Lidocaine blockade of amygdala output in fear-conditioned rats reduces Fos expression in the ventrolateral periaqueductal gray |
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| Affiliation: | 1. Department of Human Genetics, Leiden University Medical Center, Leiden, The Netherlands;2. Department of Endocrinology, Leiden University Medical Center, Leiden, The Netherlands;3. Department of Neurology, Leiden University Medical Center, Leiden, The Netherlands;4. Neurovascular Research Laboratory, Department of Radiology, MA General Hospital, Harvard Medical School, Charlestown, USA;5. Stroke Service and Neuroscience Intensive Care Unit, Department of Neurology, MA General Hospital, Harvard Medical School, Charlestown, USA;6. Department of Neuroscience and Pharmacology, University Medical Center Utrecht, Rudolf Magnus Institute of Neuroscience, Utrecht, The Netherlands;1. Institute of Neurological Sciences and Psychiatry, Hacettepe University, Ankara, Turkey;2. School of Medicine, Department of Psychiatry, Koç University & Research Center for Translational Medicine (KUTTAM), Koç University, İstanbul, Turkey;3. Neurophotonics Center, Boston University, Boston, MA, United States |
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| Abstract: | We showed recently that conditioned fear to context induces Fos expression in the ventrolateral periaqueductal gray [Neuroscience (1997) 78, 165–177]. Neurons in this region are thought to play an important role in the expression of freezing during conditioned fear. To test the possibility that this activation comes directly from the amygdala, we looked at changes in Fos expression after a unilateral blockade of the ventral amygdalofugal pathway with lidocaine. The pathway contains fibres originating from the central nucleus of the amygdala that project directly and mainly ipsilaterally to the ventrolateral periaqueductal gray. Conditioned fear was evoked by re-exposing rats to the same box in which they had previously received electric footshocks. The test re-exposure was preceded by a unilateral microinjection of lidocaine (2%, 0.5–1 μl; n=20) or saline (n=14). Lidocaine was also tested in non-conditioned animals (n=13). The results show that, when lidocaine was microinjected in the medial part of the central nucleus of the amygdala or along the ventral amygdalofugal pathway of conditioned rats, fear-induced Fos expression in the ventrolateral periaqueductal gray was reduced on the side ipsilateral to the injection (up to 37% reduction in comparison to the contralateral side). Ipsilateral reductions were also observed with saline, but they were weaker (maximum of 27% reduction). Fos expression remained low on both sides in the non-fear-conditioned animals injected with lidocaine. Finally, although freezing was only partly reduced in the conditioned animals unilaterally injected with lidocaine, it was significantly correlated to the ipsilateral reduction in Fos expression.This study provides direct evidence that the projection from the central nucleus of the amygdala to the ventrolateral periaqueductal gray is activated during fear and that it contributes to the Fos response of the ventrolateral periaqueductal gray. |
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