title: Cardiovascular and behavioural responses to conditioned fear and restraint are not affected by retrograde lesions of A5 and C1 bulbospinal neurons.
abstract: The aim of this study was to test a possible role of A5 neurons in the expression of the pressor and tachycardic responses to conditioned fear and restraint, two forms of psychological stress. Previous Fos studies have shown that the C1 adrenergic neurons and spinally projecting neurons in the vasopressor region of the rostral ventrolateral medulla are not activated by these two stressors, suggesting that these cardiovascular changes may be mediated by other premotor sympathetic (presympathetic) cell groups. The same studies also revealed that the A5 noradrenergic group was one of the main presympathetic cell groups to be activated in response to these two stressors. Thus, we hypothesized that the A5 group could mediate these cardiovascular responses. Conditioned fear and restraint were tested in rats implanted with radiotelemetric probes before and after retrograde lesion with the selective toxin anti-dopamine-beta-hydroxylase-saporin bilaterally injected in the spinal cord at T2-T3. Six animals were selected that had the most extensive loss of spinally projecting catecholaminergic neurons: A5 (81%-95%) and rostral C1 (59%-86%, which would include most C1 bulbospinal neurons). However, despite this major loss of noradrenergic and adrenergic presympathetic neurons, the magnitude of the cardiovascular response to conditioned fear and restraint was the same before and after the lesion. Associated behavioural changes were not affected either. The results indicate that A5 presympathetic neurons are not essential for the expression of the tachycardic and pressor responses to conditioned fear and restraint. They also confirm that C1 bulbospinal neurons are not involved in these responses. The presympathetic neurons driving the tachycardic and pressor responses to conditioned fear and restraint must be elsewhere.
authors.affiliation: School of Medical Sciences, University of New South Wales, NSW 2052, Australia. dmvianna@unsw.edu.au
authors.forename: D M L
authors.initials: DM
authors.lastname: Vianna
authors.forename: P
authors.initials: P
authors.lastname: Carrive
mesh_terms: D000320:Adrenergic Fibers / Q000502:physiology* / Q000648:ultrastructure; D000818:Animals; D001522:Behavior, Animal / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D001933:Brain Stem / Q000166:cytology / Q000502:physiology*; D002320:Cardiovascular Physiological Phenomena; D002395:Catecholamines / Q000502:physiology; D003213:Conditioning, Psychological / Q000502:physiology; D003714:Denervation; D004525:Efferent Pathways / Q000166:cytology / Q000502:physiology*; D005239:Fear / Q000502:physiology*; D008297:Male; D009410:Nerve Degeneration / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology; D009498:Neurotoxins / Q000633:toxicity; D051381:Rats; D017208:Rats, Wistar; D012149:Restraint, Physical / Q000502:physiology / Q000523:psychology; D013116:Spinal Cord / Q000166:cytology / Q000502:physiology; D013315:Stress, Psychological / Q000503:physiopathology*; D013610:Tachycardia / Q000209:etiology / Q000503:physiopathology; D014661:Vasoconstriction / Q000502:physiology
chemical_list: D002395:Catecholamines; D009498:Neurotoxins