Three experiments investigated the conditions under which electrolytic lesions of the dorsolateral periaqueductal grey (dlPAG) facilitate conditioned defensive freezing in the rat (Rattus norvegicus). Experiment 1 found that dlPAG lesions placed before context-shock pairings facilitated conditioned defensive freezing with massed but not distributed shock. No such effect was found in Experiment 2, when the lesions were placed after context-shock pairings. Experiment 3 found that dlPAG lesions facilitated subsequent conditioning with massed but not a single shock. In addition, no differences in sensitivity to thermal or shock pain were evident in lesioned and unlesioned rats. Taken together, these results are consistent with the suggestion that dlPAG activation interferes with the processing of contextual cues during association formation.
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http://dx.doi.org/10.1080/02724990143000126 | DOI Listing |
Pflugers Arch
August 2012
Department of Animal Morphology and Physiology, São Paulo State University-(UNESP FCAV), Jaboticabal, SP, Brazil.
The periaqueductal gray (PAG) is a midbrain structure directly involved in the modulation of defensive behaviors. It has direct projections to several central nuclei that are involved in cardiorespiratory control. Although PAG stimulation is known to elicit respiratory responses, the role of the PAG in the CO(2)-drive to breathe is still unknown.
View Article and Find Full Text PDFNeurosci Lett
February 2009
Neuroscience Research Center, Shahid Beheshti University, M.C., P.O. Box 19615-1178, Tehran, Iran.
The periaqueductal gray (PAG) and nucleus cuneiformis (CnF), like the rostral ventromedial medulla, have functional roles in descending pain-inhibitory pathway related to morphine antinociception. There is not any evidence concerning the role of different regions of the PAG on antinociceptive effect of morphine administered into the CnF in pain modulatory system. In the present study, we investigate whether electrolytic lesion of dorsolateral periaqueductal gray (dl-PAG) influence the analgesic effect of morphine microinjected into the CnF.
View Article and Find Full Text PDFIntegr Physiol Behav Sci
December 2005
University of California, Los Angeles, USA.
Defensive responses to a cat were observed in rats given excitotoxic lesions of the central nucleus of the amygdala (ACe), dorsolateral periaqueductal gray (dlPAG), ventral periaqueductal gray (vPAG), or sham lesions. Rats were placed adjacent to a compartment containing a cat. Sham-lesioned rats avoided the area nearest the cat and preferred the area furthest away from the cat.
View Article and Find Full Text PDFJ Chem Neuroanat
December 2005
Laboratory of Neuroanatomy and Neuropsychobiology, Department of Pharmacology, School of Medicine of Ribeirão Preto of the University of São Paulo FMRP-USP, Avenue of Bandeirantes, 3900, Ribeirão Preto SP 14049-900, Brazil.
In the present study, the functional neuroanatomy of nigrotectal-tectonigral pathways as well as the effects of central administration of opioid antagonists on aversive stimuli-induced responses elicited by electrical stimulation of the midbrain tectum were determined. Central microinjections of naloxonazine, a selective mu(1)-opiod receptor antagonist, in the mesencephalic tectum (MT) caused a significant increase in the escape thresholds elicited by local electrical stimulation. Furthermore, either naltrexone or naloxonazine microinjected in the substantia nigra, pars reticulata (SNpr), caused a significant increase in the defensive thresholds elicited by electrical stimulation of the continuum comprised by dorsolateral aspects of the periaqueductal gray matter (dlPAG) and deep layers of the superior colliculus (dlSC), as compared with controls.
View Article and Find Full Text PDFBrain Res Bull
December 2003
Laboratório de Psicobiologia, FFCLRP, Campus USP, Av Bandeirantes 3900, 14049-901, Ribeirão Preto, SP, Brazil.
Electrical stimulation of the dorsal regions of the periaqueductal gray (PAG) leads to defensive reactions characterized as freezing and escape responses. Until recently it was thought that this freezing behavior could be due to the recruitment of neural circuits in the ventrolateral periaqueductal gray (vlPAG), while escape would be mediated by other pathways. Nowadays, this view has been changing mainly because of evidence that freezing and escape behaviors thus elicited are not altered after lesions of the vlPAG.
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