The cholinergic stimulation of the central amygdala modifying the tonic immobility response and antinociception in guinea pigs depends on the ventrolateral periaqueductal gray.
Tonic immobility (TI), also known as death feigning or animal hypnosis, is a reversible state of motor inhibition that is triggered by postural inversion and/or movement restraining maneuvers but also by repetitive stimulation and pressure on body parts. Our previous studies demonstrated that cholinergic stimulation of the central amygdala (CEA) decreases the duration of TI in guinea pigs. Some reports have demonstrated that electrical or chemical stimulation of the CEA promotes antinociception. Evidence suggests that the CEA performs part of its functions by means of a connection with the ventrolateral periaqueductal gray (vlPAG). In the current study, we investigated the participation of a possible functional and anatomical CEA-vlPAG connection in guinea pigs in the regulation of the TI response and antinociception. Our results showed that the functional CEA-vlPAG connection is essential for the participation of the CEA in the modulation of TI and of antinociception. The reversible exclusion of the vlPAG by means of microinjection of 2% lidocaine blocked the inhibitory effect on TI duration and the antinociceptive effect, as determined by a decrease of the vocalization index (VI) obtained with the administration of carbachol (2.7 nmol/0.2 microl) into the CEA. On the other hand, the exclusion of the CEA by lidocaine did not block the antinociception or the increase in TI induced by microinjection of CCh into the vlPAG. Finally, microinjection of the retrograde neurotracer Fast Blue into the CEA or into the vlPAG demonstrated the existence of a reciprocal anatomical connection between the CEA and vlPAG.
Leite-Panissi
Christie Ramos Andrade
CR
Department of Physiology, Faculty of Medicine of Ribeirão Preto, University of São Paulo, 14049-900 Ribeirão Preto, SP, Brazil.
Coimbra
Norberto Cysne
NC
Menescal-de-Oliveira
Leda
L
D000578:Amidines / Q000378:metabolism; D000679:Amygdala / Q000187:drug effects* / Q000502:physiology; D000779:Anesthetics, Local / Q000008:administration & dosage / Q000494:pharmacology; D000818:Animals; D001931:Brain Mapping; D002217:Carbachol / Q000008:administration & dosage / Q000494:pharmacology*; D018679:Cholinergic Agonists / Q000008:administration & dosage / Q000494:pharmacology*; D005456:Fluorescent Dyes / Q000378:metabolism; D006168:Guinea Pigs; D007103:Immobilization / Q000502:physiology*; D008012:Lidocaine / Q000008:administration & dosage / Q000494:pharmacology; D008297:Male; D008845:Microinjections; D009433:Neural Inhibition / Q000502:physiology; D009434:Neural Pathways / Q000502:physiology; D010147:Pain Measurement; D010487:Periaqueductal Gray / Q000033:anatomy & histology / Q000502:physiology*; D010812:Physical Stimulation; D011930:Reaction Time; D013997:Time Factors; D014828:Vocalization, Animal
D000578:Amidines; D000779:Anesthetics, Local; D018679:Cholinergic Agonists; D005456:Fluorescent Dyes; C031455:diamidino compound 253-50; D002217:Carbachol; D008012:Lidocaine