Limits...
Shared mechanisms of alcohol and other drugs.

Cruz MT, Bajo M, Schweitzer P, Roberto M - Alcohol Res Health (2008)

Bottom Line: Thus, cannabis and opiates act via receptors intended for internally derived (i.e., endogenous) cannabinoid and opiate substances.In contrast, alcohol does not appear to activate specific receptors.However, alcohol influences the activity of many transmitter systems including GABA and endogenous opioids and cannabinoids.

View Article: PubMed Central - PubMed

Affiliation: Committee on Neurobiology of Addictive Disorders, The Scripps Research Institute, La Jolla, California.

ABSTRACT
Identifying the changes that occur in the brain as a result of alcohol and other drug (AOD) use is important to understanding the development of AOD addiction. The nerve cell signaling chemical (i.e., neurotransmitter) γ-aminobutync acid (GABA) plays an important role in the brain chemistry of addiction. Most drugs interact with binding molecules (i.e., receptors) for specific neurotransmitters and either block or facilitate binding at these receptors. Thus, cannabis and opiates act via receptors intended for internally derived (i.e., endogenous) cannabinoid and opiate substances. In contrast, alcohol does not appear to activate specific receptors. However, alcohol influences the activity of many transmitter systems including GABA and endogenous opioids and cannabinoids.

Show MeSH

Related in: MedlinePlus

Hypothetical action of alcohol on γ-aminobutyric acid (GABA)-releasing synapses in the central nucleus of the amygdala. Upper synapse: Alcohol enhances the release of GABA from the presynaptic terminals of the same or another GABAergic interneuron. Lower synapse: Activation of presynaptic opioid or cannabinoid receptors (e.g., CB1) may reduce GABA release onto this interneuron, leading to increased excitability.NOTES: CB1, cannabinoid receptor; eCBs, endocannabinoids; GABAA-R, GABAA receptor; Op-R, opioid receptor.
© Copyright Policy - public-domain
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC3860454&req=5

f2-arh-31-2-137: Hypothetical action of alcohol on γ-aminobutyric acid (GABA)-releasing synapses in the central nucleus of the amygdala. Upper synapse: Alcohol enhances the release of GABA from the presynaptic terminals of the same or another GABAergic interneuron. Lower synapse: Activation of presynaptic opioid or cannabinoid receptors (e.g., CB1) may reduce GABA release onto this interneuron, leading to increased excitability.NOTES: CB1, cannabinoid receptor; eCBs, endocannabinoids; GABAA-R, GABAA receptor; Op-R, opioid receptor.

Mentions: In summary, the findings of Roberto and colleagues (2004) point to a significant effect of alcohol on GABAergic transmission in the CeA that markedly adapts during the development of alcohol dependence. The mechanism of alcohol’s effect remains to be fully elucidated but primarily is associated with an action upon GABA release. Most of the CeA neurons used in this research are GABAergic inhibitory interneurons with inhibitory recurrent or feedforward connections as well as projections to downstream nuclei. Functionally, alcohol itself may influence the neuronal responsivity of the inhibitory CeA gating that regulates information flow through the intra-amygdaloidal circuits (e.g., by disinhibition of CeA), altering the inhibition of the downstream regions (e.g., BNST) by altering GABA release there (see figure 2).


Shared mechanisms of alcohol and other drugs.

Cruz MT, Bajo M, Schweitzer P, Roberto M - Alcohol Res Health (2008)

Hypothetical action of alcohol on γ-aminobutyric acid (GABA)-releasing synapses in the central nucleus of the amygdala. Upper synapse: Alcohol enhances the release of GABA from the presynaptic terminals of the same or another GABAergic interneuron. Lower synapse: Activation of presynaptic opioid or cannabinoid receptors (e.g., CB1) may reduce GABA release onto this interneuron, leading to increased excitability.NOTES: CB1, cannabinoid receptor; eCBs, endocannabinoids; GABAA-R, GABAA receptor; Op-R, opioid receptor.
© Copyright Policy - public-domain
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3860454&req=5

f2-arh-31-2-137: Hypothetical action of alcohol on γ-aminobutyric acid (GABA)-releasing synapses in the central nucleus of the amygdala. Upper synapse: Alcohol enhances the release of GABA from the presynaptic terminals of the same or another GABAergic interneuron. Lower synapse: Activation of presynaptic opioid or cannabinoid receptors (e.g., CB1) may reduce GABA release onto this interneuron, leading to increased excitability.NOTES: CB1, cannabinoid receptor; eCBs, endocannabinoids; GABAA-R, GABAA receptor; Op-R, opioid receptor.
Mentions: In summary, the findings of Roberto and colleagues (2004) point to a significant effect of alcohol on GABAergic transmission in the CeA that markedly adapts during the development of alcohol dependence. The mechanism of alcohol’s effect remains to be fully elucidated but primarily is associated with an action upon GABA release. Most of the CeA neurons used in this research are GABAergic inhibitory interneurons with inhibitory recurrent or feedforward connections as well as projections to downstream nuclei. Functionally, alcohol itself may influence the neuronal responsivity of the inhibitory CeA gating that regulates information flow through the intra-amygdaloidal circuits (e.g., by disinhibition of CeA), altering the inhibition of the downstream regions (e.g., BNST) by altering GABA release there (see figure 2).

Bottom Line: Thus, cannabis and opiates act via receptors intended for internally derived (i.e., endogenous) cannabinoid and opiate substances.In contrast, alcohol does not appear to activate specific receptors.However, alcohol influences the activity of many transmitter systems including GABA and endogenous opioids and cannabinoids.

View Article: PubMed Central - PubMed

Affiliation: Committee on Neurobiology of Addictive Disorders, The Scripps Research Institute, La Jolla, California.

ABSTRACT
Identifying the changes that occur in the brain as a result of alcohol and other drug (AOD) use is important to understanding the development of AOD addiction. The nerve cell signaling chemical (i.e., neurotransmitter) γ-aminobutync acid (GABA) plays an important role in the brain chemistry of addiction. Most drugs interact with binding molecules (i.e., receptors) for specific neurotransmitters and either block or facilitate binding at these receptors. Thus, cannabis and opiates act via receptors intended for internally derived (i.e., endogenous) cannabinoid and opiate substances. In contrast, alcohol does not appear to activate specific receptors. However, alcohol influences the activity of many transmitter systems including GABA and endogenous opioids and cannabinoids.

Show MeSH
Related in: MedlinePlus