Drugs of Abuse and Stress May Cause Similar Changes in the Brain

Mental and behavioural disorders

10.1093/oso/9780198843177.003.0012 ◽

2020 ◽

pp. 333-365

Author(s):

Fabrizio Benedetti

Keyword(s):

Clinical Trials ◽

Mental Disorders ◽

Placebo Effect ◽

Crucial Role ◽

Drugs Of Abuse ◽

Placebo Treatment ◽

Brain Regions ◽

Psychotherapeutic Interventions ◽

Psychotherapeutic Outcome ◽

The Brain

In this chapter some mental disorders are described. For example, in depression, fluoxetine treatment and a placebo treatment affect similar brain regions. In anxiety, patients’ expectations play a crucial role, as covert (unexpected) administration of anti-anxiety drugs is less effective than overt (expected) administration. The disruption of prefrontal executive control in Alzheimer’s disease decreases the magnitude of placebo responses. In addition, expectations appear to be particularly important when associated with the effects of drugs of abuse. Placebo effects appear to be powerful in psychotherapy as well, and the brain areas involved in the psychotherapeutic outcome are different from those involved in the placebo effect. As clinical trials for psychotherapeutic interventions represent a major problem, new recommendations are presented.

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Neurochemical Systems in the Central Nervous System

Neurobiology of Mental Illness ◽

10.1093/med/9780199934959.003.0002 ◽

2013 ◽

pp. 12-26

Author(s):

Ariel Y. Deutch ◽

Robert H. Roth

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Psychiatric Disorders ◽

Neurotrophic Factors ◽

Drugs Of Abuse ◽

Large Majority ◽

System P ◽

Target Neuron ◽

The Central Nervous System ◽

The Brain

Chapter 2 describes the neurochemical organization of the brain. It summarizes the diverse types of molecules that neurons in the brain use as neurotransmitters and neurotrophic factors, and how these molecules are synthesized and metabolized. The chapter also presents the array of receptor proteins through which these molecules regulate target neuron functioning and the reuptake proteins that generally terminate the neurotransmitter signal. Today a large majority of all drugs used to treat psychiatric disorders, as well as most drugs of abuse, still have as their initial targets proteins involved directly in neurotransmitter function.

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Cellular and Molecular Mechanisms of Addiction

10.1093/med/9780190681425.003.0046 ◽

2017 ◽

Author(s):

Kathryn J. Reissner ◽

Peter W. Kalivas

Keyword(s):

Molecular Mechanisms ◽

Drugs Of Abuse ◽

Drug Seeking ◽

Molecular Changes ◽

Cellular Changes ◽

Continued Use ◽

Brain Reward ◽

Social Use ◽

The Brain

Exposure to drugs of abuse can be a reinforcing experience that, in vulnerable individuals, can lead to continued use and the development of an addiction disorder. Evidence indicates that the escalation in use and compulsive motivation to obtain the drug is linked to long-lasting cellular changes within the brain reward neurocircuitry. In this chapter we describe the stages of transition in use from social use to habitual relapse, and within that context we describe the implicated neurocircuitry, and the enduring cellular and molecular changes that occur within that circuitry, that may mediate the preoccupation with drug seeking in addiction-vulnerable individuals.

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Caught in the Net: Perineuronal Nets and Addiction

Neural Plasticity ◽

10.1155/2016/7538208 ◽

2016 ◽

Vol 2016 ◽

pp. 1-8 ◽

Cited By ~ 16

Author(s):

Megan Slaker ◽

Jordan M. Blacktop ◽

Barbara A. Sorg

Keyword(s):

Extracellular Matrix ◽

Drugs Of Abuse ◽

Perineuronal Nets ◽

Drug Induced ◽

Brain Circuitry ◽

Induced Changes ◽

The Brain

Exposure to drugs of abuse induces plasticity in the brain and creates persistent drug-related memories. These changes in plasticity and persistent drug memories are believed to produce aberrant motivation and reinforcement contributing to addiction. Most studies have explored the effect drugs of abuse have on pre- and postsynaptic cells and astrocytes; however, more recently, attention has shifted to explore the effect these drugs have on the extracellular matrix (ECM). Within the ECM are unique structures arranged in a net-like manner, surrounding a subset of neurons called perineuronal nets (PNNs). This review focuses on drug-induced changes in PNNs, the molecules that regulate PNNs, and the expression of PNNs within brain circuitry mediating motivation, reward, and reinforcement as it pertains to addiction.

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Chronic Developmental Lead Exposure increases μ-Opiate Receptor Levels in the Adolescent Rat Brain

10.1101/2020.04.18.048264 ◽

2020 ◽

Author(s):

Damaris Albores-Garcia ◽

Jennifer L McGlothan ◽

Zoran Bursac ◽

Tomás R. Guilarte

Keyword(s):

Rat Brain ◽

Early Adolescence ◽

Drugs Of Abuse ◽

Specific Binding ◽

Biological Effects ◽

The United States ◽

Female Rats ◽

Opioid Use ◽

Male And Female Rats ◽

The Brain

AbstractOpioid use and abuse has reached epidemic proportion in the United States resulting in a significant numbers of deaths due to overdose. While environmental factors are implicated in opioid addiction, less is known about the role of exposure to environmental pollutants on the brain opioid system. Human and preclinical studies have suggested an association between childhood lead (Pb2+) intoxication and proclivity to substance abuse and delinquent behavior. Opioid receptors are involved in the biological effects of opioids and other drugs of abuse. In this study, we examine the effect of chronic developmental Pb2+ exposure on μ-opioid receptor (MOR) levels in the rat brain using [3H]-D-Ala2-MePhe4-Gly-ol5 enkephalin ([3H]-DAMGO) quantitative receptor autoradiography.Our results indicate that chronic developmental Pb2+ exposure increases the levels of [3H]-DAMGO specific binding to MOR in several limbic regions of the brain in male and female rats during the pre-adolescence (PN14) and early-adolescence (PN28) period. These changes were less pronounced in late-adolescence (PN50) and adult (PN120) animals. Our findings are important because the pre-adolescence and early adolescence period is a time in which there is higher engagement in reward and drug seeking behaviors in humans.In summary, we show that chronic exposure to Pb2+ an ubiquitous and well-known environmental contaminant and neurotoxicant, alters MOR levels in brain regions associated with addiction circuits in the adolescent period with important implications to opioid drug use and abuse.

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Investigating the Cocaine-induced Reduction of Potassium Current on the Generation of Action Potentials Using a Computational Model

Basic and Clinical Neuroscience Journal ◽

10.32598/bcn.2021.1150.2 ◽

2021 ◽

Author(s):

Hadi Borjkhani ◽

◽

Mehdi Borjkhani ◽

Morteza A. Sharif ◽

◽

...

Keyword(s):

Computational Model ◽

Action Potentials ◽

Potassium Current ◽

Drugs Of Abuse ◽

Potassium Conductance ◽

Brain Regions ◽

Chaotic Regime ◽

Chaotic Oscillations ◽

Sodium Potassium ◽

The Brain

Introduction: Drugs of abuse, including cocaine, affect different brain regions and lead to pathological memories. These abnormal memories may occur due to the changes in synaptic transmissions or variations in synaptic properties of neurons. It has been shown that cocaine inhibits delayed rectifying potassium currents in affected regions of the brain and can have a role in the formation of pathological memories. Purpose: This study investigates how the change in the conductance of delayed rectifying potassium channels can affect the produced action potentials using a computational model. Methods: We present a computational model with different channels and receptors, including sodium, potassium, calcium, NMDARs, and AMPARs, which can produce burst-type action potentials. In the simulations, by changing the delayed rectifying potassium conductance bifurcation diagram is calculated. Conclusion: Results show that for a specific range of potassium conductance, a chaotic regime emerges in produced action potentials. These chaotic oscillations may play a role in inducing abnormal memories.

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De cigalas y humanos. Perspectiva evolucionista de la adicción

Mètode Revista de difusió de la investigació ◽

10.7203/metode.12.18398 ◽

2021 ◽

Author(s):

Carmen Ferrer-Pérez ◽

José Miñarro López

Keyword(s):

Complex Disease ◽

Drugs Of Abuse ◽

Reward System ◽

Holistic View ◽

Biopsychosocial Approach ◽

Behavioural Effects ◽

The Brain

Addiction is a complex disease whose manifestation is unique to each individual patient. Despite this, our knowledge suggests that many of the consequences of using drugs of abuse are due to alterations in the brain, which would be similar from one individual to another. Specifically, abuse drugs act on the brain’s reward system to trigger behavioural effects. In this paper, we will unravel the functions and phylogenetic roots of this system and then explain how drugs of abuse can affect the functioning of the brain. Addiction research and treatment requires a biopsychosocial approach and hence, being aware of the phylogenetic side of this problem can help to build a holistic view of the disease.

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Enhanced susceptibility of CA3 hippocampus to prenatal nicotine exposure

Journal of Developmental Origins of Health and Disease ◽

10.1017/s2040174416000775 ◽

2016 ◽

Vol 8 (2) ◽

pp. 155-160 ◽

Cited By ~ 1

Author(s):

O. O. Kalejaiye ◽

M. C. Gondré-Lewis

Keyword(s):

Adverse Effects ◽

Drugs Of Abuse ◽

Emotional Memory ◽

Nicotine Exposure ◽

Glutamatergic Transmission ◽

Prenatal Nicotine Exposure ◽

Specific Manner ◽

Prenatal Nicotine ◽

The Brain ◽

Early Phases

The brain is highly susceptible to adverse effects of drugs of abuse during early phases of life. Prenatal nicotine exposure (PNE), a preventable cause of gestational and infant mortality, can alter neuron wiring and induce sustained deficits in attention and learning. Here, a rat model of PNE (embryonic days 7–21) was used to examine the maturing hippocampus, which encodes new memories and processes emotional memory. Components of synaptic signaling were evaluated at postnatal day 14 (P14), a period of prolific synaptogenesis in rats, to determine if glutamatergic transmission-associated molecules are regulated in subregions of hippocampus as early as P14. PNE resulted in reduced expression of GluN2B, GluA2 and CaMKIIα, but elevated SNAP25 proteins specifically in the CA3 but not CA1. Only CaMKIIα was regulated in dentate gyrus at this age. These results suggest that glutamatergic and synaptic dysregulation of learning and memory may occur in hippocampus in a temporally and subregionally specific manner.

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