Calcium signalling in cortical and thalamic neurons of rats with streptozotocin-induced diabetes

Intracellular Ca²⁺ transients were measured with the use of a Ca²⁺-sensitive fluorescent indicator, fura-2, in neocortical and thalamic neurons in brain slices from control rats and rats with uncompensated streptozotocin-induced diabetes. The transients were evoked by high-potassium (50 mM)-induced membrane depolarization. The amplitude of depolarization-induced Ca²⁺ transients demonstrated a tendency to increase under diabetic conditions, beeing more expressed in cortical neurons compared with thalamic ones. The transients in cortical neurons from diabetic animals became also more susceptible to the blocking action of nifedipine (100μM) and less sensitive to Ni²⁺ (50μM), indicating that diabetic changes affect mostly Ca²⁺ transients triggered by high-voltage activated (L-type) calcium channels. The duration of a statistically significant increase was observed in the residual elevation of intracellular Ca²⁺ changes. However, a statistically significant increase was observed in the residual elevation of intracellular Ca²⁺ measured 60 sec after termination of membrane depolarization in both cortical and thalamic neurons, indicating alterations in the mechanisms that restore the resting level of Ca²⁺ in the cytosol. It is concluded that uncomensated insulin-dependent diabetes, which according to earlier data substantially alters calcium signalling in primary sensory neurons, also affects such signalling in the neurons of higher brain structures including the thalamus and cortex.     

The role of the thalamic ventrolateral nucleus in the cortical effect on the activity of vestibular neurons

Electrocoagulation of lateral vestibular nucleus (NVL) reduces inhibitory effect of the motor and somatosensory areas and enhances the inhibitory effect of limbic, vestibular, and orbital cortical areas. Facilitating effect was enhanced by electrostimulation of the motor area and reduced by the stimulation of other cortical areas. Following the coagulation of the NVL, the ascending afferent flow to the cortex seems to be reduced. This results in diminishing of the cortical neurones tone and readjusts the descending influences upon the NVL neurones activity.     

Low response variability in simultaneously recorded retinal, thalamic, and cortical neurons

The response of a cortical cell to a repeated stimulus can be highly variable from one trial to the next. Much lower variability has been reported of retinal cells. We recorded visual responses simultaneously from three successive stages of the cat visual system: retinal ganglion cells (RGCs), thalamic (LGN) relay cells, and simple cells in layer 4 of primary visual cortex. Spike count variability was lower than that of a Poisson process at all three stages but increased at each stage. Absolute and relative refractory periods largely accounted for the reliability at all three stages. Our results show that cortical responses can be more reliable than previously thought. The differences in reliability in retina, LGN, and cortex can be explained by (1) decreasing firing rates and (2) decreasing absolute and relative refractory periods.     

Network bursts in cortical cultures are best simulated using pacemaker neurons and adaptive synapses

One of the most specific and exhibited features in the electrical activity of dissociated cultured neural networks (NNs) is the phenomenon of synchronized bursts, whose profiles vary widely in shape, width and firing rate. On the way to understanding the organization and behavior of biological NNs, we reproduced those features with random connectivity network models with 5,000 neurons. While the common approach to induce bursting behavior in neuronal network models is noise injection, there is experimental evidence suggesting the existence of pacemaker-like neurons. In our simulations noise did evoke bursts, but with an unrealistically gentle rising slope. We show that a small subset of ‘pacemaker’ neurons can trigger bursts with a more realistic profile. We found that adding pacemaker-like neurons as well as adaptive synapses yield burst features (shape, width, and height of the main phase) in the same ranges as obtained experimentally. Finally, we demonstrate how changes in network connectivity, transmission delays, and excitatory fraction influence network burst features quantitatively.     

Double cortical control acting upon activities of intralaminar thalamic cells

We report the effects exerted by the cortex upon the intralaminar thalamic nucleic, as revealed by reversible blockade of the cortex with spreading depression in awake rats. Extracellular recordings of spontaneous activity were made simultaneously at thalamic and cortical sites. The effect of peripheral receptive field stimulation was to decrease activity of intralaminar thalamic cells. Cortical recordings revealed the cortical regions affected by spreading depression. Two type of cells were identified depending on the changes in their sensorial responses during the cortical spreading depression propagation. The first exhibited a tonic facilitating cortical control when the cortical spreading depression was located at A 8.0 to A 10.0. The second type exhibited a disappearance of the sensorial responses when cortical spreading depression was located at A 4.0 to A 8.0 and also displayed the tonic facilitating control. This indicates that two different identified cortical regions influenced the thalamic activity.     

Temperature sensitivity of the cholinergic response in cortical neurons of guinea pigs

A temperature change from 20 to 36 degrees C results in a significant increase of neuronal responses to iontophoretic application of acetylcholine in parietal cortex slices. The most intensive changes in cholinergic responses occurred in two temperature zones: 27-29 degrees C and 34-36 degrees C. Increase in the responses to acetylcholine accompany with increasing spontaneous spike activity.     

Threshold behavior in the initiation of hippocampal population bursts

Hippocampal population discharges such as sharp waves, epileptiform firing, and GDPs recur at long and variable intervals. The mechanisms for their precise timing are not well understood. Here, we show that population bursts in the disinhibited CA3 region are initiated at a threshold level of population firing after recovery from a previous event. Each population discharge follows an active buildup period when synaptic traffic and cell firing increase to threshold levels. Single-cell firing can advance burst onset by increasing population firing to suprathreshold values. Population synchrony is suppressed when threshold frequencies cannot be reached due to reduced cellular excitability or synaptic efficacy. Reducing synaptic strength reveals partially synchronous population bursts that are curtailed by GABA(B)-mediated conductances. Excitatory glutamatergic transmission and delayed GABA(B)-mediated signals have opposing feedback effects on CA3 cell firing and so determine threshold behavior for population synchrony.     

Depth sensitivity of binocular cortical neurons of behaving monkeys.

Activity of neurons if foveal striate and prestriate cortex of trained rhesus monkeys was recorded with metal microelectrodes. While animals fixated a small spot at a given fixation distance (38 or 57 cm), bright or dark bars moving across a frontoparallel plane were presented at different depths in a range of +/- 10 cm about the fixation distance. Almost all cells showed binocular interaction. Neurons with balanced ocularity (approximately equal monocular responses) usually facilitated each other and were tuned to depth around the plane of fixation often with inhibitory flanks nearer and further. Neurons with unbalanced ocularity either inhibited each other or had asymmetric depth sensitivity profiles, i.e. activation by stimuli in front and suppression by stimuli behind the fixation plane (near cells) or vice versa (far cells). Thus striate and prestriate cortex of the monkey contains four subsets of binocular cells which may contribute to depth perception.     

Effect of morphine on the sensitivity of cerebral cortical neurons to acetylcholine

Sensitivity of sensorimotor cortical neurons to microiontophoretically applied morphine and acetylcholine has been studied in the experiments on unanesthetized rabbits. The predominant reaction to morphine and acetylcholine was decrease and increase in the rate of neuronal impulse activity, respectively. There was no correlation in the responses to morphine and acetylcholine. Atropine failed to influence the morphine effect. When both drugs are simultaneously applied to neurons, morphine decreases both excitatory and inhibitory responses to acetylcholine. This effect of morphine may occur in the case when the drug is applied in doses which do not change spontaneous neuronal activity. On the contrary, excitatory effect of glutamic acid decreased only when morphine was applied in doses causing local anesthetic effect and decreasing background neuronal activity. It is suggested that morphine can exercise a modulating influence on choline receptors of cortical neurons.     

Effect of prostaglandins on the sensitivity of cerebral cortical neurons in rabbits to cholinoreceptor agonists

The effect of prostaglandins F2a and E2 on the reaction of rabbit's brain cortex neurons provoked by arecoline and nicotine (stimulators of M- and N-cholinereceptors) has been investigated by using a microionophoretic technique. As a rule, prostaglandin F2a decreased and prostaglandin E2 increased the effects of arecoline. Prostaglandins rarely changed the effect of nicotine. The data obtained confirms the supposition that prostaglandin F2a has inhibitory effects on the synthesis in neurons of the cyclical guanosinemonophosphate. Some hypothesis of the prostaglandins participation in integrative activity mechanisms of neurons are supposed.     

Cholinergic sensitivity as an index of the functional differences in cortical neurons in young and old rabbits]

Acetylcholine-sensitivity of motor cortex neurons was studied in the young and old rabbits. Muscarinic-type excitation in the neurons of old animals was revealed twice less frequently compared to the young ones. The age-related fall in the number of cholinoceptive neurons may be due to general decrease of neuronal activation in the motor cortex during aging. Changes in functional properties of motor cortex neurons with age may have a result that firing rate of movement related neurons becomes insufficient for the effective control of motor function.