Neonatal development of projections to the basolateral amygdala from prefrontal and thalamic structures in rat.
Recently an animal model for neurodevelopmental disorders has been developed. In this model the effects of an early neonatal [postnatal day 7 (Pd7)] basolateral amygdala lesion are compared with the effects of a lesion later in life (Pd21). Early amygdala damage results in enduring behavioral disturbances that become more manifest after puberty. These disturbances were not present in animals lesioned at Pd21. Accordingly it was postulated that the early damage may affect the neuroanatomical and neurochemical organization and functioning of other brain structures. To obtain information on the innervation of the amygdala during normal development, we used the retrograde tracer fluoro-gold. From neonatal day 7 onward (studied until Pd19), retrogradely labeled cells were present in the caudal and rostral thalamus, the substantia innominata, and the prefrontal but not the caudal cortex. Development of the topography of the projecting cells differed substantially for the thalamic regions and substantia innominata vs. the cortical regions. In thalamic regions and substantia innominata, no changes were observed during the studied period (Pd7-Pd9). In the prefrontal cortex, the number of labeled cells increased (from Pd7 to Pd13), the topography of the location of the cells changed from unilateral to bilaminar (from Pd9 to Pd13), and the number of subareas in which the cells were present increased (from Pd7 to Pd13). In the caudal cortex, relatively few cells were present up to Pd15. From Pd17 onward, a bilaminar topography of the location of the cells was observed. These data provide information on the circuitry that may be involved in the aberrant neurodevelopment of neonatally amygdala-lesioned rats, which has been proposed as an animal model for neurodevelopmental psychopathological disorders.
Bouwmeester
Hans
H
Rudolf Magnus Institute of Neuroscience, Department of Pharmacology and Anatomy, University Medical Center Utrecht, 3584 CG Utrecht, The Netherlands.
Smits
Kim
K
Van Ree
Jan M
JM
D000375:Aging / Q000502:physiology*; D000679:Amygdala / Q000166:cytology / Q000254:growth & development* / Q000502:physiology; D000818:Animals; D000831:Animals, Newborn; D002454:Cell Differentiation / Q000502:physiology; D004195:Disease Models, Animal; D005260:Female; D005456:Fluorescent Dyes; D007150:Immunohistochemistry; D008297:Male; D001523:Mental Disorders / Q000473:pathology / Q000503:physiopathology; D009434:Neural Pathways / Q000166:cytology / Q000254:growth & development* / Q000502:physiology; D009474:Neurons / Q000166:cytology / Q000502:physiology; D017397:Prefrontal Cortex / Q000166:cytology / Q000254:growth & development* / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar / Q000033:anatomy & histology / Q000254:growth & development* / Q000502:physiology; D013266:Stilbamidines; D013788:Thalamus / Q000166:cytology / Q000254:growth & development* / Q000502:physiology
C049774:2-hydroxy-4,4'-diamidinostilbene, methanesulfonate salt; D005456:Fluorescent Dyes; D013266:Stilbamidines