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Depending on the level of arousal identical sensory stimuli result in different neuronal and behavioral responses. This effect may depend on thalamo-cortical network mechanism directing sensory information to the cortex either through a first-order or higher-order thalamic relay nuclei. Using multichannel chronic recordings from the thalamo-cortical part of the somatosensory system of behaving rats, we have shown that in low arousal the information flow reaches primary sensory (S1) cortex mainly via first-order ventral posteromedial (VPM) nucleus and that a higher-order relay – posterior medial nucleus (PoM), receives this information later, via feedback input from S1. In contrast, during high arousal substantial part of the sensory information flow to S1 is passed also through the PoM nucleus. We propose that direct opening of peripheral inputs transmission through PoM follows the release of this nucleus from feed-forward inhibition exerted by zona incerta. This mechanism may serve to supply fast sensory information about salient stimuli not only to S1 but also, in parallel, to higher order sensory and motor cortices in order to facilitate behavioral reactions. Although such mechanism may lower the accuracy of detailed stimulus feature processing but may play a vital role during dangerous situations. Research was supported by the National Science Centre grant N N401 533040.
Local fi eld potential (LFP) – the result of summed postsynaptic potentials from cell populations – reveal the most characteristic neural activity at the recording site in the brain. Thus LFPs are well suited for study of neural networks, specifi cally those involved in processing of sensory information. We propose a method of assessing functional brain connectivity through LFP analysis. The method is applied to multi-site signals representing potentials evoked by a repeated, stereotyped stimulus. In spite of a stereotyped stimulus, all responses are different due to, inter alia, ongoing background activity of the brain and this trial-to-trial variability is utilized in our analysis. The method is based on calculation of correlations between trial-to-trial LFP variations at every post-stimulus latency at every recoding site. The results show how neuronal activities at different sites and latencies correspond to activation at other sites with a given time delays. We used this method to analyze the functional connectivity in thalamocortical network involved in processing of somatosensory (vibrissal) information in non-anaesthetised rat. One result is that the cortical activation at 25–50 ms post-stimulus correlates with thalamic LFP measured at 50–150 ms post stimulus, thus implying this late latency thalamic activity depends on a corticothalamic feedback. Apart from raw LFP, the method is applicable to results of various decomposition methods of brain signals (PCA, ICA, etc.)
BACKGROUND AND AIMS: Thalamic relay cells constitute important node of reciprocal sensory processing which is highly dependent on current behavioral demands realized by brainstem neuromodulatory systems. In these experiments, performed on rats’ thalamic brain slices, we have investigated cholinergic influence on synaptic transmission from cortical layer 6 to the posteromedial thalamic nucleus (PoM). METHODS: Neuronal membrane potentials and currents were recorded with whole-cell patch-clamp method and general cholinergic agonist carbachol was added to the bath in order to mimic cholinergic activation. Excitatory postsynaptic responses were evoked in PoM cells by repetitive trains of 5 electrical stimuli delivered at 20 Hz through bipolar electrode placed at the corticothalamic fibers in the internal capsule. RESULTS: In all investigated cells, consecutive postsynaptic responses in the train showed pronounced frequency facilitation (i.e. increase in amplitude). Carbachol substantially decreased postsynaptic response amplitudes, but at the same time it enhanced the magnitude of frequency facilitation. Moreover, the amplitudes of each consecutive postsynaptic potential in the train were characterized by much higher trial-to-trial coefficient of variation (SD/ mean). These effects suggested presynaptic action of carbachol. To prove this, we measured the failure rate of excitatory postsynaptic currents in PoM cells in response to minimum stimulation of corticothalamic fibers. CONCLUSION: The substantial increase of failure rate in the presence of carbachol supports the hypothesis that observed effects of cholinergic modulation relay on decreased probability of transmitter release from presynaptic site. This research and SN were supported by the European Union Regional Development Fund through the Foundation for Polish Science within the frames of International PhD Program in Neurobiology.
Higher order posteromedial thalamic nucleus of the rat (PoM) receives cholinergic (Ach) and noradrenergic (NA) neuromodulatory projections originating from the brain stem. With a whole-cell patch-clamp method we investigated influence of these neuromodulators on membrane potential of PoM neurons in the thalamic slices. Ach (carbachol) or NA (norepinephrine) agonists were added to the bath to mimic the activation of appropriate neuromodulatory system. Both agonists induced slow depolarization of membrane potential by about 9 mV. However, carbachol but not norepinephrine substantially enhanced amplitude of membrane potential fluctuations in the frequency range from 8 to 500 Hz (reaching more than two-fold elevation between 25–180 Hz). These carbachol induced fluctuations were not blocked neither by manual membrane repolarization to the control level, nor by the blockage of GABA-A receptors. Our results suggest that this increase of fluctuation strength might result mainly from activation of muscarinic receptors. This research and SN were supported by the European Union Regional Development Fund through the Foundation for Polish Science within the frames of International PhD Program in Neurobiology.
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