolonged cocaine self-administration decreases ex vivo intrinsic excitability of deep-layer pyramidal neurons in the Prelimbic Cortex, which was significantly more pronounced in compulsive drug-seeking animals. Furthermore, compensating for hypoactive Prelimbic Cortex neurons with in vivo optogenetic Prelimbic Cortex stimulation significantly prevented compulsive cocaine seeking, whereas optogenetic Prelimbic Cortex inhibition significantly increased compulsive cocaine seeking. Our results show a marked reduction in Prelimbic Cortex excitability in compulsive cocaine-seeking rats, and that in vivo optogenetic Prelimbic Cortex stimulation decreased compulsive drug-seeking behaviours. Thus, targeted stimulation of the prefrontal Cortex could serve as a promising therapy for treating compulsive drug use.

  • rescuing cocaine induced prefrontal Cortex hypoactivity prevents compulsive cocaine seeking
    Nature, 2013
    Co-Authors: Billy T Chen, Christina Hatch, Ikue Kusumotoyoshida, Woodward F Hopf, Antonello Bonci, Hau Jie Yau, Saemi L Cho
    Abstract:

    Loss of control over harmful drug seeking is one of the most intractable aspects of addiction, as human substance abusers continue to pursue drugs despite incurring significant negative consequences. Human studies have suggested that deficits in prefrontal cortical function and consequential loss of inhibitory control could be crucial in promoting compulsive drug use. However, it remains unknown whether chronic drug use compromises cortical activity and, equally important, whether this deficit promotes compulsive cocaine seeking. Here we use a rat model of compulsive drug seeking in which cocaine seeking persists in a subgroup of rats despite delivery of noxious foot shocks. We show that prolonged cocaine self-administration decreases ex vivo intrinsic excitability of deep-layer pyramidal neurons in the Prelimbic Cortex, which was significantly more pronounced in compulsive drug-seeking animals. Furthermore, compensating for hypoactive Prelimbic Cortex neurons with in vivo optogenetic Prelimbic Cortex stimulation significantly prevented compulsive cocaine seeking, whereas optogenetic Prelimbic Cortex inhibition significantly increased compulsive cocaine seeking. Our results show a marked reduction in Prelimbic Cortex excitability in compulsive cocaine-seeking rats, and that in vivo optogenetic Prelimbic Cortex stimulation decreased compulsive drug-seeking behaviours. Thus, targeted stimulation of the prefrontal Cortex could serve as a promising therapy for treating compulsive drug use.

Christina Hatch - One of the best experts on this subject based on the ideXlab platform.

  • rescuing cocaine induced prefrontal Cortex hypoactivity prevents compulsive cocaine seeking
    Nature, 2013
    Co-Authors: Billy T Chen, Christina Hatch, Ikue Kusumotoyoshida, Woodward F Hopf, Antonello Bonci
    Abstract:

    A study of compulsive drug-seeking behaviour in rats reveals that prolonged cocaine self-administration decreases Prelimbic Cortex activity resulting in increased compulsive drug-seeking actions; conversely, increasing activity in the Prelimbic Cortex decreases drug-seeking behaviour, a finding relevant to addiction treatment. Antonello Bonci and colleagues use a rodent model for compulsive cocaine usage to show that in animals expressing the strongest drug-seeking behaviours, there is a prolonged reduction in activity in the deeper layers of the Prelimbic Cortex, part of the brain thought to be associated with compulsive drug seeking. Correcting this hypoactivity using optogenetic strategies prevents cocaine-seeking behaviours. In addition, optogenetic inhibition of Prelimbic activity was sufficient to drive compulsive drug seeking. This work identifies Prelimbic stimulation as a possible therapy in compulsive drug users. Loss of control over harmful drug seeking is one of the most intractable aspects of addiction, as human substance abusers continue to pursue drugs despite incurring significant negative consequences1. Human studies have suggested that deficits in prefrontal cortical function and consequential loss of inhibitory control2,3,4 could be crucial in promoting compulsive drug use. However, it remains unknown whether chronic drug use compromises cortical activity and, equally important, whether this deficit promotes compulsive cocaine seeking. Here we use a rat model of compulsive drug seeking5,6,7,8 in which cocaine seeking persists in a subgroup of rats despite delivery of noxious foot shocks. We show that prolonged cocaine self-administration decreases ex vivo intrinsic excitability of deep-layer pyramidal neurons in the Prelimbic Cortex, which was significantly more pronounced in compulsive drug-seeking animals. Furthermore, compensating for hypoactive Prelimbic Cortex neurons with in vivo optogenetic Prelimbic Cortex stimulation significantly prevented compulsive cocaine seeking, whereas optogenetic Prelimbic Cortex inhibition significantly increased compulsive cocaine seeking. Our results show a marked reduction in Prelimbic Cortex excitability in compulsive cocaine-seeking rats, and that in vivo optogenetic Prelimbic Cortex stimulation decreased compulsive drug-seeking behaviours. Thus, targeted stimulation of the prefrontal Cortex could serve as a promising therapy for treating compulsive drug use.

  • rescuing cocaine induced prefrontal Cortex hypoactivity prevents compulsive cocaine seeking
    Nature, 2013
    Co-Authors: Billy T Chen, Christina Hatch, Ikue Kusumotoyoshida, Woodward F Hopf, Antonello Bonci, Hau Jie Yau, Saemi L Cho
    Abstract:

    Loss of control over harmful drug seeking is one of the most intractable aspects of addiction, as human substance abusers continue to pursue drugs despite incurring significant negative consequences. Human studies have suggested that deficits in prefrontal cortical function and consequential loss of inhibitory control could be crucial in promoting compulsive drug use. However, it remains unknown whether chronic drug use compromises cortical activity and, equally important, whether this deficit promotes compulsive cocaine seeking. Here we use a rat model of compulsive drug seeking in which cocaine seeking persists in a subgroup of rats despite delivery of noxious foot shocks. We show that prolonged cocaine self-administration decreases ex vivo intrinsic excitability of deep-layer pyramidal neurons in the Prelimbic Cortex, which was significantly more pronounced in compulsive drug-seeking animals. Furthermore, compensating for hypoactive Prelimbic Cortex neurons with in vivo optogenetic Prelimbic Cortex stimulation significantly prevented compulsive cocaine seeking, whereas optogenetic Prelimbic Cortex inhibition significantly increased compulsive cocaine seeking. Our results show a marked reduction in Prelimbic Cortex excitability in compulsive cocaine-seeking rats, and that in vivo optogenetic Prelimbic Cortex stimulation decreased compulsive drug-seeking behaviours. Thus, targeted stimulation of the prefrontal Cortex could serve as a promising therapy for treating compulsive drug use.

Ikue Kusumotoyoshida - One of the best experts on this subject based on the ideXlab platform.

  • rescuing cocaine induced prefrontal Cortex hypoactivity prevents compulsive cocaine seeking
    Nature, 2013
    Co-Authors: Billy T Chen, Christina Hatch, Ikue Kusumotoyoshida, Woodward F Hopf, Antonello Bonci
    Abstract:

    A study of compulsive drug-seeking behaviour in rats reveals that prolonged cocaine self-administration decreases Prelimbic Cortex activity resulting in increased compulsive drug-seeking actions; conversely, increasing activity in the Prelimbic Cortex decreases drug-seeking behaviour, a finding relevant to addiction treatment. Antonello Bonci and colleagues use a rodent model for compulsive cocaine usage to show that in animals expressing the strongest drug-seeking behaviours, there is a prolonged reduction in activity in the deeper layers of the Prelimbic Cortex, part of the brain thought to be associated with compulsive drug seeking. Correcting this hypoactivity using optogenetic strategies prevents cocaine-seeking behaviours. In addition, optogenetic inhibition of Prelimbic activity was sufficient to drive compulsive drug seeking. This work identifies Prelimbic stimulation as a possible therapy in compulsive drug users. Loss of control over harmful drug seeking is one of the most intractable aspects of addiction, as human substance abusers continue to pursue drugs despite incurring significant negative consequences1. Human studies have suggested that deficits in prefrontal cortical function and consequential loss of inhibitory control2,3,4 could be crucial in promoting compulsive drug use. However, it remains unknown whether chronic drug use compromises cortical activity and, equally important, whether this deficit promotes compulsive cocaine seeking. Here we use a rat model of compulsive drug seeking5,6,7,8 in which cocaine seeking persists in a subgroup of rats despite delivery of noxious foot shocks. We show that prolonged cocaine self-administration decreases ex vivo intrinsic excitability of deep-layer pyramidal neurons in the Prelimbic Cortex, which was significantly more pronounced in compulsive drug-seeking animals. Furthermore, compensating for hypoactive Prelimbic Cortex neurons with in vivo optogenetic Prelimbic Cortex stimulation significantly prevented compulsive cocaine seeking, whereas optogenetic Prelimbic Cortex inhibition significantly increased compulsive cocaine seeking. Our results show a marked reduction in Prelimbic Cortex excitability in compulsive cocaine-seeking rats, and that in vivo optogenetic Prelimbic Cortex stimulation decreased compulsive drug-seeking behaviours. Thus, targeted stimulation of the prefrontal Cortex could serve as a promising therapy for treating compulsive drug use.

  • rescuing cocaine induced prefrontal Cortex hypoactivity prevents compulsive cocaine seeking
    Nature, 2013
    Co-Authors: Billy T Chen, Christina Hatch, Ikue Kusumotoyoshida, Woodward F Hopf, Antonello Bonci, Hau Jie Yau, Saemi L Cho
    Abstract:

    Loss of control over harmful drug seeking is one of the most intractable aspects of addiction, as human substance abusers continue to pursue drugs despite incurring significant negative consequences. Human studies have suggested that deficits in prefrontal cortical function and consequential loss of inhibitory control could be crucial in promoting compulsive drug use. However, it remains unknown whether chronic drug use compromises cortical activity and, equally important, whether this deficit promotes compulsive cocaine seeking. Here we use a rat model of compulsive drug seeking in which cocaine seeking persists in a subgroup of rats despite delivery of noxious foot shocks. We show that prolonged cocaine self-administration decreases ex vivo intrinsic excitability of deep-layer pyramidal neurons in the Prelimbic Cortex, which was significantly more pronounced in compulsive drug-seeking animals. Furthermore, compensating for hypoactive Prelimbic Cortex neurons with in vivo optogenetic Prelimbic Cortex stimulation significantly prevented compulsive cocaine seeking, whereas optogenetic Prelimbic Cortex inhibition significantly increased compulsive cocaine seeking. Our results show a marked reduction in Prelimbic Cortex excitability in compulsive cocaine-seeking rats, and that in vivo optogenetic Prelimbic Cortex stimulation decreased compulsive drug-seeking behaviours. Thus, targeted stimulation of the prefrontal Cortex could serve as a promising therapy for treating compulsive drug use.

Woodward F Hopf - One of the best experts on this subject based on the ideXlab platform.

  • rescuing cocaine induced prefrontal Cortex hypoactivity prevents compulsive cocaine seeking
    Nature, 2013
    Co-Authors: Billy T Chen, Christina Hatch, Ikue Kusumotoyoshida, Woodward F Hopf, Antonello Bonci
    Abstract:

    A study of compulsive drug-seeking behaviour in rats reveals that prolonged cocaine self-administration decreases Prelimbic Cortex activity resulting in increased compulsive drug-seeking actions; conversely, increasing activity in the Prelimbic Cortex decreases drug-seeking behaviour, a finding relevant to addiction treatment. Antonello Bonci and colleagues use a rodent model for compulsive cocaine usage to show that in animals expressing the strongest drug-seeking behaviours, there is a prolonged reduction in activity in the deeper layers of the Prelimbic Cortex, part of the brain thought to be associated with compulsive drug seeking. Correcting this hypoactivity using optogenetic strategies prevents cocaine-seeking behaviours. In addition, optogenetic inhibition of Prelimbic activity was sufficient to drive compulsive drug seeking. This work identifies Prelimbic stimulation as a possible therapy in compulsive drug users. Loss of control over harmful drug seeking is one of the most intractable aspects of addiction, as human substance abusers continue to pursue drugs despite incurring significant negative consequences1. Human studies have suggested that deficits in prefrontal cortical function and consequential loss of inhibitory control2,3,4 could be crucial in promoting compulsive drug use. However, it remains unknown whether chronic drug use compromises cortical activity and, equally important, whether this deficit promotes compulsive cocaine seeking. Here we use a rat model of compulsive drug seeking5,6,7,8 in which cocaine seeking persists in a subgroup of rats despite delivery of noxious foot shocks. We show that prolonged cocaine self-administration decreases ex vivo intrinsic excitability of deep-layer pyramidal neurons in the Prelimbic Cortex, which was significantly more pronounced in compulsive drug-seeking animals. Furthermore, compensating for hypoactive Prelimbic Cortex neurons with in vivo optogenetic Prelimbic Cortex stimulation significantly prevented compulsive cocaine seeking, whereas optogenetic Prelimbic Cortex inhibition significantly increased compulsive cocaine seeking. Our results show a marked reduction in Prelimbic Cortex excitability in compulsive cocaine-seeking rats, and that in vivo optogenetic Prelimbic Cortex stimulation decreased compulsive drug-seeking behaviours. Thus, targeted stimulation of the prefrontal Cortex could serve as a promising therapy for treating compulsive drug use.

  • rescuing cocaine induced prefrontal Cortex hypoactivity prevents compulsive cocaine seeking
    Nature, 2013
    Co-Authors: Billy T Chen, Christina Hatch, Ikue Kusumotoyoshida, Woodward F Hopf, Antonello Bonci, Hau Jie Yau, Saemi L Cho
    Abstract:

    Loss of control over harmful drug seeking is one of the most intractable aspects of addiction, as human substance abusers continue to pursue drugs despite incurring significant negative consequences. Human studies have suggested that deficits in prefrontal cortical function and consequential loss of inhibitory control could be crucial in promoting compulsive drug use. However, it remains unknown whether chronic drug use compromises cortical activity and, equally important, whether this deficit promotes compulsive cocaine seeking. Here we use a rat model of compulsive drug seeking in which cocaine seeking persists in a subgroup of rats despite delivery of noxious foot shocks. We show that prolonged cocaine self-administration decreases ex vivo intrinsic excitability of deep-layer pyramidal neurons in the Prelimbic Cortex, which was significantly more pronounced in compulsive drug-seeking animals. Furthermore, compensating for hypoactive Prelimbic Cortex neurons with in vivo optogenetic Prelimbic Cortex stimulation significantly prevented compulsive cocaine seeking, whereas optogenetic Prelimbic Cortex inhibition significantly increased compulsive cocaine seeking. Our results show a marked reduction in Prelimbic Cortex excitability in compulsive cocaine-seeking rats, and that in vivo optogenetic Prelimbic Cortex stimulation decreased compulsive drug-seeking behaviours. Thus, targeted stimulation of the prefrontal Cortex could serve as a promising therapy for treating compulsive drug use.