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Opioid Receptor-Mediated Regulation of Neurotransmission in the Brain

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TLDR
The similarities and differences in opioid receptor-mediated regulation of neurotransmission across different brain regions are explored and how future studies can consider potential cell-type, regional, and neural pathway-specific effects of opioid receptors in order to better understand how opioid receptors modulate brain function is understood.
Abstract
Opioids mediate their effects via opioid receptors: mu, delta, and kappa. At the neuronal level, opioid receptors are generally inhibitory, presynaptically reducing neurotransmitter release and postsynaptically hyperpolarizing neurons. However, opioid receptor-mediated regulation of neuronal function and synaptic transmission is not uniform in expression pattern and mechanism across the brain. The localization of receptors within specific cell types and neurocircuits determine the effects that endogenous and exogenous opioids have on brain function. In this review we will explore the similarities and differences in opioid receptor-mediated regulation of neurotransmission across different brain regions. We discuss how future studies can consider potential cell-type, regional, and neural pathway-specific effects of opioid receptors in order to better understand how opioid receptors modulate brain function.

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Effects of prenatal opioid exposure on synaptic adaptations and behaviors across development

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Opioids induce bidirectional synaptic plasticity in a brainstem pain centre in the rat.

TL;DR: In this paper , the authors demonstrate a concentration-dependent, bimodal effect of opioids on excitatory synaptic transmission in the lateral parabrachial nucleus (LPBN) in the brainstem.
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Shared Mechanisms of GABAergic and Opioidergic Transmission Regulate Corticolimbic Reward Systems and Cognitive Aspects of Motivational Behaviors

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References
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Journal ArticleDOI

NEURAL MECHANISMS OF ADDICTION: The Role of Reward-Related Learning and Memory

TL;DR: Progress in identifying candidate mechanisms of addiction is reviewed, including molecular and cellular mechanisms that underlie long-term associative memories in several forebrain circuits (involving the ventral and dorsal striatum and prefrontal cortex) that receive input from midbrain dopamine neurons.
Journal ArticleDOI

The structure and function of G-protein-coupled receptors

TL;DR: G-protein-coupled receptors mediate most of the authors' physiological responses to hormones, neurotransmitters and environmental stimulants, and so have great potential as therapeutic targets for a broad spectrum of diseases.
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Opioids excite dopamine neurons by hyperpolarization of local interneurons.

TL;DR: It is concluded that hyperpolarization of the interneurons by opioids reduces the spontaneous GABA-mediated synaptic input to the dopamine cells in vivo, which would be expected to contribute to the positive reinforcement seen with mu-receptor agonists such as morphine and heroin.
Journal ArticleDOI

Synaptic plasticity: multiple forms, functions, and mechanisms.

TL;DR: Current understanding of the mechanisms of the major forms of synaptic plasticity at excitatory synapses in the mammalian brain are reviewed.
Journal ArticleDOI

The Amygdaloid Complex: Anatomy and Physiology

TL;DR: The anatomical and physiological substrates proposed to underlie amygdala function are examined, suggesting that long-term synaptic plasticity of inputs to the amygdala underlies the acquisition and perhaps storage of the fear memory.
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