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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.

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Related in: MedlinePlus

WIN, an agonist* for the cannabinoid receptor CB1, prevents alcohol from increasing transmission of the neurotransmitter γ-aminobutyric acid (GABA). Inhibitory synaptic responses were evoked in slices from the central nucleus of the amygdala (CeA) by locally stimulating the recorded neurons. A) Average of inhibitory postsynaptic currents (IPSC) amplitude over time. The application of 2 μM WIN (applied at t = 0) in the bathing media decreased IPSC amplitude. Further addition of 44 mM ethanol in the continued presence of WIN had no effect on CeA inhibitory transmission. B) On average (n = 7), 2 μM WIN decreased GABA transmission to 60 ± 5 percent of control (pre-WIN) values. The addition of 44 mM ethanol did not alter IPSC amplitude (63 ± 6% of control).*NOTE: For a definition of this and other technical terms, see the glossary pp. 177–179
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f3-arh-31-2-137: WIN, an agonist* for the cannabinoid receptor CB1, prevents alcohol from increasing transmission of the neurotransmitter γ-aminobutyric acid (GABA). Inhibitory synaptic responses were evoked in slices from the central nucleus of the amygdala (CeA) by locally stimulating the recorded neurons. A) Average of inhibitory postsynaptic currents (IPSC) amplitude over time. The application of 2 μM WIN (applied at t = 0) in the bathing media decreased IPSC amplitude. Further addition of 44 mM ethanol in the continued presence of WIN had no effect on CeA inhibitory transmission. B) On average (n = 7), 2 μM WIN decreased GABA transmission to 60 ± 5 percent of control (pre-WIN) values. The addition of 44 mM ethanol did not alter IPSC amplitude (63 ± 6% of control).*NOTE: For a definition of this and other technical terms, see the glossary pp. 177–179

Mentions: In the BLA, eCB signaling has been implicated in the extinction of aversive memories (Marsicano et al. 2002). Zhu and Lovinger (2005) used freshly isolated BLA neurons to provide solid evidence of a retrograde eCB signaling16 in the BLA. Little information is available on the expression and function of CB1 in the CeA. Katona and colleagues (2001) reported that CB1 is expressed at high levels in certain amygdala nuclei, especially the lateral and basal nuclei, but are absent in the CeA. However, the authors recently conducted electrophysiological experiments in CeA slices to investigate the cellular interactions of the CB1 system and alcohol on GABAergic transmission (see below). These studies (Roberto et al., preliminary data) showed that superfusion of the CB1 agonist WIN onto CeA neurons markedly reduced GABA transmission (see figure 3).


Shared mechanisms of alcohol and other drugs.

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

WIN, an agonist* for the cannabinoid receptor CB1, prevents alcohol from increasing transmission of the neurotransmitter γ-aminobutyric acid (GABA). Inhibitory synaptic responses were evoked in slices from the central nucleus of the amygdala (CeA) by locally stimulating the recorded neurons. A) Average of inhibitory postsynaptic currents (IPSC) amplitude over time. The application of 2 μM WIN (applied at t = 0) in the bathing media decreased IPSC amplitude. Further addition of 44 mM ethanol in the continued presence of WIN had no effect on CeA inhibitory transmission. B) On average (n = 7), 2 μM WIN decreased GABA transmission to 60 ± 5 percent of control (pre-WIN) values. The addition of 44 mM ethanol did not alter IPSC amplitude (63 ± 6% of control).*NOTE: For a definition of this and other technical terms, see the glossary pp. 177–179
© Copyright Policy - public-domain
Related In: Results  -  Collection

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

f3-arh-31-2-137: WIN, an agonist* for the cannabinoid receptor CB1, prevents alcohol from increasing transmission of the neurotransmitter γ-aminobutyric acid (GABA). Inhibitory synaptic responses were evoked in slices from the central nucleus of the amygdala (CeA) by locally stimulating the recorded neurons. A) Average of inhibitory postsynaptic currents (IPSC) amplitude over time. The application of 2 μM WIN (applied at t = 0) in the bathing media decreased IPSC amplitude. Further addition of 44 mM ethanol in the continued presence of WIN had no effect on CeA inhibitory transmission. B) On average (n = 7), 2 μM WIN decreased GABA transmission to 60 ± 5 percent of control (pre-WIN) values. The addition of 44 mM ethanol did not alter IPSC amplitude (63 ± 6% of control).*NOTE: For a definition of this and other technical terms, see the glossary pp. 177–179
Mentions: In the BLA, eCB signaling has been implicated in the extinction of aversive memories (Marsicano et al. 2002). Zhu and Lovinger (2005) used freshly isolated BLA neurons to provide solid evidence of a retrograde eCB signaling16 in the BLA. Little information is available on the expression and function of CB1 in the CeA. Katona and colleagues (2001) reported that CB1 is expressed at high levels in certain amygdala nuclei, especially the lateral and basal nuclei, but are absent in the CeA. However, the authors recently conducted electrophysiological experiments in CeA slices to investigate the cellular interactions of the CB1 system and alcohol on GABAergic transmission (see below). These studies (Roberto et al., preliminary data) showed that superfusion of the CB1 agonist WIN onto CeA neurons markedly reduced GABA transmission (see figure 3).

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