Ethanol Inhibits Persistent Activity in Prefrontal Cortical Neurons

Tu, Y.; Kroener, Sven; Abernathy, Kenneth; Lapish, Christopher C.; Seamans, Jeremy K.; Chandler, L. Judson; Woodward, John J.

doi:10.1523/jneurosci.5378-06.2007

Cited by 96 publications

(103 citation statements)

References 65 publications

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“…The dose of ethanol (20 mmol/L) used in the current study is safe and effective according to previous reports [1,37]. In many previous studies, blood concentrations ranging from 20 to 90 mg/dL (5-20 mmol/ L) have been defined as indicating low to moderate ethanol consumption [1].…”

Section: Drugs and Microinjectionsmentioning

confidence: 89%

“…ACSF served as the vehicle control in all experiments. Rats received bilateral microinjections of ethanol (20 mmol/L, *90 mg/dL, equivalent to a peak blood concentration of 1.0 g/kg, defined as moderate consumption), bicuculline (20 lmol/ L), or muscimol (5 mmol/L) in a volume of 0.5 lL over 60 s using a Hamilton syringe attached to polyethylene tubing as in previous studies [1,14,37,38]. The microinjections started 5 min after injector insertion, and the injectors remained in place for full drug diffusion.…”

Section: Drugs and Microinjectionsmentioning

confidence: 99%

“…In many previous studies, blood concentrations ranging from 20 to 90 mg/dL (5-20 mmol/ L) have been defined as indicating low to moderate ethanol consumption [1]. Ethanol at 25-100 mmol/L has also been demonstrated to washout-reversibly suppress the persistent activity of PFC neurons in brain slice patch-clamp recordings [37]. Systemic administration of 0.375-3.5 g/kg of ethanol to rats has been shown to result in blood concentrations ranging from *50 to 350 mg/dL (10-70 mmol/L) which also dose-dependently reduces spike activity in PFC neurons 30 min after treatment [37].…”

Section: Drugs and Microinjectionsmentioning

confidence: 99%

“…Ethanol at 25-100 mmol/L has also been demonstrated to washout-reversibly suppress the persistent activity of PFC neurons in brain slice patch-clamp recordings [37]. Systemic administration of 0.375-3.5 g/kg of ethanol to rats has been shown to result in blood concentrations ranging from *50 to 350 mg/dL (10-70 mmol/L) which also dose-dependently reduces spike activity in PFC neurons 30 min after treatment [37]. In that study, a dose of 20 mmol/L ethanol (90 mg/dL; equivalent to 1.0 g/kg) was effective and believed to be moderate in amount [37].…”

Section: Drugs and Microinjectionsmentioning

confidence: 99%

“…Systemic administration of 0.375-3.5 g/kg of ethanol to rats has been shown to result in blood concentrations ranging from *50 to 350 mg/dL (10-70 mmol/L) which also dose-dependently reduces spike activity in PFC neurons 30 min after treatment [37]. In that study, a dose of 20 mmol/L ethanol (90 mg/dL; equivalent to 1.0 g/kg) was effective and believed to be moderate in amount [37]. In a pilot study, we also demonstrated that intra-PFC microinjection of 20 mmol/L ethanol induced bicuculline-reversible mechanical pain hypersensitivity.…”

Section: Drugs and Microinjectionsmentioning

confidence: 99%

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Ethanol Increases Mechanical Pain Sensitivity in Rats via Activation of GABAA Receptors in Medial Prefrontal Cortex

Geng

Wang

et al. 2016

Neurosci. Bull.

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Ethanol is widely known for its ability to cause dramatic changes in emotion, social cognition, and behavior following systemic administration in humans. Human neuroimaging studies suggest that alcohol dependence and chronic pain may share common mechanisms through amygdala-medial prefrontal cortex (mPFC) interactions. However, whether acute administration of ethanol in the mPFC can modulate pain perception is unknown. Here we showed that bilateral microinjections of ethanol into the prelimbic and infralimbic areas of the mPFC lowered the bilateral mechanical pain threshold for 48 h without influencing thermal pain sensitivity in adult rats. However, bilateral microinjections of artificial cerebrospinal fluid into the mPFC or bilateral microinjections of ethanol into the dorsolateral PFC (also termed as motor cortex area 1 in Paxinos and Watson's atlas of The Rat Brain. Elsevier Academic Press, Amsterdam, 2005) failed to do so, suggesting regional selectivity of the effects of ethanol. Moreover, bilateral microinjections of ethanol did not change the expression of either pro-apoptotic (caspase-3 and Bax) or anti-apoptotic (Bcl-2) proteins, suggesting that the dose was safe and validating the method used in the current study. To determine whether c-aminobutyric acid A (GABA A ) receptors are involved in mediating the ethanol effects, muscimol, a selective GABA A receptor agonist, or bicuculline, a selective GABA A receptor antagonist, was administered alone or co-administered with ethanol through the same route into the bilateral mPFC. The results showed that muscimol mimicked the effects of ethanol while bicuculline completely reversed the effects of ethanol and muscimol. In conclusion, ethanol increases mechanical pain sensitivity through activation of GABA A receptors in the mPFC of rats.

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Section: Drugs and Microinjectionsmentioning

confidence: 89%

Section: Drugs and Microinjectionsmentioning

confidence: 99%

Section: Drugs and Microinjectionsmentioning

confidence: 99%

Section: Drugs and Microinjectionsmentioning

confidence: 99%

Section: Drugs and Microinjectionsmentioning

confidence: 99%

See 3 more Smart Citations

Ethanol Increases Mechanical Pain Sensitivity in Rats via Activation of GABAA Receptors in Medial Prefrontal Cortex

Geng

Wang

et al. 2016

Neurosci. Bull.

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Postnatal binge‐like alcohol exposure decreases dendritic complexity while increasing the density of mature spines in mPFC Layer II/III pyramidal neurons

Hamilton

Whitcher

Klintsova

2009

Synapse

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Prenatal exposure to alcohol in humans can result in a wide range of deficits collectively referred to as Fetal Alcohol Spectrum Disorders. Of these deficits, cognitive impairments are among the most debilitating and long-lasting. Specifically, cognitive impairments in executive functioning suggest damage to the prefrontal cortex (PFC). Several external stimuli, such as morphine, chronic stress and maternal stress have been found to alter the dendritic structure of cells within the PFC. In this study, three groups of rat pups were used: intubated with alcohol (5.25g/kg/day; AE), sham intubated (SI), or suckle controls (SC) on PD4-9. On PD26-30 rats were anesthetized, perfused with saline and brains were processed for Golgi-Cox staining. Basilar dendrite complexity, spine density and spine phenotypes were evaluated for Layer II/III neurons in the medial PFC. Results indicate that AE rats have an altered basilar dendritic tree complexity due to a significant decrease in both length and number of intersections in proximity to the neuronal soma. Furthermore, spine density patterns of basilar dendrites remain unchanged while the density of mature versus immature spines significantly changes. These effects were not seen in the apical dendrites, indicating alcohol’s influence on different neuronal parts in a single cell. In addition, these results suggest that the innervations of the soma and basilar dendrites by thalamic projections may play a role. Thus, our data demonstrates that postnatal exposure to alcohol produces changes in the neuronal organization of rat adolescent PFC that may affect the performance on prefrontal-dependant behavioral tasks.

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Understanding How Acute Alcohol Impacts Neural Encoding in the Rodent Brain

Lapish

2024

Current Topics in Behavioral Neurosciences

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Ethanol Inhibits Persistent Activity in Prefrontal Cortical Neurons

Cited by 96 publications

References 65 publications

Ethanol Increases Mechanical Pain Sensitivity in Rats via Activation of GABAA Receptors in Medial Prefrontal Cortex

Ethanol Increases Mechanical Pain Sensitivity in Rats via Activation of GABAA Receptors in Medial Prefrontal Cortex

Postnatal binge‐like alcohol exposure decreases dendritic complexity while increasing the density of mature spines in mPFC Layer II/III pyramidal neurons

Understanding How Acute Alcohol Impacts Neural Encoding in the Rodent Brain

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