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In cats with pretrigeminal brainstem transections, reversible inactivation of the primary visual cortex by cooling results in changes of the magnitude of response and spatio-temporal structure of receptive fi elds of neurons from lateral geniculate and perigeniculate nuclei (LGNd and PGN; Waleszczyk et al. 2005). Since cortical inactivation changes also the spontaneous activity of these thalamic neurons, we hypothesized that cortical feedback affects their membrane potential. Both types of investigated cells displayed two modes of activity: a tonic mode, during depolarization; and a burst mode, when the cell is hyperpolarized. In this report we investigated the effect of elimination of cortical feedback by cooling on the temporal pattern of the spontaneous "bursty" activity of single neurons in LGNd and PGN. During such reversible inactivation of areas 17 and 18, in both LGNd and PGN cells, spontaneously occurring bursts exhibited longer interspike intervals (ISIs) and lower number of spikes, while the average burst duration remained unchanged. Longer ISIs suggest that cortical feedback infl uences not only visual responsiveness of thalamic neurons, but also temporal pattern of their spontaneous fi ring, in line with the hypothesis of a tonic cortical modulation of their membrane potential. Supported by the Ministry of Science and Higher Education grant COST/127/2007.
In laboratory animals, exposure to the enriched environment (EE) induces broad range of modifications in nerve cells at both molecular and anatomical levels. EE also improves animal’s cognitive performance in learning and memory tasks. Despite some progress in revealing the effects of EE on synaptic transmission in the hippocampus, scant and inconsistent data are available on the impact of EE on synaptic properties in the neocortex. The aim of the present study was to examine the influence of the EE exposure on neuronal properties in layer IV of the barrel cortex. Twenty five days old mice (bred under standard laboratory conditions) were put for two weeks to the enriched environment (i.e. to bigger cage with playing tools: tunnels, ladders, a running wheel, spatial maze box and with a set of objects of different shape, made from various fabrics). Control mice were housed in standard laboratory cages during the same period of time. Next, we prepared brain slices containing the barrel cortex and performed visually guided whole-cell recordings from excitatory layer IV neurons within barrels B-D. The results were compared between control and EE-exposed animals. We found that EE experience increased the spontaneous firing rate of excitatory layer IV cells. This phenomenon seems to be due to stronger excitatory synaptic input to these neurons, because both frequency and amplitude of spontaneous excitatory postsynaptic currents were bigger after EE exposure, while kinetic properties of spontaneous inhibitory postsynaptic currents as well as intrinsic excitability remained unchanged. Our results indicate that EE selectively enhances excitatory transmission within the cortical representation of whiskers. The research was supported by the Ministry of Science and Higher Education “PolPostDoc” grant PBZ/MNiSW/07/2006/09 to GY.
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.
The second order somatosensory thalamic nucleus (posteromedial nucleus, PoM) receives excitatory projection from layer VI of somatosensory cortex. While it is known that layer VI cortical input to first order, ventrobasal nucleus (VB) is modulated by cholinergic projections from the brainstem, no such data exists concerning the PoM nucleus. In order to study if layer VI corticothalamic transmission to PoM is also modulated we used patch-clamp recording in thalamocortical slices from the rat's brain. Excitatory postsynaptic potentials (EPSPs) were evoked in PoM cells by trains of 5 electrical pulses at 20 Hz frequency applied to corticothalamic fibers. After carbachol was applied to mimic activation of the cholinergic neuromodulatory system corticothalamic EPSP amplitudes were reduced, while facilitation of EPSP amplitudes was enhanced for each next pulse in the series. Such cholinergic control of layer VI corticothalamic synapses in PoM may be used as gain modulator for the transfer of the peripheral sensory information to the cortex.
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