Altered noradrenergic function is associated with alcoholism. Reduced
brain norepinephrine (NE) concentrations and beta-adrenergic receptor
supersensitivity following chronic alcohol consumption suggest a reduc
ed level of noradrenergic neurotransmission. To further elucidate the
reason for changes in noradrenergic function, we determined the number
of melanin-containing noradrenergic neurons in the locus coeruleus (L
C) postmortem from 11 controls and 7 alcoholics. Controls did not have
a known history of psychiatric or neurologic disorders and were drug-
free by toxicological screen. The diagnosis of alcohol-depend ence was
based on DSM-III-R criteria. Alcoholics differed from controls in hav
ing 23% fewer LC neurons (control: 43,472 +/- 1,021; alcoholic: 33,398
+/- 2184; P < 0.0005) and 46% lower density of neurons (control: 1,22
7 +/- 89 cells per mm(3); alcoholic: 663 +/- 94 cells per mm(3); P = 0
.001). The reduction in neurons was bilateral and throughout the middl
e third of the LC. The two groups did not differ with respect to LC le
ngth (control: 16.1 +/- 0.6 mm; alcoholic: 15.3 +/- 0.9 mm; P = 0.47)
or total LC volume (control: 37.3 +/- 2.8 mm(3); alcoholic: 46.5 +/- 4
.2 mm(3); P = 0.09). Changes in noradrenergic neurotransmission in alc
oholics may be due to fewer noradrenergic neurons in the locus coerule
us and may contribute to memory loss and depression, common consequenc
es of alcoholism.