This Article  • References  • Full text PDF  • Reply to article  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Contact me when this article is cited  Related Content  • Similar articles in this journal  Social Bookmarking   What's this?

David L. Braff, MD; Mark A. Geyer, PhD
Department of Psychiatry, T-004 University of California, San Diego La Jolla, CA 92093

Arch Gen Psychiatry. 1991;48(4):380.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

In Reply.—

We would like to address the issue raised above. First, we did not mean to deify molecular biology. It is our belief that ultimately, molecular biological data will need to be translated into a brain-compatible language (eg, regional dopamine excess) to be understood.

Second, there is the broader issue of the role of dopamine transmission in patients with schizophrenia. In our own work, we do not endorse a simplistic "one neurotransmitter" theory of schizophrenic cognitive deficits. In fact, animal model data implicate a critical hippocampal—nucleus accumbens—ventral pallidal circuit that relies on multiple neurotransmitters at these various sites.^1-3 Dopamine is involved primarily in the nucleus accumbens, but the roles of -aminobutyric acid in the ventral pallidum, cholinergic, and/or noradrenergic systems in the hippocampus, as well as glutamate systems, point to the complexity of the circuit underlying the gating/inhibitory mechanisms.

Third, the statement that "the one known attribute that neuroleptic . . . [Full Text PDF of this Article]

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter     What's this?