PURPOSE: The ascending reticular activating system (ARAS) is responsible for regulation of consciousness. In this study, using diffusion tensor imaging (DTI), we attempted to reconstruct the thalamocortical projections between the intralaminar thalamic nuclei and the frontoparietal cortex in normal subjects. METHODS: DTI data were acquired in 24 healthy subjects and eight kinds of thalamocortical projections were reconstructed: the seed region of interest (ROI) - the intralaminar thalamic nuclei and the eight target ROIs - the medial prefrontal cortex, dorsolateral prefrontal cortex, ventrolateral prefrontal cortex, orbitofrontal cortex, premotor cortex, primary motor cortex, primary somatosensory cortex, and posterior parietal cortex. RESULTS: The eight thalamocortical projections were reconstructed in each hemisphere and the pathways were visualized: projections to the prefrontal cortex ascended through the anterior limb and genu of the internal capsule and anterior corona radiata. Projections to the premotor cortex passed through the genu and posterior limb of the internal capsule and middle corona radiata; in contrast, projections to the primary motor cortex, primary somatosensory cortex, and posterior parietal cortex ascended through the posterior limb of the internal capsule. No significant difference in fractional anisotropy, mean diffusivity, and fiber volume of all reconstructed thalamocortical projections was observed between the right and left hemispheres (p>0.05). CONCLUSION: We reconstructed the thalamocortical projections between the intralaminar thalamic nuclei and the frontoparietal cortex in normal subjects. We believe that our findings would be useful to clinicians involved in the care of patients with impaired consciousness and for researchers in studies of the ARAS.
Anisotropy ; Brain* ; Cerebral Cortex* ; Consciousness ; Diffusion Tensor Imaging ; Extremities ; Healthy Volunteers ; Humans* ; Internal Capsule ; Intralaminar Thalamic Nuclei* ; Motor Cortex ; Parietal Lobe ; Prefrontal Cortex ; Somatosensory Cortex ; Thalamus

It has been suggested that epileptic seizures can be interrupted by deep brain stimulation (DBS) of various deep brain structures which may exert a therapeutic control on seizure generators or correspond to ictal onset zone themselves. Several groups have used DBS in drug-resistant epilepsy cases for which resective surgery cannot be applied. The promising subcortical brain structures are anterior and centromedian nucleus of the thalamus, subthalamic nucleus, and other nuclei to treat epilepsy in light of previous clinical and experimental data. Recently two randomized trials of neurostimulation for controlling refractory epilepsy employed the strategies to stimulate electrodes placed on both anterior thalamic nuclei or near seizure foci in response to electroencephalographically detected epileptiform activity. However, the more large-scale, long-term clinical trials which elucidates optimal stimulation parameters, ideal selection criteria for epilepsy DBS should be performed before long.
Anterior Thalamic Nuclei ; Brain ; Deep Brain Stimulation ; Electrodes ; Epilepsy ; Intralaminar Thalamic Nuclei ; Light ; Patient Selection ; Seizures ; Subthalamic Nucleus ; Thalamus

OBJECTIVETo examine the antagonization of phentolamine against the effects of norepinephrine (NE) on the activity of pain-related neurons in the parafascicular nucleus of morphine-dependent rats.

METHODSElectric impulses were applied as nociceptive stimulus to the right sciatic nerve of morphine-dependent rats, and the discharges of the pain-related neurons in the parafascicular nucleus were recorded by extracellular recording method with glass microelectrodes.

RESULTSIntracerebroventricular injection of norepinephrine resulted in the inhibition of evoked response of the pain-excited neurons as well as the excitation of evoked response of the pain-inhibiting neurons. Both the inhibitory effect on the electric discharges of the pain-excited neurons and the excitatory effect on the pain-inhibiting neurons of norepinephrine were almost completely blocked by intracerebroventricular administration of phentolamine.

CONCLUSIONPhentolamine antagonizes the inhibitory effect of norepinephrine on the activity of pain-related neurons in the parafascicular nucleus in morphine-dependent rats, and norepinephrine may play an important role in the integration of the pain signal through the alpha-receptors.

Animals ; Drug Antagonism ; Electrophysiology ; Intralaminar Thalamic Nuclei ; cytology ; drug effects ; Neurons ; drug effects ; Norepinephrine ; antagonists & inhibitors ; pharmacology ; Pain ; physiopathology ; Phentolamine ; pharmacology ; Rats ; Rats, Wistar

The present study was designed to investigate the function and mechanism of high-frequency stimulation (HFS) of the parafascicular nucleus (PF) used as a therapeutic approach for Parkinson's disease (PD). PD rat model was built by injecting 6-hydroxydopamine (6-OHDA) into the substartia nigra pars compacta of adult male Sprague-Dawley rats. Using the ethological methods, we examined the effect of electrical stimulation of PF on the apomorphine-induced rotational behavior in PD rats. Moreover, Electrophysiological recordings were made in rats to investigate the effects of electrical stimulation of PF on the neuronal activities of the subthalamic nucleus (STN) and the ventromedial nucleus (VM). Our results showed that one week after HFS (130 Hz, 0.4 mA, 5 s) of PF, there was significant improvement in apomorphine-induced rotational behavior in PD rats. HFS of PF caused an inhibition of the majority of neurons (84%) recorded in the STN in PD rats. The majority of cells recorded in the VM of the thalamus responded to the HFS with an increase in their unitary discharge activity (81%). These effects were in a frequency-dependent manner. Only stimulus frequencies above 50 Hz were effective. Furthermore, employing microelectrophoresis, we demonstrated that glutamatergic and GABAergic afferent nerve fibers converged on the same STN neurons. These results show that the HFS of PF induces a reduction of the excitatory glutamatergic output from the PF which in turn results in deactivation of STN neurons. The reduction in tonic inhibitory drive from the basal ganglia induces a disinhibition of activity in the VM, a motor thalamic nucleus. In conclusion, the results suggest that HFS of PF may produce a therapeutic effect in PD rats, which is mediated by the nuclei of PF, STN and VM.
Action Potentials ; physiology ; Animals ; Electric Stimulation ; Intralaminar Thalamic Nuclei ; physiopathology ; Male ; Neurons ; physiology ; Parkinson Disease ; physiopathology ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Subthalamic Nucleus ; physiopathology ; Ventral Thalamic Nuclei ; physiopathology

To study the antiepileptic mechanism of vagus nerve stimulation (VNS), we used the methods of in situ hybridyzation and image analysis to detect the expression of NMDAR1 mRNA and GABAA receptor alpha 1 subunit mRNA (GABAAR alpha 1 mRNA) in the thalamic reticular nuclus. The results show that the NMDAR1 mRNA expression of rats administered pentylenetetrazole(PTZ) is higher than that of control group. By treating with VNS, it decreased. On the contrary, the expression of GABAAR alpha 1 mRNA in the thalamic reticular nuclus of PTZ group rats is lower than that of control group. For rats treated with VNS, it increased. Therefore, it is concluded that VNS may reduce the excitability of cerebral cortices by depressing the activities of glutamic acid receptors (GluR) and by promoting the activities of gamma-aminobutyric acid receptors(GABAR) in thalamic reticular nuclus. So the formation and development of seizures are inhibited.
Animals ; Electric Stimulation Therapy ; methods ; Epilepsy ; chemically induced ; therapy ; Intralaminar Thalamic Nuclei ; metabolism ; Male ; Pentylenetetrazole ; toxicity ; RNA, Messenger ; biosynthesis ; Rats ; Rats, Wistar ; Receptors, GABA-A ; biosynthesis ; genetics ; Receptors, N-Methyl-D-Aspartate ; biosynthesis ; genetics ; Vagus Nerve ; physiopathology

Nitric oxide(NO) is thought to play an important role in development and plasticity of brain. In this study, we aimed to examine the expression of neuronal NOS and NADPH-diaphorase (NADPH-d) activity in the developing rat brain. The results show that there is a great variation in the time of appearance of the earliest NOS containing cells depending on their location: At the 15th embryonic day weakly stained cells were present in caudate-putamen, and neurons in the sensory trigeminal nucleus and the solitary nucleus displayed an intense staining. The NOS neurons in orbital neocortex, bed nucleus of stria terminalis, paraventricular hypothalamic nucleus, lateral hypothalamic area and mammillary body appeared first at the 18th embryonic day. The supraoptic nucleus and superior and inferior colliculi also weakly labeled at the 18th embryonic day, At the loth embryonic day, positive cells appeared in horizontal limb of diagonal band, anterior olfactory nucleus and parafascicular thalamic nucleus. In the cerebellum, weak NOS staining was present in fibers and cells situated below Purkinje cert layer. The Purkinje cell layer displayed a weak, rather diffuse activity throughout the cerebellum at postnatal day 0. At the 4th postnatal day. the reaction product in the Purkinje cell layer became more distinct. At the 10th postnatal day, the inner part of molecular layer became populated by NOS positive basket cells, and the reaction products on the Purkinje cells began to disappear. The present results showed that NOS in the rat brain is expressed in different populations of neurons at different stages of development. This expression pattern of NOS suggests that NO may play a role in the developmental remodelling of the mammalian brain.
Animals ; Brain* ; Cerebellum ; Extremities ; Hypothalamic Area, Lateral ; Inferior Colliculi ; Intralaminar Thalamic Nuclei ; Mamillary Bodies ; Neocortex ; Neurons ; Nitric Oxide Synthase* ; Nitric Oxide* ; Orbit ; Paraventricular Hypothalamic Nucleus ; Plastics ; Purkinje Cells ; Rats* ; Septal Nuclei ; Solitary Nucleus ; Supraoptic Nucleus ; Trigeminal Nuclei