Pathologic role of neuronal nicotinic acetylcholine receptors in epileptic disorders: implication for pharmacological interventions.

Accumulating evidence suggests that neuronal nicotinic acetylcholine receptors (nAChRs) may play a key role in the pathophysiology of some neurological diseases such as epilepsy. Based on genetic studies in patients with epileptic disorders worldwide and animal models of seizure, it has been demonstrated that nAChR activity is altered in some specific types of epilepsy, including autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) and juvenile myoclonic epilepsy (JME). Neuronal nAChR antagonists also have antiepileptic effects in pre-clinical studies.

Extrastriatal D2-like receptors modulate basal ganglia pathways in normal and Parkinsonian monkeys.

According to traditional models of the basal ganglia-thalamocortical network of connections, dopamine exerts D2-like receptor (D2LR)-mediated effects through actions on striatal neurons that give rise to the "indirect" pathway, secondarily affecting the activity in the internal and external pallidal segments (GPi and GPe, respectively) and the substantia nigra pars reticulata (SNr). However, accumulating evidence from the rodent literature suggests that D2LR activation also directly influences synaptic transmission in these nuclei. To further examine this issue in primates, we combined in vivo electrophysiological recordings and local intracerebral microinjections of drugs with electron microscopic immunocytochemistry to study D2LR-mediated modulation of neuronal activities in GPe, GPi, and SNr of normal and MPTP-treated (parkinsonian) monkeys.

Impairment of retention but not acquisition of a visuomotor skill through time-dependent disruption of primary motor cortex.

Learning a visuomotor skill involves a distributed network which includes the primary motor cortex (M1). Despite multiple lines of evidence supporting the role of M1 in motor learning and memory, it is unclear whether M1 plays distinct roles in different aspects of learning such as acquisition and retention. Here, we investigated the nature and chronometry of that processing through a temporally specific disruption of M1 activity using single-pulse transcranial magnetic stimulation (TMS).

A computational model of how an interaction between the thalamocortical and thalamic reticular neurons transforms the low-frequency oscillations of the globus pallidus.

In Parkinson's disease, neurons of the internal segment of the globus pallidus (GPi) display the low-frequency tremor-related oscillations. These oscillatory activities are transmitted to the thalamic relay nuclei. Computer models of the interacting thalamocortical (TC) and thalamic reticular (RE) neurons were used to explore how the TC-RE network processes the low-frequency oscillations of the GPi neurons.

Effects of the activity of the internal globus pallidus-pedunculopontine loop on the transmission of the subthalamic nucleus-external globus pallidus-pacemaker oscillatory activities to the cortex.

Resting tremor is the most specific sign for idiopathic Parkinson' disease. It has been proposed that parkinsonian tremor results from the activity of the central oscillators. One of the hypotheses, which have been proposed about the possible principles underlying such central oscillations, is the subthalamic nucleus (STN)-external globus pallidus (GPe)-pacemaker hypothesis.

Discussion on the reverberatory model of short-term memory: a computational approach.

Up to now a number of models have been proposed to underlie memory formation in the central nervous system. Two of these models are the reverberatory circuit model and the other one the self-feedback loop model. This paper considers these two models regarding their ability to preserve neural activity and to hold information.

Transmission of the subthalamic nucleus oscillatory activity to the cortex: a computational approach.

Parkinsonian tremor is most likely due to oscillatory neuronal activities of central oscillators such as the subthalamic nucleus (STN)-external segment of the globus pallidus (GPe) pacemaker within the basal ganglia (BG). Activity from the central oscillator is proposed to be transmitted via transcortical pathways to the periphery. A computational model of the BG is proposed for simulating the transmission of the STN oscillatory activity to the cortex, based closely on known anatomy and physiology of the BG.