Thalamus & related systems最新文献

The involvement of the thalamus in infectious diseases of the nervous system has been hitherto rather neglected by investigators in clinical and basic neuroscience, despite numerous reports indicating that the thalamus, and territories within this region, can be attacked by different types of microbes. This topic is here reviewed. First, an overview is provided on general principles of spread of microbes to the brain (through peripheral nerves, or through the blood or cerebrospinal fluid) and their interactions with neurons and immune cells to cause acute, transient or persistent infections. Examples are given on how non-cytolytic infections can cause long-lasting disturbances in synaptic activities and neuronal networks as a result of a “hit-and-run” mechanism, or as an effect of factors released in the microenvironment to control the neuronal infection. Emerging data on how molecules functioning at the “immunological synapse” (the site of contact between immune cells and target infected cells) may affect nervous system synapses are pointed out. An account is then given of clinical and experimental infections of the thalamus caused by viruses (rabies and herpes viruses, influenza A virus, flaviviruses, HIV virus), the parasite Toxoplasma gondii, and prions. The implications and consequences of the attack of these microbes to the thalamus are discussed. Of special interest is the potential persistence of latent infections in thalamic neurons, which could cause disturbances of neuronal functions in the absence of overt structural lesions. Altogether these data recall attention on the pathogenesis and consequences of acute and persistent infections in the mammalian thalamus.

The intrinsic electrophysiological properties of medial geniculate body (MGB) neurons and their responses to noise bursts/pure tones were examined in the pentobarbital anesthetized guinea pig through intracellular recording. Discharge rate was calculated in the absence of acoustic stimuli over varied membrane potentials which were changed by intracellular injection of current or through automatic drifting. The non-acoustically-driven firing rate was 45.8±23.3 Hz (mean±S.D., n=8) at membrane potentials of −45 mV, 30.6±19.4 Hz (n=14) at −50 mV, 18.0±12.9 Hz (n=14) at −55 mV, and significantly decreased to 5.7±7.4 Hz at −60 mV, and to 0.7±1.5 Hz (n=10) at −65 mV (ANOVA, P<0.001). The maximum non-acoustically-driven rate observed in the present study was 160 Hz. The auditory responsiveness of the MGB neurons was examined at membrane potentials over a range of −45 to −75 mV: the higher the membrane potential, the greater the responsiveness and vice versa. A putative non-low-threshold calcium spike (non-LTS) burst was observed in the present study. It showed significantly longer inter-spike intervals (11.6±6.0 ms, P<0.001, t-test) than those associated with the putative LTS bursts (6.7±2.4 ms, P<0.001, t-test). The dependence of the temporal structure of the spikes/spike bursts on the stimulus may provide insight into the temporal coding of sound information in the auditory system.

The basic electrophysiological properties and responses to serotonin of thalamocortical (TC) neurons in the ferret, cat, and monkey pulvinar were compared. Morphologically, thalamocortical neurons in these three species were similar, except for the presence of beaded dendrites in many monkey neurons. In all three species, the neurons exhibited two distinct firing modes: single spike activity and low threshold Ca²⁺-spike mediated bursting. However, in monkeys, the low threshold Ca²⁺ spikes were followed by a prominent 50–100 ms afterhyperpolarization that could result in the generation of an additional rebound Ca²⁺ spike. The application of 5-HT to thalamocortical neurons in cat and monkey pulvinar resulted in a depolarization and an increase in membrane conductance through an enhancement of the hyperpolarization-activated cation current, I_h, apparently through the activation of 5-HT₇ receptors. In contrast, the application of serotonin to ferret pulvinar neurons resulted in a prominent hyperpolarization, owing to an increase in membrane potassium conductance. In monkey and ferret, application of serotonin could result in barrages of IPSPs in thalamocortical neurons. These results indicate that there are significant species-dependent differences in both the electrophysiological and pharmacological properties of pulvinar thalamocortical neurons.

The goal of the present study was to determine the ascending sources to the pre-supplementary motor area (pre-SMA) in macaque monkeys using multiple labeling techniques. We labeled the pallidothalamic projections using biotinylated dextran amine (BDA) and the cerebellothalamic projections using wheatgerm agglutinin conjugated to horseradish peroxidase. The pre-SMA thalamocortical projections neurons were also labeled using cholera toxin subunit b following identification of the pre-SMA by location, and by movements evoked by intracortical microstimulation. The extent of pre-SMA was later confirmed by identifying characteristics from Nissl cytoarchitecture and SMI-32 immunoreactivity. Thalamic nuclear boundaries were based on Nissl cytoarchitecture, acetylcholinesterase chemoarchitecture and Cat-301 immunoreactivity. Cerebellothalamic afferents were distributed predominantly to ventral lateral posterior nucleus (VLp), including medial and dorsal VLp, while the pallidothalamic afferents projected more rostrally to ventral lateral anterior nucleus (VLa) and ventral anterior nucleus (VA). The pre-SMA thalamocortical projection neurons were primarily found in VA and medial VLp. However, scattered cells were also found in VLa, dorsal VLp, central lateral nucleus (CL) and mediodorsal nucleus (MD). Scattered pre-SMA projecting cells overlapped foci of cerebellar label in medial VLp. Additionally, limited overlap of pre-SMA cells and pallidothalamic labeling was found in caudal VA. These findings suggest that the pre-SMA is uniquely positioned to integrate ascending basal ganglia and cerebellar information after a relay from VA and medial VLp. These anatomical findings are consistent with the recent hypothesis that the pre-SMA acts as the coordinator of visual and motor loops in motor learning [J. Cogn. Neurosci. 13 (2001) 626].

The terminals formed by the corticothalamic axons are of two types, small and giant endings. This dual mode of corticothalamic projection has been found to be consistent across species (mouse, rat, cat, monkey) and across systems (visual, auditory, somatosensory and motor). In the monkey, this dual mode of projection has been demonstrated for the motor system in the case of the primary motor cortical area, the supplementary motor area and the caudal part of the dorsal premotor cortex. Based on biotinylated dextran amine anterograde tracing experiments, a similar dual mode of termination morphology was found here for corticothalamic axons originating from the other three distinct sub-divisions of the premotor cortex. Furthermore, the pattern of arrangement of giant endings originating from the premotor cortex was found to be similar to that from the supplementary motor area but different to that from the primary motor cortex.

Sleep deprivation impairs alertness and cognitive performance, and these deficits suggest decreases in brain activity and function, particularly in the prefrontal cortex, a region subserving alertness, attention, and higher-order cognitive processes and in the thalamus, a subcortical structure involved in alertness and attention. To substantiate this premise, we characterized the effects of 24, 48, and 72 h of progressive sleep deprivation on brain activity by assessing regional cerebral metabolic rate for glucose (CMRglu) during complex cognitive task performance in 17 young, normal, healthy male volunteers using positron emission tomography (PET) and ${}^{18}\text{Fluoro}$-2-deoxyglucose (${}^{18}\text{FDG}$). The results of prolonged sleep deprivation, 48 and 72 h, are reported here. Compared to rested baseline (RB), global CMRglu decreased by 6% at 48 and 72 h sleep deprivation (SD) and approximated the 8% decrease seen at 24 h SD. Absolute and relative regional CMRglu decreased at 48 and 72 h SD primarily in the prefrontal and parietal cortices and in the thalamus, the same areas that showed decreases at 24 h SD. Compared to 24 h SD, relative regional CMRglu decreased further in the prefrontal cortex and dorsal thalamus at 48 and 72 h, and at 72 h SD in a limited area of medial visual cortex. Relative regional CMRglu increased in lateral superior occipital cortices, lingual and fusiform gyri, anterior cerebellum, and in primary and supplementary motor cortices at 48 and 72 h SD, indicating a rebound CMRglu activity response from 24 h SD. Polysomnographic monitoring confirmed that subjects were awake. Behavioral outcomes showed continuing decreases in alertness, cognitive performance, and saccadic velocity (a measure of oculomotor response) with prolonged sleep deprivation. Progressive decreases in relative CMRglu values in prefrontal, thalamic, and primary visual areas were correlated positively with the impairments in cognitive performance and saccadic velocity across the 72 h sleep deprivation period. Relative thalamic activity was also correlated with the alterations in alertness. The prefrontal and thalamic regions were positively correlated, suggesting that sleep deprivation impacted these areas together as a functional network.

We propose that the decreases in CMRglu induced in the prefrontal-thalamic network by prolonged sleep deprivation underlie the decline in alertness and cognitive performance and signify the brain’s involuntary progression toward sleep onset, while the increases in visual and motor areas express the brain’s exertion of voluntary control to remain awake and perform. This ex