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Updated: Jun 18, 2025
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Published on: February 25, 2011
Nitric oxide-signalling affects panic-like defensive behaviour and defensive antinociception neuromodulation in the
Renato Leonardo de Freitas1, Renata Moreira Acunha2, Fernando René Bendaña-Córdoba2
1Laboratory of Neuroanatomy and Neuropsychobiology, Department of Pharmacology, Ribeirão Preto Medical School of the University of São Paulo (FMRP-USP), Av. Bandeirantes, 3900, Ribeirão Preto, São Paulo 14049-900, Brazil; Laboratory of Neurosciences of Pain & Emotions and Multi-User Centre of Neuroelectrophysiology, Department of Surgery and Anatomy, FMRP-USP, Av. Bandeirantes, 3900, Ribeirão Preto, São Paulo 14049-900, Brazil; Institute of Neuroscience and Behaviour (INeC) Ophidiarium, Av. Bandeirantes, 3900, Ribeirão Preto, São Paulo 14040-901, Brazil; Department of Experimental Medicine, University of Campania "Luigi Vanvitelli", Naples 80138, Italy; Institute of Natural Sciences, Federal University of Alfenas (UNIFAL-MG), Str. Gabriel Monteiro da Silva, 700, Alfenas, 37130-000 Minas Gerais (MG), Brazil.
Rationale:
The prelimbic division (PrL) of the medial prefrontal cortex (mPFC) is a key structure in panic.
Objectives:
To evaluate the role of nitric oxide (NO) in defensive behaviour and antinociception.
Methods:
Either Nω-propyl-L-arginine (NPLA) or Carboxy-PTIO was microinjected in the PrL cortex, followed by hypothalamic treatment with bicuculline. The exploratory behaviours, defensive reactions and defensive antinociception were recorded. Encephalic c-Fos protein was immunolabelled after escape behaviour.
Results:
NPLA (an inhibition of nNOs) decreased panic-like responses and innate fear-induced antinociception. The c-PTIO (a membrane-impermeable NO scavenger) decreased the escape behaviour. PrL cortex pre-treatment with c-PTIO at all doses decreased defensive antinociception. c-Fos protein was labelled in neocortical areas, limbic system, and mesencephalic structures.
Conclusion:
The NPLA and c-PTIO in the PrL/mPFC decreased the escape behaviour and defensive antinociception organised by medial hypothalamic nuclei. The oriented escape behaviour recruits neocortical areas, limbic system, and mesencephalic structures. These findings suggest that the organisation of defensive antinociception recruits NO-signalling mechanisms within the PrL cortex. Furthermore, the present findings also support the role of NO as a retrograde messenger in the PrL cortex during panic-like emotional reactions.
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