Continuous white noise exposure during and after auditory critical period differentially alters bidirectional thalamocortical plasticity in rat auditory cortex in vivo

Abstract

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.

Chronic Fluoxetine Treatment Suppresses Plasticity (Long-Term Potentiation) in the Mature Rodent Primary Auditory CortexIn Vivo

“…Previous work has shown that local application of an NMDA receptor antagonist directly in A1 of rats blocks the induction of LTP elicited by MGN stimulation in vivo [22, 34]. It is well documented that the precise subunit composition of the NMDA receptor exerts profound effects on LTP induction by altering the level of calcium influx across the postsynaptic membrane.…”

Spine formation and maturation in the developing rat auditory cortex

“…Immediately following hearing onset, P11–P14, is the auditory critical period, a restricted window of time during which the functional tonotopic organization of the auditory cortex can be manipulated by environmental auditory stimuli (Zhang et al, 2001; Nakahara et al, 2004; Norena et al, 2006; de Villers-Sidani et al, 2007). For example, constant exposure to a specific sound frequency during the second and third postnatal week results in its overrepresentation in the auditory tonotopic map (Zhang et al, 2001); elimination of patterned auditory input during the second and third postnatal weeks by constant exposure to broadband noise results in an immature tonotopic map (Chang and Merzenich, 2003; Speechley et al, 2007). Expression of the NR1 subunit of the N-methyl-D-aspartic acid receptor (NMDAR) increases rapidly between P7 and P14 (Lu et al, 2007), suggesting changes in synaptic physiology during the critical period.…”

Physiological consequences of selective suppression of synaptic transmission in developing cerebral cortical networks in vitro: Differential effects on intrinsically generated bioelectric discharges in a living ‘model’ system for slow-wave sleep activity

“…Burst firing in particular has recently been postulated to preferentially drive those target neurons the intrinsic postsynaptic oscillatory membrane tendencies of which match intraburst firing frequencies in the presynaptic input (Izhikevich, 2002;Izhikevich et al, 2003;Sasaki et al, 2006;Villacorta and Panetsos, 2005). Spontaneous bioelectric discharge levels appear to be able throughout life, furthermore, to determine the vector of activitydependent plasticity, thus acting as a 'meta-plasticity' factor favoring potentiation over depression when background firing is strong and the reverse when it is weak (e.g., Castro-Alamancos et al, 1995;Milner et al, 2004;Speechley et al, 2007;Xiao et al, 1995). Perhaps surprisingly, high levels of ongoing neuronal activity can, in addition, reduce the ability of stimulation to induce any plastic reaction at all (Crochet et al, 2006).…”