Inhibition of substance P-induced defensive behavior via neurokinin-1 receptor antagonism in the central and medial but not basolateral nuclei of the amygdala in male Wistar rats
| Autor: | Gabriel Shimizu Bassi, Marcus Lira Brandão, Milene Cristina de Carvalho, Rafael Carvalho Almada |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
Male
0301 basic medicine Elevated plus maze Microinjections medicine.drug_class Neuropeptide Substance P Pharmacology Amygdala 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Neurochemical Neurokinin-1 Receptor Antagonists Tachykinin receptor 1 medicine Animals Maze Learning Receptor Biological Psychiatry Analgesics Behavior Animal Fear Receptors Neurokinin-1 Receptor antagonist Rats 030104 developmental biology medicine.anatomical_structure chemistry Vocalization Animal Neuroscience 030217 neurology & neurosurgery |
| Zdroj: | Progress in Neuro-Psychopharmacology and Biological Psychiatry. 77:146-154 |
| ISSN: | 0278-5846 |
| DOI: | 10.1016/j.pnpbp.2017.03.026 |
| Popis: | Rationale The production of unconditioned defensive behaviors has been related to the amygdala, a key component of the encephalic aversion system. Microinjection of the neuropeptide substance P (SP) in the amygdala elicits defensive behaviors via the activation of type 1 neurokinin (NK-1) receptors. However, no studies have investigated whether intra-amygdala SP/NK-1 mechanisms can elicit other types of defensive responses, such as antinociception and ultrasonic vocalizations (USVs). Methods The present study investigated the effects of SP-induced activation of the neurokininergic system in three main nuclei of the amygdala—basolateral (BLA), central (CeA), and medial (MeA) nuclei—in rats that were subjected to the elevated plus maze (EPM), tail-flick test, and USV recording. The effects of SP in these amygdaloid nuclei were challenged with combined injections of the NK-1 receptor antagonist spantide. Results The present study showed that SP injections in the CeA and MeA but not BLA exerted anxiogenic-like effects. In contrast to the CeA, the anxiogenic-like effects of SP in the MeA were not dependent on NK-1 mechanisms. In the tail-flick test, SP microinjections produced antinociceptive effects only in the MeA through NK-1 receptor activation. No USV emissions were detected after the SP microinjections. Conclusions The present study showed that NK-1 receptors in the CeA and MeA but not BLA are involved in defensive reactions to conditions of fear. The present results may provide a better understanding of the neurochemical mediation of fear states. |
| Databáze: | OpenAIRE |
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