. 2021 May 1:188:108501.

doi: 10.1016/j.neuropharm.2021.108501. Epub 2021 Feb 24.

Alcohol reduces the activity of somatostatin interneurons in the mouse prefrontal cortex: A neural basis for its disinhibitory effect?

Miao Li¹, David Cabrera-Garcia¹, Michael C Salling², Edmund Au³, Guang Yang⁴, Neil L Harrison⁵

Affiliations

¹ Columbia University, Department of Anesthesiology, 630 West 168th Street, New York, NY, 10032, USA.
² Louisiana State University, Department of Anatomy, New Orleans, LA, 1901 Perdido Street, New Orleans, LA, 70112, USA.
³ Columbia University, Department of Pathology & Cell Biology and Rehabilitative Medicine and Regeneration, Columbia Translational Neuroscience Initiative Scholar, 630 West 168th Street, New York, NY, 10032, USA.
⁴ Columbia University, Department of Anesthesiology, 630 West 168th Street, New York, NY, 10032, USA. Electronic address: gy2268@cumc.columbia.edu.
⁵ Columbia University, Department of Anesthesiology, 630 West 168th Street, New York, NY, 10032, USA; Columbia University, Department of Molecular Pharmacology and Therapeutics, 630 West 168th Street, New York, NY, 10032, USA. Electronic address: nh2298@columbia.edu.

PMID: 33636191
PMCID: PMC8820125
DOI: 10.1016/j.neuropharm.2021.108501

Alcohol reduces the activity of somatostatin interneurons in the mouse prefrontal cortex: A neural basis for its disinhibitory effect?

Miao Li et al. Neuropharmacology. 2021.

. 2021 May 1:188:108501.

doi: 10.1016/j.neuropharm.2021.108501. Epub 2021 Feb 24.

Authors

Miao Li¹, David Cabrera-Garcia¹, Michael C Salling², Edmund Au³, Guang Yang⁴, Neil L Harrison⁵

Affiliations

¹ Columbia University, Department of Anesthesiology, 630 West 168th Street, New York, NY, 10032, USA.
² Louisiana State University, Department of Anatomy, New Orleans, LA, 1901 Perdido Street, New Orleans, LA, 70112, USA.
³ Columbia University, Department of Pathology & Cell Biology and Rehabilitative Medicine and Regeneration, Columbia Translational Neuroscience Initiative Scholar, 630 West 168th Street, New York, NY, 10032, USA.
⁴ Columbia University, Department of Anesthesiology, 630 West 168th Street, New York, NY, 10032, USA. Electronic address: gy2268@cumc.columbia.edu.
⁵ Columbia University, Department of Anesthesiology, 630 West 168th Street, New York, NY, 10032, USA; Columbia University, Department of Molecular Pharmacology and Therapeutics, 630 West 168th Street, New York, NY, 10032, USA. Electronic address: nh2298@columbia.edu.

PMID: 33636191
PMCID: PMC8820125
DOI: 10.1016/j.neuropharm.2021.108501

Abstract

The prefrontal cortex (PFC) is involved in executive ("top-down") control of behavior and its function is especially susceptible to the effects of alcohol, leading to behavioral disinhibition that is associated with alterations in decision making, response inhibition, social anxiety and working memory. The circuitry of the PFC involves a complex interplay between pyramidal neurons (PNs) and several subclasses of inhibitory interneurons (INs), including somatostatin (SST)-expressing INs. Using in vivo calcium imaging, we showed that alcohol dose-dependently altered network activity in layers 2/3 of the prelimbic subregion of the mouse PFC. Low doses of alcohol (1 g/kg, intraperitoneal, i.p.) caused moderate activation of SST INs and weak inhibition of PNs. At moderate to high doses, alcohol (2-3 g/kg) strongly inhibited the activity of SST INs in vivo, and this effect may result in disinhibition, as the activity of a subpopulation of PNs was simultaneously enhanced. In contrast, recordings in brain slices using ex vivo electrophysiology revealed no direct effect of alcohol on the excitability of either SST INs or PNs over a range of concentrations (20 and 50 mM) consistent with the blood alcohol levels reached in the in vivo experiments. This dose-dependent effect of alcohol on SST INs in vivo may reveal a neural basis for the disinhibitory effect of alcohol in the PFC mediated by other neurons within or external to the PFC circuitry.

Keywords: Alcohol; Calcium imaging; Disinhibition; Interneurons; Prefrontal cortex; Somatostatin.

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Conflict of interest statement

Competing Financial Interests

The authors declare no competing financial interests.

Figures

**Fig. 1.. Low doses of alcohol decrease PN activity in the PL *in vivo*.**
Schematic showing *in vivo* two-photon imaging in the prelimbic (PL) region of PFC through a glass window. Dashed lines indicate the region of PL and the bottom of L2/3 of the cortex. M2, secondary motor cortex. Whole cell recordings were performed in L2/3 of acute PFC slices. (B) Blood alcohol concentrations (BACs) after a bolus injection of alcohol at different doses. At 10 min, the corresponding BACs (in mM) for 0.5, 1, 2 and 3 g/kg were, respectively, 7.9 ± 1.6, 28.5 ± 1.2, 39.4 ± 5.9 and 63.4 ± 4.5. (C) Representative time lapse images and fluorescence traces of PNs expressing GCaMP6s in L2/3 of PL before and after saline injection. Scale bar, 20 μm. (D) Average integrated Ca²⁺ activity of L2/3 PNs before and after saline injection. (Baseline: 18.57 ± 0.50%, 10 min: 18.28 ± 0.37%, P = 0.3274, 30 min: 18.71 ± 0.53%, P = 0.7785, 60 min: 18.23 ± 0.48%, P = 0.7947, 120 min: 17.91 ± 0.39%, P = 0.3725, n = 225 cells from 4 mice). (E) Average integrated Ca²⁺ activity of L2/3 PNs before and after 0.5 g/kg ethanol (EtOH) injection. (Baseline: 18.67 ± 0.54%, 10 min: 17.91 ± 0.44%, P = 0.5373, 30 min: 18.39 ± 0.64%, P = 0.1279, 60 min: 18.72 ± 0.53%, P = 0.6874, 120 min: 18.03 ± 0.45%, P = 0.7231; n = 184 cells from 3 mice). (F) Average integrated Ca²⁺ activity of L2/3 PNs before and after 1 g/kg alcohol injection. (Baseline: 18.38 ± 0.37%, 10 min: 17.78 ± 0.57%, P = 0.0007, 30 min: 17.80 ± 0.60%, P = 0.0007, 60 min: 18.13 ± 0.35%, P = 0.8302, 120 min: 19.31 ± 0.44%, P = 0.0543, n = 212 cells from 4 mice). (**D-F**) Bottom, the proportions of neurons showing increases, decreases or no change in Ca²⁺ activity after injection. (G) Average integrated Ca²⁺ activity of L2/3 PNs at 30 min after saline, 0.5 g/kg and 1 g/kg alcohol injection. (Saline: 18.71 ± 0.53%, n = 225 cells from 4 mice, 0.5 g/kg: 18.39 ± 0.64%, P = 0.2077, n = 184 from 3 mice, 1 g/kg: 17.80 ± 0.60%, P = 0.0038, n = 212 from 4 mice). (H) Amplitude of L2/3 PN Ca²⁺ transients at 30 min after saline, 0.5 g/kg and 1 g/kg alcohol injection. (Saline: 48.81 ± 1.08%, n = 225 cells from 4 mice, 0.5 g/kg: 46.69 ± 1.02%, P = 0.5662, n = 184 from 3 mice, 1 g/kg: 48.43 ± 1.30%, P = 0.2868, n = 212 from 4 mice). (I) Frequency of L2/3 PN Ca²⁺ transients at 30 min after saline, 0.5 g/kg and 1 g/kg alcohol injection. (Saline: 4.24 ± 0.14, n = 225 cells from 4 mice, 0.5 g/kg: 3.39 ± 0.11, P = 0.0002, n = 184 from 3 mice, 1 g/kg: 3.31 ± 0.14, P < 0.0001, n = 212 from 4 mice). (J) Duration (s) of L2/3 PN Ca²⁺ transients at 30 min after saline, 0.5 g/kg and 1 g/kg alcohol injection. (Saline: 2.11 ± 0.08, n = 225 cells from 4 mice, 0.5 g/kg: 2.03 ± 0.08, P > 0.9999, n = 184 from 3 mice, 1 g/kg: 2.07 ± 0.11, P = 0.8774, n = 212 from 4 mice). Data in (**D-J**) are presented as mean ± s.e.m. n.s., not signification, **P < 0.01, ***P < 0.001, ****P < 0.0001 vs. baseline or saline by Dunn’s *post hoc* multiple comparison test. (K) Confocal image of a representative biocytin-filled pyramidal neuron in L2/3 section stained with DAPI (blue). Scale bar, 100 μm. (L) Representative recordings in L2/3 PNs before (gray) and in the presence of 20 mM ethanol (red) in response to −200 and +200 pA stimulus. Rheobase traces (in response to a +80 pA current step) are shown in black. Gray arrow indicates voltage sag and black arrows indicate ADP (top arrow) and mAHP (bottom arrown). (M) Comparison of the excitability of PNs by eliciting APs during 500 ms, 20 pA current steps and examining input-output curves during ACSF (open circles), 20 mM ethanol (red solid circles) and washout (gray solid circles). 20 mM ethanol did not alter the number of elicited spikes and did not change after washout compared to ACSF (two-way mixed ANOVA, P = 0.6348, n = 10 cells, except washout: n = 8 cells, from 8 mice). The values plotted in the I-V graph are expressed as mean ± s.e.m.

**Fig. 2.. Moderate to high doses of alcohol increase PN activity in the PL cortex *in vivo* but not intrinsic excitability *ex vivo*.**
**(A)** Representative time lapse images and fluorescence traces of PNs expressing GCaMP6s in L2/3 of PL before and after 3 g/kg alcohol injection. Scale bar, 20 μm. (B) Average integrated Ca²⁺ activity of L2/3 PNs before and after 2 g/kg alcohol injection. (Baseline: 18.57 ± 0.40%, 10 min: 22.34 ± 0.73%, P < 0.0001, 30 min: 24.16 ± 1.05%, P < 0.0001, 60 min: 23.13 ± 0.85%, P < 0.0001, 120 min: 18.42 ± 0.47%, P = 0.1633; n = 264 cells from 3 mice). (C) Average integrated Ca²⁺ activity of L2/3 PNs before and after 3 g/kg alcohol injection. (Baseline: 18.95 ± 0.48%, 10 min: 20.17 ± 0.49%, P = 0.0563, 30 min: 23.13 ± 0.74%, P < 0.0001, 60 min: 24.33 ± 0.88%, P < 0.0001, 120 min: 20.32 ± 0.47%, P = 0.0008; n = 271 cells from 4 mice). (**B-C**) Bottom, the proportions of neurons showing increases, decreases or no change in Ca²⁺ activity after injection. (D) Average integrated Ca²⁺ activity of L2/3 PNs at 30 min after saline, 2 and 3 g/kg alcohol injection. (Saline: 18.71 ± 0.53%, n = 225 cells from 4 mice, 2 g/kg: 24.16 ± 1.05%, P < 0.0001, n = 264 from 3 mice, 3 g/kg: 23.13 ± 0.74%, P < 0.0001, n = 271 from 4 mice). (E) Amplitude of L2/3 PN Ca²⁺ transients at 30 min after saline, 2 g/kg and 3 g/kg alcohol injection. (Saline: 48.81 ± 1.08%, n = 225 cells from 4 mice, 2 g/kg: 58.92 ± 1.88%, P < 0.0001, n = 264 from 3 mice, 3 g/kg: 49.03 ± 1.13%, P > 0.9999, n = 271 from 4 mice). (F) Frequency of Ca²⁺ transients at 30 min after saline, 2 g/kg and 3 g/kg alcohol injection. (Saline: 4.24 ± 0.14, n = 225 cells from 4 mice, 2 g/kg: 4.79 ± 0.13, P = 0.0223, n = 264 from 3 mice, 3 g/kg: 6.15 ± 0.27, P < 0.0001, n = 271 from 4 mice). (G) Duration of Ca²⁺ transients at 30 min after saline, 2 and 3 g/kg alcohol injection. (Saline: 2.11 ± 0.08, n = 225 cells from 4 mice, 2 g/kg: 2.60 ± 0.17, P = 0.4864, n = 264 from 3 mice, 3 g/kg: 2.13 ± 0.09, P > 0.9999, n = 271 from 4 mice). Data in (**B-G**) are presented as mean ± s.e.m. n.s., not signification, *P < 0.05, **P < 0.01, ****P < 0.0001 vs. baseline or saline by Dunn’s *post hoc* multiple comparison test. (H) Representative traces in response to current injection steps (−200, +80, +200 pA) do not show differences in action potential spiking in the presence of 50 mM ethanol (brown) compared with control (gray). (I) Ethanol (50 mM, brown circles) did not alter cell firing (mean spikes ± s.e.m) of L2/3 PNs compared to ACSF (open circles) (mixed model two-way ANOVA, treatment F_{(2, 18)} treatment = 1.448, P = 0.2703, n = 10 cells, except washout: n = 6 cells, from 9 mice).

**Fig. 3.. Low doses of alcohol increase SST activity in the PL *in vivo*.**
(A) Representative time lapse images and fluorescence traces of SST INs expressing GCaMP6s in the PL before and after 1 g/kg alcohol injection. Scale bar, 20 μm. (B) Average integrated Ca²⁺ activity of L2/3 SST INs before and after saline injection. (Baseline: 28.23 ± 1.23%, 10 min: 28.01 ± 0.99%, P = 0.3348; 30 min: 26.79 ± 0.87%, P = 0.7135; 60 min: 26.92 ± 0.87%, P = 0.7163; 120 min: 26.97 ± 1.01%, P = 0.9655; n = 156 cells from 7 mice). (C) Average integrated Ca²⁺ activity of L2/3 SST INs before and after 0.5 g/kg alcohol injection. (Baseline: 28.22 ± 2.58%, 10 min: 27.13 ± 1.79%, P = 0.3355; 30 min: 29.98 ± 1.92%, P = 0.0186; 60 min: 32.10 ± 3.13%, P = 0.2658; 120 min: 37.57 ± 3.10%, P = 0.0002; n = 103 cells from 4 mice). (D) Average Ca²⁺ activity of L2/3 SST INs before and after 1 g/kg alcohol injection. (Baseline: 28.44 ± 1.04%, 10 min: 25.74 ± 1.15%, P = 0.0049, 30 min: 29.75 ± 1.31%, P = 0.6992, 60 min: 32.99 ± 1.51%, P = 0.0695, 120 min: 34.89 ± 1.84%, P = 0.0040, n = 107 cells from 5 mice). (**B-D**) Bottom, the proportions of neurons showing increases, decreases or no change in Ca²⁺ activity after injection. (E) Average integrated Ca²⁺ activity of SST INs at 120 min after saline, 0.5 and 1 g/kg alcohol injection. (Saline: 26.97 ± 1.01%, n = 156 cells from 7 mice, 0.5 g/kg: 37.57 ± 3.10%, P = 0.0066, n = 103 from 4 mice, 1 g/kg: 34.89 ± 1.84%, P < 0.0001, n = 107 from 5 mice). (F) Amplitude of Ca²⁺ transients at 120 min after saline, 0.5 and 1 g/kg alcohol injection. (Saline: 58.90 ± 1.48%, n = 156 cells from 7 mice, 0.5 g/kg: 80.39 ± 5.37%, P = 0.0089, n = 103 from 4 mice, 1 g/kg: 68.10 ± 2.49%, P = 0.0046, n = 107 from 5 mice). (G) Frequency of Ca²⁺ transients at 120 min after saline, 0.5 and 1 g/kg alcohol injection. (Saline: 2.50 ± 0.17, n = 156 cells from 7 mice, 0.5 g/kg: 2.34 ± 0.18, P > 0.9999, n = 103 from 4 mice, 1 g/kg: 4.03 ± 0.19, P < 0.0001, n = 107 from 5 mice). (H) Duration of Ca²⁺ transients at 120 min after saline, 0.5 and 1 g/kg alcohol injection. (Saline: 4.45 ± 0.52, n = 156 cells from 7 mice, 0.5 g/kg: 6.33 ± 1.05, P = 0.1184, n = 103 from 4 mice, 1 g/kg: 3.80 ± 0.48, P > 0.9999, n = 107 from 5 mice). Data in (**B-H**) are presented as mean ± s.e.m. n.s., not signification, *P < 0.05, **P < 0.01, ****P < 0.0001 vs. baseline or saline by Dunn’s *post hoc* multiple comparison test. (I) In the left panel, confocal image showing the distribution of Cre-SST/Td-Tomato cells (in red) in the PL cortex. Scale bar, 200 μm. The right panel shows enlarged view of a representative L2/3 SST IN filled with biocytin (green) during patch-clamp recording. In red, neurons of SST-Cre line expressing td-Tomato. CC: corpus callosum. Scale bar, 100 μm. (J) Representative traces of L2/3 SST INs in ACSF (gray) and during bath application of 20 mM ethanol (red) in response to −200 and +200 pA pulses. Rheobase traces induced by +40 pA current injection are shown in black. (K) Input-output curve of the number of spikes (mean ± s.e.m.) of SST interneurons before (open circles), during exposure to 20 mM (red circles) and after washout (gray circles). Ethanol (20 mM) did not affect the excitability of the L2/3 SST interneurons (mixed model two-way ANOVA, F_{(2, 20)} treatment = 0.2483 P = 0.7825, n = 11 cells, except washout: n = 7 cells, from 9 mice). Data in I-V plot are presented as mean ± s.e.m.

**Fig. 4.. Moderate to high doses of alcohol decrease SST IN activity in the PL *in vivo*.**
(A) Representative time lapse images and fluorescence traces of SST INs expressing GCaMP6s in L2/3 of the PL before and after 2 g/kg alcohol injection. Scale bar, 20 μm. (B) Average integrated Ca²⁺ activity of L2/3 SST INs before and after 2 g/kg alcohol injection. (Baseline: 27.97 ± 1.06%, 10 min: 20.33 ± 1.19%, P < 0.0001, 30 min: 24.73 ± 1.71%, P < 0.0001, 60 min: 28.70 ± 1.44%, P = 0.6202, 120 min: 30.24 ± 1.58%, P = 0.8417; n = 137 cells from 5 mice). (C) Average integrated Ca²⁺ activity of L2/3 SST INs before and after 3 g/kg alcohol injection. (Baseline: 28.96 ± 1.30%, 10 min: 15.33 ± 1.22%, P < 0.0001, 30 min: 17.60 ± 1.11%, P < 0.0001, 60 min: 24.64 ± 2.04%, P < 0.0001, 120 min: 34.48 ± 3.07%, P = 0.7042; n = 132 cells from 4 mice). (**B-C**) Bottom, the proportions of neurons showing increases, decreases or no change in Ca²⁺ activity after injection. (D) Average integrated Ca²⁺ activity of SST INs at 30 min after saline, 2 and 3 g/kg alcohol injection. (Saline: 26.79 ± 0.87%, n = 156 cells from 7 mice, 2 g/kg: 24.73 ± 1.71%, P = 0.0002, n = 137 from 5 mice, 3 g/kg: 17.60 ± 1.11%, P < 0.0001, n = 132 from 4 mice). (E) Amplitude of L2/3 SST Ca²⁺ transients at 30 min after saline, 2 g/kg and 3 g/kg alcohol injection. (Saline: 61.87 ± 1.35%, n = 156 cells from 7 mice, 2 g/kg: 54.37 ± 2.46%, P < 0.0001, n = 137 from 5 mice, 3 g/kg: 39.20 ± 1.43%, P < 0.0001, n = 132 from 4 mice). (F) Frequency of Ca²⁺ transients at 30 min after saline, 2 and 3 g/kg alcohol injection. (Saline: 2.77 ± 0.17, n = 156 cells from 7 mice, 2 g/kg: 1.72 ± 0.14, P < 0.0001, n = 137 from 5 mice, 3 g/kg: 1.03 ± 0.10, P < 0.0001, n = 132 from 4 mice). (G) Duration of Ca²⁺ transients at 30 min after saline, 2 g/kg and 3 g/kg alcohol injection. (Saline: 3.66 ± 0.33, n = 156 cells from 7 mice, 2 g/kg: 5.64 ± 1.02, P = 0.0003, n = 137 from 5 mice, 3 g/kg: 2.45 ± 0.62, P < 0.0001, n = 132 from 4 mice). Data in (**B-G**) are presented as mean ± s.e.m. ***P < 0.001, ****P < 0.0001 vs. baseline or saline by Dunn’s *post hoc* multiple comparison test. (H) Bath application of 50 mM ethanol (brown) had no effect on firing rate in L2/3 SST INs compared to ACSF (gray). Representative traces in response to current injection steps (−200, +60, +120 pA). Rheobase traces are shown in black. (I) High concentration of ethanol (50 mM, brown circles) and washout (gray circles) did not alter cell firing of SST INs compared to ACSF (open circles) (two-way ANOVA, F_{(2, 20)} treatment = 0.098, P = 0.9064, n = 11 cells, except washout: n = 10 cells, from 8 mice). Data in I-V plot are presented as mean ± s.e.m.

**Fig. 5.. Dose- and time-dependent effects of moderate to high doses of alcohol on SST IN and PN activity in the PL *in vivo*.**
(**A-D**) Normalized Ca²⁺ activity of L2/3 PNs (open circles) and SST INs (squares) after 0.5 g/kg (A), 1 g/kg (B), 2 g/kg (C) and 3 g/kg (D) alcohol injection. Dotted line indicates normalized Ca²⁺ baseline. (A) 0.5 g/kg EtOH (120 min: PN, 0.97 ± 0.02, SST, 1.3 ± 0.11, P = 0.0142). (B) 1 g/kg EtOH (60 min: PN, 0.99 ± 0.02, SST, 1.16 ± 0.05, P = 0.0398, 120 min: PN, 1.05 ± 0.02, SST, 1.23 ± 0.06, P = 0.0268). (C) 2 g/kg EtOH (10 min: PN, 1.20 ± 0.04, SST, 0.73 ± 0.04, P < 0.0001, 30 min: PN, 1.30 ± 0.06, SST, 0.88 ± 0.06, *P <* 0.0001, 60 min: PN, 1.25 ± 0.05, SST, 1.03 ± 0.05, P = 0.0390). (D) 3 g/kg EtOH (10 min: PN, 1.03 ± 0.03, SST, 0.53 ± 0.04, P <0.0001, 30 min: PN, 1.22 ± 0.04, SST, 0.61 ± 0.04, *P <* 0.0001, 60 min: PN, 1.28 ± 0.05, SST, 0.85 ± 0.07, *P <* 0.0001). Data are presented as means ± s.e.m. *P < 0.05, ****P < 0.0001, PN vs SST by two-way ANOVA and Sidak’s *post hoc* multiple comparison test. (**E-F**). Proportions of PNs (circles) and SST INs (squares) that show decreases (in blue) or increases (in red) in Ca²⁺ activity after 0.5 g/kg (E), 1 g/kg (F), 2 g/kg (G) and 3 g/kg (H) alcohol injection. Dotted line indicates mean proportion (6.5%) of neurons showing increases and decreases in Ca²⁺ activity after saline injection. Responsive neurons (%) as the proportion of neurons that show increases or decreases in Ca²⁺ activity 3 s.d. above or below the mean baseline activity.

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Alcohol reduces the activity of somatostatin interneurons in the mouse prefrontal cortex: A neural basis for its disinhibitory effect?

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Alcohol reduces the activity of somatostatin interneurons in the mouse prefrontal cortex: A neural basis for its disinhibitory effect?

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