|
TABLE 1.
Phenomena in the course of mood disorders modeled by kinding and behavioral
sensitization
|
|||
| Descriptors | Kinding | Sensitization | Phenomenona |
| Stressor vulnerability | + + | + + | Initial stressors early in
development may be
without effect but predispose to greater reactivity upon rechallenge |
| Stressor precipitation | + + | + + | Later stress may precipitate full-blown episode |
| Conditioning may be involved | ¾ | + + | Stressors may become more symbolic |
| Episode autonomy | + + | ¾ | Initially-precipitated episodes
may occur
spontaneously |
| Cross-sensitization with
stimulants |
¾ | + + | Comorbidity with drug abuse
may work in both
directions (affective illness {ewc MVIMG, MVIMAGE,!biarrow.BMP} drug abuse) |
| Vulnerability to relapse | + + | + + | S and K demonstrate long-term
increases in
responsivity |
| Episodes may
a. become more severe
b. show more rapid onsets |
+ + |
+ +
+ + |
S and K both show behavioral evolution in severity or stages Hyperactivity and stereotypy show more rapid onsets |
| Anatomical and biochemical
substrates evolve |
+ + | + + | K memory-trace evolves from unilateral to bilateral |
| IEGs involved | + + | + + | IEGs, such as c-fos induced |
| Alterations in gene
expression occur |
+ + | + + | IEGs may change gene expression,
especially of
peptides over long time domains |
| Change in synaptic
microstructure occurs |
+ + | ¾ | Neuronal sprouting and cell
loss indicate structural
changes |
| Pharmacology differs as a
function or stage as a evolution |
+ + | + + | K differs as a function of
stage; S differs as a
function of development versus expression |
a S, sensitization; K, kinding.
published 2000