Lesion of the ventral periaqueductal gray reduces conditioned fear but does not change freezing induced by stimulation of the dorsal periaqueductal gray - PubMed
Lesion of the ventral periaqueductal gray reduces conditioned fear but does not change freezing induced by stimulation of the dorsal periaqueductal gray
D M Vianna et al. Learn Mem. 2001 May-Jun.
Abstract
Previously-reported evidence showed that freezing to a context previously associated with footshock is impaired by lesion of the ventral periaqueductal gray (vPAG). It has also been shown that stepwise increase in the intensity of the electrical stimulation of the dorsal periaqueductal gray (dPAG) produces alertness, then freezing, and finally escape. These aversive responses are mimicked by microinjections of GABA receptor antagonists, such as bicuculline, or blockers of the glutamic acid decarboxylase (GAD), such as semicarbazide, into the dPAG. In this work, we examined whether the expression of these defensive responses could be the result of activation of ventral portion of the periaqueductal gray. Sham- or vPAG electrolytic-lesioned rats were implanted with an electrode in the dPAG for the determination of the thresholds of freezing and escape responses. The vPAG electrolytic lesions were behaviorally verified through a context-conditioned fear paradigm. Results indicated that lesion of the vPAG disrupted conditioned freezing response to contextual cues associated with footshocks but did not change the dPAG electrical stimulation for freezing and escape responses. In a second experiment, lesion of the vPAG also did not change the amount of freezing and escape behavior produced by microinjections of semicarbazide into the dPAG. These findings indicate that freezing and escape defensive responses induced by dPAG stimulation do not depend on the integrity of the vPAG. A discussion on different neural circuitries that might underlie different inhibitory and active defensive behavioral patterns that animals display during threatening situations is presented.
Figures

Schematic drawing of target brain sites. (A) Representative ventral periaqueductal gray lesion. (B) Sites of stimulation electrodes in the dorsal periaqueductal gray. Sham-lesion animals submitted to electrical (ο) or chemical stimulation (⋆). vPAG-lesion animals submitted to electrical (·) or chemical stimulation (★), respectively.

(A) Aversive thresholds determined in rats bearing (hatched columns) or not bearing (sham-open columns) electrolytic lesion of the vPAG. (B) Percentage of time spent freezing by rats with sham (hatched columns) or vPAG (open columns) lesions during 6 min. Pre refers to the baseline period; Post, to the testing session 24 h after conditioning. N = 8 for all groups, except for the freezing threshold (lesion = 8, control = 7).

(A) Freezing and escape behaviors induced by microinjections of semicarbazide (8.0 μg/0.2μL) into the dPAG in rats bearing (hatched columns) or not bearing (open columns) electrolytic lesion of the vPAG. N = 9 for both groups.
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