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. Author manuscript; available in PMC: 2010 Oct 31.
Published in final edited form as: Neurosci Lett. 2007 Jun 2;421(3):270–274. doi: 10.1016/j.neulet.2007.05.052

Table 1.

Endocannabinoids and N-acetylethanolamine levels in the hypothalamus, amygdala, caudate-putamen and prefrontal cortex of rats exposed to alcohol for 24 h and their corresponding controls

HYPOTHALAMUS AMYGDALA

Compound levels
(pmol/g tissue)
Control Alcohol Control Alcohol
AEA 30.06 ± 3.46 20.32 ± 2.46 * 53.18 ± 5.13 32.83 ± 3.14 **
2-AG 3311.7 ± 258.4 2659.1 ± 202.0 1935.8 ± 196.6 1744.5 ± 93.0
LEA 5.77 ± 0.98 4.40 ± 0.57 3.36 ± 0.60 6.09 ± 0.70 *
PEA 290.6 ± 14.2 249.5 ± 13.7 132.9 ± 12.5 104.1 ± 7.1
OEA 341.4 ± 27.9 267.4 ± 15.3 * 204.5 ± 25.6 164.9 ± 16.4
SEA 79.9 ± 5.1 65.1 ± 4.7 52.1 ± 2.6 37.2 ± 3.2 *


CAUDATE-PUTAMEN PREFRONTAL CORTEX

Compound levels
pmol/g tissue)
Control Alcohol Control Alcohol

AEA 25.6 ± 2.1 19.8 ± 1.3 * 16.7 ± 1.4 14.6 ± 0.6
2-AG 1022.6 ± 98.4 974.9 ± 56.7 558.7 ± 31.8 413.0 ± 15.4 ***
LEA 8.9 ± 3.1 5.2 ± 0.6 6.8 ± 1.2 5.1 ± 0.3
PEA 337.3 ± 10.9 293.8 ± 12.3 * 144.6 ± 2.8 134.9 ± 5.7
OEA 386.9 ± 22.3 293.1 ± 13.6 ** 240.9 ± 16.1 196.8 ± 9.2 *
SEA 65.7 ± 4.4 58.4 ± 1.7 38.2 ± 3.1 36.7 ± 1.1

Data are means ± SEM of 8 animals in the alcohol group and 4 in the control group. Values were assessed by the two-way (brain region × alcohol treatment) analysis of variance followed by the Student-Newman-Keuls test (*p0.05, **p<0.01 and ***p<0.001 versus the control group).