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|Title:||Modulation of the thalamocortical projections on different layers of auditory cortex in guinea pigs||Authors:||Wang, Ningqian||Degree:||Ph.D.||Issue Date:||2009||Abstract:||The goal of this study was to understand the spontaneous neuronal activities and acoustic responses of neurons in the primary auditory cortex (AI), and the modulation of different divisions of the medial geniculate body (MGB) on different layers of the auditory cortex (AC) especially AI, through in vivo intracellular recordings and/or extracellular recordings in adult urethane-anesthetized guinea pigs. One hundred and eighty nine neurons/units in AC, distributed among all six cortical layers, were recorded intracellularly and/or extrcellularly. Thirty-one of forty intracellular recorded neurons (77.50 %) and one hundred and thirty of one hundred and forty nine extracellular recorded units (87.25%) showed excitatory responses to a noise burst stimulus applied to the contralateral ear of the animals. The extracellularly recorded neurons showed synchronized spikes with the excitatory postsynaptic potential (EPSP), action potential (AP) and/or rhythmic oscillation of the intracellularly recorded neurons. The rhythmic oscillations evoked by the acoustic stimuli were predominantly in the spindle frequency band (14.77 +- 5.26 Hz) and had a long latency (75.37 +- 26.15 ms). Acoustic responses appeared among the auditory cortical layers in a general sequence from the deep layers to the superficial layers. A number of neurons in upper sublayer I and lower sublayer II responded first. Then layers IV, III, and VI responded, while finally layers I, II and V responded (P < 0.05). The direct, short latency projection from dorsal cochlear nucleus (DCN) to MGm and the projection from MGm to different layers of AC may explain why layer VI, upper sublayer I and lower sublayer II were activated first by the acoustic stimuli (Anderson et al., 2004; Anderson et al., 2006). The neuronal responses in Al to electrical stimulation applied to different divisions of the MGB were recorded intracellularly and/or extracellularly. A stimulation electrode array containing three electrodes was implanted into the MGB, targeted to the medial and ventral divisions (MGm and MGv). The stimulation sites in different divisions of MGB and extracellular recording sites in AC were confirmed by electrical lesions. Intracellularly recorded neurons were labeled with Neurobiotin after physiological recordings. Neurons in the AC showed spontaneous discharges, with occasional oscillatory activity. Similar to the acoustic stimuli, electrical stimulation of different MGB divisions evoked synchronized neuronal responses in AC layers. Neurons in layer I of Al were predominantly modulated by electrical stimulation of the MGm. Electrical stimulation of different areas of the MGm had different effects on layer I neurons. Stimulation of some areas of the MGm increased the MP of layer I neurons, inhibited the spontaneous oscillation, and changed the neuronal activity. Stimulation of other areas of the MGm decreased the MP to tonic discharging or decreased the discharging rate of APs. This two-direction modulatory effect that different areas of the MGm have on layer I may be involved in the maintenance of the state of layer I neuronal activity. In auditory cortical layers II and III, more neurons responded to the electrical stimulation applied to MGm than MGv. Layers II and III responded to the thalamic electrical stimulation differently. Electrical stimulation of MGv induced long delayed oscillations or short delayed AP, followed by long lasting oscillations on layer II neurons. Similar long delayed oscillation was also observed on layer III neurons following electrical stimulation of MGv. The sequence of thalamic stimulation-induced oscillations was the same as that of the acoustic response, from bottom to upper layers. The MGm stimulation induced EPSP/AP followed by rhythmic oscillation on layer III neurons had similar latencies to their acoustic responses while layer II neurons had shorter delayed response. The difference may be related to the activation of different projections from MGm to cortical layer III maybe via layer I when MGm was stimulated electrically (Andersen et al., 1980; Huang and Winer, 2000; Lee and Winer, 2008a). Acoustic responses could be inhibited or prolonged by thalamic electrical stimulation applied 20 or 50 ms before the acoustic stimuli. This is due to the lower excitabilities of the neurons, since thalamic electrical stimulation induced EPSP/AP or oscillaiton. Spontaneous neuronal activity in layers I, II and III were always inhibited by the electrical stimulation of MGm. GABAergic neurons in cortical layers I and II were likely involved in this process. However, spontaneous activity of some neurons in layers IV and V could be changed from tonic discharging to rhythmic oscillation by the electrical stimulation of MGm. The present results indicate there is a functional segregation of the parallel pathways from the MGv and MGm to the AC. The thalamocortical projection from the MGv is the major pathway of auditory information, while the projection from the MGm is likely modulatory. The pathway from the MGm could regulate the general arousal of the auditory cortex. A fast feedforward modulation of the upper layers of the auditory cortex through the MGm pathway might enable the preparation of the auditory cortex to receive the auditory information forwarded from the MGv.||Subjects:||Hong Kong Polytechnic University -- Dissertations.
Medial geniculate body.
|Pages:||138 leaves : ill. (some col.) ; 30 cm.|
|Appears in Collections:||Thesis|
View full-text via https://theses.lib.polyu.edu.hk/handle/200/3722
Citations as of May 22, 2022
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