Anatomical and physiological considerations in thalamic rhythm generation

Abstract

SUMMARYThe thalamus, known as the pacemaker for spindle rhythms in sleep, has several enabling features that promote such pacemaking. These include a circuitry that interconnects large groups of excitatory and inhibitory neurons, all of which are essentially capable of firing high-frequency`bursts' of discharges. Bursts in thalamic reticular neurons produce powerful inhibition in thalamic relay neurons, which leads to rebound excitation. The timing properties of the inhibition regulate the network activity by controlling rebound burst latency. Anatomical features within thalamus such as convergence and divergence determine the spread and synchronization of pacemaking activity. The anatomical basis of divergence, i.e. the degree of axonal arborization of elements within the thalamic circuit, can be functionally modified in a dynamic fashion by biochemical pathways that regulate the properties of synaptic release. These data suggest that it will be possible to therapeutically regulate the thalamus to modify not only the propensity to sleep but also forms of epilepsy that rely on similar thalamic circuitry.

Membrane Resonance in Bursting Pacemaker Neurons of an Oscillatory Network Is Correlated with Network Frequency

“…One exception has been thalamic neurons. The thalamus is composed of a conglomerate of nuclei involving neurons with significantly different properties and is believed by many researchers to be the pacemaker network for spindle rhythms during sleep (Huguenard, 1998). Neurons of the medial geniculate nucleus, for example, demonstrate a resonance peak at 1 Hz which is influenced by a T-type Ca current (Tennigkeit et al, 1997).…”

Neuronal Voltage-Gated Calcium Channels: Structure, Function, and Dysfunction

“…This causes a low-threshold calcium potential that facilitates the activation of voltage-gated sodium channels to give rise to a burst of action potentials (Alviñ a et al, 2009;Destexhe et al, 1998). This phenomenon is termed ''rebound bursting'' and is of critical importance for the output of many different types of neurons (Molineux et al, 2006), perhaps most notably in thalamocortical relay neurons and in thalamic reticular neurons (Huguenard, 1998;Ulrich and Huguenard, 1997) (Figure 3). It should also be noted that Cav1.3 calcium channels display a relatively hyperpolarized range of activation (Xu and Lipscombe, 2001), and given their dendritic localization, it is possible that these channels could act like T-type channels in regulating postsynaptic activity.…”

MicroRNA 132 alters sleep and varies with time in brain

“…miRNA-132 was selected because it varies with sleep loss (11) and with the time of day (7). Further, miRNA-132 is linked to circadian rhythm entrainment (7) and to dendritic modifications (51), processes associated with sleep regulation (15,19,23,35,47). First, we investigated the effects of intracerebroventricular (ICV) microinjections of preMIR-132; during the light phase, it decreased duration of non-rapideye-movement sleep (NREMS) and increased duration of rapid eye movement sleep (REMS).…”