The formation and erasure of drug addiction memories / 复旦学报（医学版）

Psychoactive substance abuse has been a public health and social problem in the world.The essence of psychoactive substance addiction is a pathological memory (addiction memory) based on alterations in gene expression and synapticplasticity.Here we summarize recent findings in the neurobiological mechanisms of psychoactive substance addiction.

Neurobiological Mechanism of Memory

Memory is one of the most important mental mechanisms which is crucial for us to adapt to environmental surroundings and to maintain our identity. The neurobiological mechanisms for memory are based upon the synaptic plasticity that involve both functional and structural changes at the synapses in the neural circuits participating in learning and memory. Memory is not a single process but has two forms of short-term and long-term memory that are two independent but overlapping processes that blend into one another. The short-term memory depends upon the functional change of synaptic strength but the long-term memory requires anatomic changes of synapses in the neural circuit. Memory storage seems to use elements of a common genetic switch, involving cyclic adenosine monophospate (cAMP)-dependent protein kinase, mitogen activated protein kinase, and cAMP response element-binding protein, to convert short-term memory into long-term memory.

Understanding of the sensorimotor-cognitive difficulties in attention deficit and hyperactivity disorders children / 中华实用儿科临床杂志

Attention deficit and hyperactivity disorders (ADHD),a neurodevelopmental disability with core symptoms of inattention,hyperactivity and impulsivity increases the risk of many cognitive problems.However,the brain structures and pathways involved in the interplays between the core symptoms,such as activity deficits,and cognitive impairments have remained unknown over the past decades.This article review the academic developments in recent years that elucidate the neural mechanisms involved in the sensorimotor-cognitive difficulties at systematic,circuitry,cellular,and molecular levels.The treatment potentials of physical activity enhancement were addressed,as a new alternative and supplementary therapeutic strategy for ADHD,based on our current understanding of the neurobiology of cognitive-sensorimotor interaction.

Understanding Stress by Neuroscience

Stress can be defined generally as reponses to stressors on the body or in a definition more focused on the central nervous system, it can be defined as alterations in neuro-psychological homeostatic processes. There is a psychological aspect to stress, related to issues such as memory, emotion, arousal, and also a biological aspect which included activation of specific brain and endocrine circuits. This article reviews a series of neurobiological mechanisms aimed at understanding what are pathways by which stress is perceived, processed, and transduced into a neuroendocrine response. Multiple brain structures are involved in the organization of responses to stressful stimuli. Among them the hypothalamus, septohippocampal structures, amygdala, cingulate and prefrontal cortices, hindbrain regions such as the brainstem catecholamine cell body group (A2/C2 cell groups in the nucleus of the tractus solitaris; A1/C1 cell groups in the ventrolateral medulla; A6 cell groups in the locus ceruleus), the parabrachial nucleus, cuneiform nucleus, and dorsal raphe nucleus are prominent structures. We reviewed with the focus on the classic stress circuits: the limbic- hypothalamic-pituitary- adrenal axis (LHPA) and locus ceruleus-norepinephrine (LC-NE) system. Our review indicates that the LHPA stress circuit and LC- NE system are the complex systems with multiple control mechanisms and that these mechanisms are altered in pathological states, such as chronic stress and depression. The holistic features described in this reviews can provide insight into the nature and location of brain circuits and neurotransmitter receptors involved in stress and the treatment of stress-related disorders.

Neurobiological Mechanism of Nicotine Dependence / 대한정신약물학회지

Nicotine, the primary psychoactive components of tobacco smoke, produce diverse neurophysiological and behavioral effects through several brain regions and neurochemical pathways. It acts as an agonist to activate and desensitize nicotinic acetylcholine receptors. Nicotinic signaling leads to activation of reward centers in the CNS, including the mesoaccumbens dopamine system, which ultimately leads to behavioral reinforcement and addiction. Indeed, the actions of nicotine on many systems, including brainstem cholinergic, GABAergic, glutaminergic, noradrenergic, and serotonergic systems, may help to mediate nicotine effects related to addiction. And many years of smoking induces neuroadaptations in acetylcholine and dopamine systems. Moreover, the long-term synaptic changes results in learned behaviors and memory which are associated with smoking. We reviewed the nicotinic synaptic mechanisms in midbrain dopaminergic areas. In summary, nicotine as obtained from tobacco interacts with multiple nicotinic acetylcholine receptor subtypes on dopamine, GABA, glutaminergic neuron to produce not only the acute positive reinforcement but also the synaptic changes associated with learning and memory.