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Research article summary (published 30 Dec 1989):

Pharmacological and anatomical analysis of fear conditioning.

Full Abstract

The potentiated startle paradigm measures conditioned fear by an increase in the amplitude of a simple reflex (the acoustic startle reflex) in the presence of a cue previously paired with shock. This paradigm offers a number of advantages as an alternative to most animal tests of fear or anxiety, since it involves no operant and is reflected by an enhancement rather than a suppression of ongoing behavior. Lesion and electrical stimulation studies on fear-potentiated startle and startle increased by electrical stimulation of the amygdala are being used to define the neural pathways necessary for a visual conditioned stimulus to alter the acoustic startle reflex. The current working hypothesis is that the conditioned stimulus activates the central nucleus of the amygdala through a pathway involving the lateral geniculate nucleus and insular cortex. The central nucleus of the amygdala may then project directly to the acoustic startle pathway, modulating the startle response. More work has to be done to define conclusively the relevant neural pathways involved in fear-potentiated startle. Nonetheless, by combining behavioral, anatomical, physiological, and pharmacological approaches, it will be possible to determine each step along the pathway that mediates the ability of a stimulus signaling fear to alter behavior. Once the exact structures are delineated, it should be possible to determine the neurotransmitters that are released during a state of fear and how this chemical information is relayed along these pathways to affect behavior. Eventually, this approach should help to determine where plastic changes take place along these pathways to mediate the conditioned effects that are being measured and the biochemical processes that are involved.

 

Author information

Author/s: Davis, M (M);

Affiliation: Department of Psychiatry, Ribicoff Research Facilities of the Connecticut Mental Health Center, Yale University School of Medicine, New Haven 06508.

Grants: MH-00004 (Agency:NIMH NIH HHS) ; MH-41928 (Agency:NIMH NIH HHS) ; NS-18033 (Agency:NINDS NIH HHS)

Journal and publication information

Publication Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.; Review

Journal: NIDA research monograph (NIDA Res Monogr), published in UNITED STATES. (Language: eng)

Reference: 1990-; vol 97 (issue ) : pp 126-62

Dates: Created 1991/01/09; Completed 1991/01/09; Revised 2007/11/14;

PMID: 2247135, status: MEDLINE (last retrieval date: 2/18/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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