Continuous white noise exposure during and after auditory critical period differentially alters bidirectional thalamocortical plasticity in rat auditory cortex in vivo.
Long-term potentiation (LTP) and long-term depression are thought to mediate activity-dependent brain plasticity but their role in the development of the thalamocortical auditory system in vivo has not been investigated. In adult urethane-anaesthetized rats, theta-burst stimulation of the medial geniculate nucleus produced robust LTP (40% amplitude enhancement) of field post-synaptic evoked potentials recorded in the superficial layers of the primary auditory cortex. Low-frequency (1-Hz) stimulation resulted in transient depression ( approximately 40%) of field post-synaptic evoked potential amplitude. Both LTP and synaptic depression were found to be dependent on cortical N-methyl-d-aspartate receptors. Thalamocortical plasticity was also assessed after continuous white noise exposure, thought to arrest auditory cortex maturation when applied during the critical period of post-natal primary auditory cortex development. Rats housed in continuous white noise for the first 50 days of post-natal life exhibited greater LTP ( approximately 80%) than controls reared in unaltered acoustic environments. The protocol used to elicit depression also resulted in substantial LTP ( approximately 50%) in white noise-reared animals. Adults housed in white noise for the same length of time exhibited normal LTP but displayed greater and persistent levels of synaptic depression ( approximately 70%). Thus, the absence of patterned auditory stimulation during early post-natal life appears to retard sensory-dependent thalamocortical synaptic strengthening, as indicated by the preferential readiness for synaptic potentiation over depression. The fact that the same auditory manipulation in adults results in synapses favouring depression demonstrates the critical role of developmental stage in determining the direction of synaptic modification in the thalamocortical auditory system.
Speechley
William J
WJ
Department of Psychology, Queen's University, Kingston, Ontario, K7L 3N6, Canada.
Hogsden
Jennifer L
JL
Dringenberg
Hans C
HC
D000161:Acoustic Stimulation; D000375:Aging / Q000502:physiology*; D000818:Animals; D000831:Animals, Newborn; D001303:Auditory Cortex / Q000033:anatomy & histology / Q000187:drug effects / Q000254:growth & development*; D001306:Auditory Pathways / Q000033:anatomy & histology / Q000254:growth & development*; D001307:Auditory Perception / Q000502:physiology*; D003423:Critical Period, Psychological; D004558:Electric Stimulation; D005072:Evoked Potentials, Auditory / Q000187:drug effects / Q000502:physiology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology; D005260:Female; D005829:Geniculate Bodies / Q000033:anatomy & histology / Q000254:growth & development*; D017774:Long-Term Potentiation / Q000187:drug effects / Q000502:physiology; D036881:Long-Term Synaptic Depression / Q000187:drug effects / Q000502:physiology; D008297:Male; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D020318:Rats, Long-Evans; D011930:Reaction Time / Q000187:drug effects / Q000502:physiology; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors / Q000378:metabolism; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology
D018691:Excitatory Amino Acid Antagonists; D016194:Receptors, N-Methyl-D-Aspartate