TY - JOUR
T1 - Deafferentation-induced apoptosis of neurons in thalamic somatosensory nuclei of the newborn rat
T2 - Critical period and rescue from cell death by peripherally applied neurotrophins
AU - Baldi, Alfonso
AU - Calia, Eustachio
AU - Ciampini, Alessandro
AU - Riccio, Massimo
AU - Vetuschi, Antonella
AU - Persico, Antonio M.
AU - Keller, Flavio
PY - 2000
Y1 - 2000
N2 - This study shows that unilateral transection of the infraorbital nerve (ION) in newborn (PO) rats induces apoptosis in the contralateral ventrobasal thalamic (VB) complex, as evidenced by terminal transferase-mediated deoxyuridine triphosphate-biotin nick end labelling (TUNEL) and electron miscroscopy. Double-labelling experiments using retrograde transport of labelled microspheres injected into the barrel cortex, followed by TUNEL staining, show that TUNEL-positive cells are thalamocortical neurons. The number of TUNEL-positive cells had begun to increase by 24 h postlesion, increased further 48 h after nerve section, and decreased to control levels after 120 h. Lesion-induced apoptosis in the VB complex is less pronounced if ION section is performed at P4, and disappears if the lesion is performed at P7. This time course closely matches the critical period of lesion-induced plasticity in the barrel cortex. Nerve growth factor (NGF) or brain-derived neurotrophic factor (BDNF), applied on the ION stump alone or in combination, are able to partially rescue thalamic neurons from apoptosis. Total cell counts in the VB complex of P7 animals that underwent ION section at PO confirm the rescuing effect of BDNF and NGF. Blockade of axonal transport in the ION mimics the effect of ION section. These data suggest that survival-promoting signals from the periphery, maybe neurotrophins, are required for the survival of higher-order neurons in the somatosensory system during the period of fine-tuning of neuronal connections. We also propose that anterograde transneuronal degeneration in the neonatal rat trigeminal system may represent a new animal model for studying the pathways of programmed cell death in vivo.
AB - This study shows that unilateral transection of the infraorbital nerve (ION) in newborn (PO) rats induces apoptosis in the contralateral ventrobasal thalamic (VB) complex, as evidenced by terminal transferase-mediated deoxyuridine triphosphate-biotin nick end labelling (TUNEL) and electron miscroscopy. Double-labelling experiments using retrograde transport of labelled microspheres injected into the barrel cortex, followed by TUNEL staining, show that TUNEL-positive cells are thalamocortical neurons. The number of TUNEL-positive cells had begun to increase by 24 h postlesion, increased further 48 h after nerve section, and decreased to control levels after 120 h. Lesion-induced apoptosis in the VB complex is less pronounced if ION section is performed at P4, and disappears if the lesion is performed at P7. This time course closely matches the critical period of lesion-induced plasticity in the barrel cortex. Nerve growth factor (NGF) or brain-derived neurotrophic factor (BDNF), applied on the ION stump alone or in combination, are able to partially rescue thalamic neurons from apoptosis. Total cell counts in the VB complex of P7 animals that underwent ION section at PO confirm the rescuing effect of BDNF and NGF. Blockade of axonal transport in the ION mimics the effect of ION section. These data suggest that survival-promoting signals from the periphery, maybe neurotrophins, are required for the survival of higher-order neurons in the somatosensory system during the period of fine-tuning of neuronal connections. We also propose that anterograde transneuronal degeneration in the neonatal rat trigeminal system may represent a new animal model for studying the pathways of programmed cell death in vivo.
KW - Brain-derived neurotrophic factor
KW - Electron microscopy
KW - Fluorescent microspheres
KW - Infraorbital nerve
KW - Nerve growth factor
KW - Stereology
KW - Thalamocortical neuron
KW - TUNEL
KW - Vinblastine
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UR - http://www.scopus.com/inward/citedby.url?scp=0033931256&partnerID=8YFLogxK
U2 - 10.1046/j.1460-9568.2000.00119.x
DO - 10.1046/j.1460-9568.2000.00119.x
M3 - Article
C2 - 10947807
AN - SCOPUS:0033931256
VL - 12
SP - 2281
EP - 2290
JO - European Journal of Neuroscience
JF - European Journal of Neuroscience
SN - 0953-816X
IS - 7
ER -