Thalamic Relay Nuclei Research Articles

Thalamic neuronal and EMG activity in psychogenic dystonia compared with organic dystonia

This is a retrospective analysis of thalamic neuronal and electromyogram activities between subjects with organic dystonia and a subject with psychogenic dystonia in whom a thalamotomy was carried out before the diagnosis of psychogenic dystonia was made. The signal-to-noise ratio in the lowest frequency band (dystonia frequency < 0.76 Hz) in the electromyogram was not significantly different by diagnosis or muscle. The coherence at dystonia frequency for wrist flexors X biceps electromyograms was significantly higher in organic dystonia, whereas the phase was not apparently different from zero for either diagnosis. In a thalamic pallidal relay nucleus (ventral oral posterior), neuronal firing rates were not apparently different between psychogenic and organic dystonia. The neuronal signal-to-noise ratio in ventral oral posterior was significantly higher in organic dystonia than in psychogenic dystonia, whereas both were greater than in controls with chronic pain. Spike X electromyogram coherence apparently was not different between psychogenic and organic dystonia. The proportion of thalamic cells responding to joint movements was higher in the cerebellar relay nucleus (ventral intermediate) of psychogenic dystonia than in organic dystonia. These results suggest that some features, such as firing rates and thalamic reorganization, are similar in psychogenic and organic dystonia. Other features differ, such as the coherence between the electromyograms from different muscles and the thalamic neuronal signal-to-noise ratio, which may reflect pathophysiological factors in organic dystonia. © 2011 Movement Disorder Society.

Vaginal allodynia as the presentation of a thalamic tumor

Central pain syndromes associated with damage to the thalamic sensory relay nuclei have been described predominantly in the stroke literature; however, pain syndromes associated with thalamic neoplasms are much less common. We describe a woman with dyspareunia secondary to vaginal allodynia as the presenting sign of a left thalamic juvenile pilocytic astrocytoma. Subsequent to an uneventful stereotactic biopsy, her vaginal allodynia progressed to hemi-body allodynia. We believe that this is the first reported case of isolated vaginal allodynia associated with a thalamic neoplasm or any other structural pathology of the central nervous system.Dyspareunia secondary to vaginal allodynia as the presenting sign of a left thalamic juvenile pilocytic astrocytoma is reported, in a rare case underscoring that thalamic pathology including neoplasms should be considered in evaluating patients with longstanding and unexplained pain syndromes.

Nozizeptives System

In order to transform a nociceptive stimulus into a painful perception, a highly specialized chain of structural and functional elements is necessary. This system comprises nociceptors in the periphery with specific molecular properties for differential coding of noxious submodalities, ascending and descending tracts that can control the input into the dorsal horn of the spinal cord as well as supraspinal processing that regulates the integration of nociceptive information with other sensory modalities and autonomic function. In this article, structures involved in nociceptive signal processing starting from the periphery up to spinal and cerebral structures are discussed in the order of their spatio-temporal activation sequence - as far as these are known. Already from the basis of the different receptor subtypes found on the thinly or unmyelinated nerve fibers in the periphery, the predominant principle of polymodality is demonstrated. Different input to the dorsal horn of the spinal cord by different nerve fiber populations to superficial and deep layers is explained, ascending tracts as well as descending systems capable of either facilitating or inhibiting the upstream flow of nociceptive information, together with their known transmitters. Finally, thalamic relay nuclei for sensory and nociceptive signals, as well as subcortical and cortical projection targets are discussed. To complete the current view of the nociceptive system, information from molecular biology and anatomic tracing studies as well as data from functional electrophysiologic cell recordings in animals and imaging studies in humans are assembled.

Selective Excitatory Actions of DNQX and CNQX in Rat Thalamic Neurons

The thalamic reticular nucleus (TRN) consists of GABA-containing neurons that form reciprocal synaptic connections with thalamic relay nuclei. Excitatory synaptic innervation of TRN neurons arises from glutamatergic afferents from thalamocortical relay neurons and deep layer corticothalamic neurons, and they produce excitation via both N-methyl-D-aspartate (NMDA) and non-NMDA receptors. Quinoxaline derivatives [e.g., 6,7-dinitroquinoxaline-2,3-dione (DNQX), 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX)] have routinely been used as non-NMDA receptor antagonists over the last two decades. In this study, we examined whether quinoxaline derivatives alter the intrinsic properties of thalamic neurons in light of recent findings indicating that these compounds can alter neuronal excitability in hippocampal and cerebellar neurons via transmembrane AMPA receptor (AMPAR) regulatory proteins (TARPs). Whole cell recordings were obtained from TRN and ventrobasal (VB) thalamic relay neurons in vitro. DNQX and CNQX produced a consistent depolarization in all TRN neurons tested. The depolarization persisted in tetrodotoxin and low Ca²+/high Mg²+ conditions, suggesting a postsynaptic site of action. In contrast, DNQX and CNQX produced little or no change in VB thalamocortical relay neurons. The nonspecific ionotropic glutamate receptor antagonist, kynurenic acid, and the selective AMPAR antagonist, 4-(8-methyl-9H-1,3-dioxolo[4,5-h][2,3]benzodiazepin-5-yl)-benzenamine hydrochloride, blocked the DNQX-mediated depolarizations. Our results indicate that the DNQX- and CNQX-mediated depolarizations are mediated by AMPAR but not kainate receptors in TRN neurons. The AMPAR-positive allosteric modulator, trichloromethiazide, potentiated the DNQX-mediated depolarization in TRN neurons but did not unmask any excitatory actions of DNQX/CNQX in relay neurons. This selective action may not only reveal a differential TARP distribution among thalamic neurons but also may provide insight into distinct characteristics of AMPA receptors of thalamic neurons that could be exploited by future pharmacological development. Furthermore, these data suggest that quinoxaline derivatives could modulate synaptic transmission and alter neuronal excitability.

「難治性疼痛の診断と最新の治療」神経障害性疼痛の治療：脳脊髄刺激療法と低用量ケタミン点滴療法

For the treatment of intractable neuropathic pain, drug challenge test is necessary and useful to examine the pharmacological background of the pain in each case. Based on the results of drug challenge test, we can select the candidates for low-dose ketamine drip infusion (LDKDI) therapy and cerebrospinal stimulation therapy. In cerebrospinal stimulation therapy, dual-lead spinal cord stimulation should be selected at first, since we can insert electrodes percutaneously and this is suitable for both the test stimulation and chronic implantation. For the treatment of peripheral deafferentation pain, which includes phantom limb pain and peripheral nerve injury pain, deep brain stimulation therapy of the thalamic relay nucleus is suitable. Motor cortex stimulation therapy is suitable for the treatment of central deafferentation pain, which includes post-stroke pain. LDKDI therapy combined with cerebrospinal stimulation therapy achieves remarkable pain reduction in the treatment of neuropathic pain.

Functional Organization of the Somatosensory Cortical Layer 6 Feedback to the Thalamus

The pathway from cortical layer 6 to the thalamus is a property of all thalamic relay nuclei. This pathway, as a population, directly excites relay cells and indirectly inhibits them via the thalamic reticular nucleus. To understand the circuit organization of this cortical feedback, we used laser-scanning photostimulation, which specifically activates somata or dendrites, to stimulate the primary somatosensory cortex in an in vitro thalamocortical slice preparation while recording from neurons of the ventral posterior medial nucleus. Layer 6 photostimulation evoked biphasic excitatory postsynaptic current/inhibitory postsynaptic current (EPSC/IPSC) responses in the neurons of the ventral posterior medial nucleus, indicating that such photostimulation strongly activates reticular cells. These disynaptic IPSCs were greatly suppressed or abolished by bath application of the muscarinic agonist acetyl-beta-methylcholine. Our results suggest that the top-down modulation of thalamic neurons from cortical layer 6 involves an inhibitory component via the thalamic reticular nucleus, and this component can be selectively reduced by cholinergic input. Finally, we found the footprints for the excitatory corticothalamic and the inhibitory cortico-reticulo-thalamic inputs to be located in similar positions, though in some cases they are offset. Both patterns have implications for cortico-reticulo-thalamic circuitry.

Progressive thalamocortical neuron loss in Cln5 deficient mice: Distinct effects in Finnish variant late infantile NCL

Finnish variant LINCL (vLINCL Fin) is the result of mutations in the CLN5 gene. To gain insights into the pathological staging of this fatal pediatric disorder, we have undertaken a stereological analysis of the CNS of Cln5 deficient mice ( Cln5 −/− ) at different stages of disease progression. Consistent with human vLINCL Fin, these Cln5 −/− mice displayed a relatively late onset regional atrophy and generalized cortical thinning and synaptic pathology, preceded by early and localized glial responses within the thalamocortical system. However, in marked contrast to other forms of NCL, neuron loss in Cln5 −/− mice began in the cortex and only subsequently occurred within thalamic relay nuclei. Nevertheless, as in other NCL mouse models, this progressive thalamocortical neuron loss was still most pronounced within the visual system. These data provide unexpected evidence for a distinctive sequence of neuron loss in the thalamocortical system of Cln5 −/− mice, diametrically opposed to that seen in other forms of NCL.

Parvalbumin neurons in the forebrain as revealed by parvalbumin-Cre transgenic mice

Neurons expressing the calcium-binding protein parvalbumin (PV) constitute an abundant subpopulation of GABAergic neurons in the cerebral cortex. However, PV is not unique to the GABAergic neurons of the forebrain, but is also expressed in a small number of pyramidal neurons and in a large number of thalamic neurons. In order to summarize the PV neurons in the forebrain, we employed the PV-Cre transgenic mice in the present study. In the progeny of crossbreed between PV-Cre mice and GFP-Cre reporter mice, we found that the GFP-positive neurons include many excitatory neurons in the neocortex and the thalamus as well as GABAergic neurons in the cerebral cortex and basal ganglia. All the reported PV-positive GABAergic neurons in the cerebral cortex and the basal ganglia seemed to be included in the GFP-positive cells. We found GFP-positive layer V pyramidal neurons inhabit a broader neocortical area than was previously reported. They were located in the primary somatosensory, motor, and visual areas. The somatosensory area of the neocortex contained the greatest number of PV-positive pyramidal neurons. A large number of thalamic relay neurons and virtually all the reticular thalamic neurons appeared as GFP-positive. Thalamic relay nucleus and a neocortical area for the same modality corresponded and seemed to contain a characteristic amount of PV-positive excitatory neurons.

Correlation between single unit activity and local field potentials

Event Abstract Back to Event Correlation between single unit activity and local field potentials Agnes Ilona Farkas1*, Péter Gombkötő1, Alice Rokszin1, Gyorgy Benedek1, Attila Nagy1 and Antal Berényi1 1 Department of Physiology, University of Szeged, Hungary The mechanism of encoding of visual information involves complex interactions between intrinsic neuronal discharge and dendrosomatic potentials generated by multiple types of synapses. The correlation between local field potentials (LFPs) and single-unit activity (SUA) has already been studied in the visual cortex and other cortical structures but less interest was focused on subcortical areas. The dorsal lateral geniculate nucleus (LGNd) is one of the thalamic visual relay nuclei in which this correlation was not investigated. We have, therefore obtained simultaneous multielectrode SUA and LFP recordings using four microelectrodes from the LGNd of three anesthetized, immobilized artificially ventilated cats. The stimulus was firstly presented in the receptive field of each unit; afterwards all four receptive fields were simultaneously stimulated. We have analyzed the signal of each electrode in each condition. We found that responses were present in both LFPs and SUA in many cases even if extra-receptive field stimulus was applied, which can be due to intragenicular connections and spreading potentials from neighboring cells. We found a characteristic positive LFP response with short latency which was in phase with the SUA of the “ON”, or „ON-OFF” cells. Some consequent, out-of-phase negative late components of the LFP were also found that showed no correlation with the SUA pattern. Despite of this finding these components were also different among the electrode positions that recorded “ON” or “OFF” or “ON-OFF” neurons, which can be explained with a domination of one cell type in one electrode area. Conference: 12th Meeting of the Hungarian Neuroscience Society, Budapest, Hungary, 22 Jan - 24 Jan, 2009. Presentation Type: Poster Presentation Topic: Research on the cerebral cortex and related structures Citation: Farkas A, Gombkötő P, Rokszin A, Benedek G, Nagy A and Berényi A (2009). Correlation between single unit activity and local field potentials. Front. Syst. Neurosci. Conference Abstract: 12th Meeting of the Hungarian Neuroscience Society. doi: 10.3389/conf.neuro.01.2009.04.192 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 06 Mar 2009; Published Online: 06 Mar 2009. * Correspondence: Agnes Ilona Farkas, Department of Physiology, University of Szeged, Szeged, Hungary, agiko12@freemail.hu Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Agnes Ilona Farkas Péter Gombkötő Alice Rokszin Gyorgy Benedek Attila Nagy Antal Berényi Google Agnes Ilona Farkas Péter Gombkötő Alice Rokszin Gyorgy Benedek Attila Nagy Antal Berényi Google Scholar Agnes Ilona Farkas Péter Gombkötő Alice Rokszin Gyorgy Benedek Attila Nagy Antal Berényi PubMed Agnes Ilona Farkas Péter Gombkötő Alice Rokszin Gyorgy Benedek Attila Nagy Antal Berényi Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Physiology and anatomy of possible oscillators in the central nervous system.

Pathologic tremors occur when the normal, continuous pattern of muscle activation is replaced by relatively synchronous bursting. This article discusses the possible roles of stretch reflex and central oscillators in producing tremor. The gain and conduction delay in some reflex arcs places the stretch reflex close to oscillation in some muscles during normal operation. Within the brain, cells in the thalamic relay nuclei and inferior olive contain a set of ionic conductancies in the cell membrane that can interact to produce oscillations in membrane potential. This tendency is exaggerated by hyperpolarizing or depolarizing the cell away from the normal resting potential. The activity of neighboring cells can be coupled (by electrotonic gap junctions in the olive and by recurrent axonal projections from the reticular nucleus in the thalamus), thus a large population of cells can oscillate together and exert a powerful rhythmic influence on motor output.

Modeling absence seizure dynamics: Implications for basic mechanisms and measurement of thalamocortical and corticothalamic latencies

A successful physiologically based continuum model of the corticothalamic system is applied to determine the relative contributions of axonal and intrinsic cellular delays to the waveforms of absence seizures. The predicted period of the absence seizure depends linearly on model parameters describing thalamocortical, corticothalamic, intracortical, and synaptodendritic delays, and these dependences are linked to the seizure mechanism by showing how time intervals between peaks in the waveforms depend on the parameters. Counterintuitively, it is found that a peak in the local field potential recorded in the thalamic relay nuclei can precede the peak in the cortical field that drove it, without violating causality, but rendering naive interpretation of time intervals between peaks invalid. We argue that a thalamocortical loop mechanism for absence seizures is consistent with intrathalamic cellular properties being the leading determinant of the frequency of spike-wave discharges in rat genetic models, with the combination of network and cellular properties providing a natural explanation for the lower frequency of human absence seizures. Finally, our results imply that the seizure frequency is not determined by the fastest thalamocortical and corticothalamic fibers, but rather depends on an effective weighted conduction velocity of all pathways present.

Expression of vesicular glutamate transporters 1 and 2 in the cells of origin of the rat thalamostriatal pathway

The present study is focused on the analysis of the vesicular glutamate transporters 1 and 2 (VGLUT1 and VGLUT2) used by thalamic neurons giving rise to the thalamostriatal system. Instead of studying the distribution of VGLUT proteins at the level of thalamostriatal terminals, this report is focused on identifying the expression of the VGLUT mRNAs within the parent cell bodies of thalamic neurons innervating the striatum. For this purpose, we have combined dual in situ hybridization to detect both VGLUT1 and VGLUT2 mRNAs together with retrograde tracing with cholera toxin. Our results show that VGLUT2 is the only vesicular glutamate transporter expressed in thalamostriatal-projecting neurons located in the midline and intralaminar nuclei, whereas all neurons from the ventral thalamic nuclei innervating the striatum express both VGLUTs, at least at the mRNA level. Indeed, the mRNAs encoding for VGLUT1 and VGLUT2 displayed a sharp complementary subcellular distribution within neurons from the ventral thalamic nuclei giving rise to thalamostriatal projections. The differential distribution of VGLUT mRNAs lead us to conclude that the thalamostriatal pathway is a dual system, composed by a preponderant projection arising from the midline and intralaminar nuclei using VGLUT2 as the glutamate transporter, together with another important source of striatal afferents arising from neurons in the ventral thalamic relay nuclei containing both kinds of vesicular glutamate transporters.

Heterogeneity of firing properties among rat thalamic reticular nucleus neurons

The thalamic reticular nucleus (TRN) provides inhibitory innervation to most thalamic relay nuclei and receives excitatory innervation from both cortical and thalamic neurons. Ultimately, information transfer through the thalamus to the neocortex is strongly influenced by TRN. In addition, the reciprocal synaptic connectivity between TRN with associated thalamic relay nuclei is critical in generating intrathalamic rhythmic activities that occur during certain arousal states and pathophysiological conditions. Despite evidence suggesting morphological heterogeneity amongst TRN neurons, the heterogeneity of intrinsic properties of TRN neurons has not been systematically examined. One key characteristic of virtually all thalamic neurons is the ability to produce action potentials in two distinct modes: burst and tonic. In this study, we have examined the prevalence of burst discharge within TRN neurons. Our intracellular recordings revealed that TRN neurons can be differentiated by their action potential discharge modes. The majority of neurons in the dorsal TRN (56%) lack burst discharge, and the remaining neurons (35%) show an atypical burst that consists of an initial action potential followed by small amplitude, long duration depolarizations. In contrast, most neurons in ventral TRN (82%) display a stereotypical burst discharge consisting of a transient, high frequency discharge of multiple action potentials. TRN neurons that lack burst discharge typically did not produce low threshold calcium spikes or produced a significantly reduced transient depolarization. Our findings clearly indicate that TRN neurons can be differentiated by differences in their spike discharge properties and these subtypes are not uniformly distributed within TRN. The functional consequences of such intrinsic differences may play an important role in modality-specific thalamocortical information transfer as well as overall circuit level activities.

GABAergic mechanisms in absence epilepsy: a computational model of absence epilepsy simulating spike and wave discharges after vigabatrin in WAG/Rij rats

In this study, the effects of vigabatrin on spike-and-wave discharges (SWDs) were measured in WAG/Rij rats, an animal model of absence epilepsy. Vigabatrin was used with the aim of enhancing GABAergic neurotransmission, and in this way to investigate the role of this process in the properties of SWDs. The study was carried out both in the rat, in vivo, and also using a computational model, in order to test different mechanisms that may account for the changes in SWDs after vigabatrin. The model parameters, representing GABA levels, were changed according to the known, and assumed, mechanism of action of the drug. The results show that the computational model can most adequately simulate the data obtained in vivo on the assumption that the enhancement of GABAergic neurotransmission due to application of vigabatrin is most pronounced at the level of the thalamic relay nuclei (TC cells). Furthermore, vigabatrin was shown to affect both the SWD starting and stopping mechanisms, as reflected by hazard rates. Based on these results, we suggest that GABAergic neurotransmission in TC cells is actively involved in the SWD termination.

Recovery from optic neuritis: an ROI-based analysis of LGN and visual cortical areas

Optic neuritis (ON) is the first clinical manifestation in approximately 20% of patients with multiple sclerosis (MS). The inflammation and demyelination of the optic nerve are characterized by symptomatic visual impairment and retrobulbar pain, and associated with decreased visual acuity, decreased colour and contrast sensitivity, delayed visual evoked potentials and visual field defects. Spontaneous recovery of vision typically occurs within weeks or months after onset, depending on the resolution of inflammation, remyelination, restoration of conduction in axons which persist demyelinated and neuronal plasticity in the cortical and subcortical visual pathways. To assess where recovery takes place along the visual pathway, visual activation was studied in the lateral geniculate nucleus (LGN), the main thalamic relay nucleus in the visual pathway and in three areas of the visual cortex: the lateral occipital complexes (LOC), V1 and V2. We conducted a longitudinal functional magnetic resonance imaging (fMRI) study of regions of interest (ROI) of activation in LGN and visual cortex in 19 patients with acute ON at onset, 3 and 6 months from presentation. With fMRI we measured the activation in the ROIs and compared activation during monocular stimulation of the affected and unaffected eye. In the acute phase the activation of LGN during visual stimulation of the affected eye was significantly reduced (P < 0.01) compared to the unaffected eye. This difference in LGN activation between the affected and unaffected eye diminished during recovery, and after 180 days the difference was no longer significant (P = 0.59). The decreased difference during recovery was mainly due to an increase in the fMRI signal when stimulating the affected eye, but included a component of a decreasing fMRI signal from LGN when stimulating the unaffected eye. In LOC, V1 and V2 activation during visual stimulation of the affected eye in the acute phase was significantly reduced (P < 0.01) compared to the unaffected eye, and during recovery the difference diminished with no significant differences left after 180 days. As the pattern of activation in LOC, V1 and V2 resembled the development in LGN we found no evidence of additional cortical adaptive changes. The reduced activation of the LGN to stimulation of the unaffected eye is interpreted as a shift away from early compensatory changes established in the acute phase in LGN and may indicate very early plasticity of the visual pathways.

Rapid contact call-driven induction of NR2A and NR2B NMDA subunit mRNAs in the auditory thalamus of the budgerigar ( Melopsittacus undulatus)

In situ hybridization histochemistry was used to assess the effect of auditory stimulation with natural contact calls on expression of NR2A and NR2B NMDA subunit mRNAs in neurons of the thalamic auditory relay nucleus ovoidalis (Ov) of a vocal learning parrot species, the budgerigar ( Melopsittacus undulatus). The results showed that both the core (Ov) and ventromedial shell subdivisions (Ovm) of ovoidalis contained neurons expressing NR2A and NR2B mRNA in no-stimulation control subjects and that the distributions of neurons expressing these subunit mRNAs were very similar in both the core and shell of Ov. Contact call stimulation (5, 30 and 180 min) resulted in substantial increases of 50–60% in the number of neurons expressing NR2A and NR2B mRNAs in both the core and shell. Staining intensity, as measured by the optical density of stained somata approximately doubled compared to controls for both NR2 subunits in the 5 and 30 min conditions, but declined from 30 to 180 min. In all conditions, the density, but not staining intensity, of neurons expressing NR2B exceeded NR2A expression. Furthermore, the density of neurons expressing both subunit mRNAs in call stimulation conditions was greater in the core than in the shell despite the fact that total neuronal density was approximately 20% higher in the shell. Previous experiments have shown that call stimulation is more effective at inducing expression of the immediate early gene zenk in the Ov shell than core; however the present results do not indicate that either NR2A or NR2B mRNA expression mediates this effect since neither subunit exhibits greater expression in Ovm. Ca ++ release is needed for immediate early gene expression, however and, notably, Ovm contains large numbers of neurons containing CGRP, a peptide which has been shown to increase cytosolic Ca ++ levels.

Thalamic sensory relay nucleus stimulation and phantom limb pain

Thalamic sensory relay nucleus stimulation and phantom limb pain

NPY signaling through Y 1 receptors modulates thalamic oscillations

Neuropeptide Y is the ligand of a family of G-protein coupled receptors (Y 1 to Y 6). In the thalamus, exogenous and endogenously released NPY can shorten the duration of thalamic oscillations in brain slices from P13 to P15 rats, an in vitro model of absence seizures. Here, we examine which Y receptors are involved in this modulation. Application of the Y 1 receptor agonist Leu 31Pro 34NPY caused a reversible reduction in the duration of thalamic oscillations (−26.6 ± 7.8%), while the Y 2 receptor agonist peptideYY (3–36) and the Y 5 receptor agonist BWX-46 did not exert a significant effect. No Y receptor agonist affected oscillation period. Application of antagonists of Y 1, Y 2 and Y 5 receptors (BIBP3226, BIIE0246 and L152,806, respectively) produced results consistent with those obtained from agonists. BIBP3226 caused a reversible disinhibition, an effect that increases oscillation duration (18.2 ± 9.7%) while BIIE0246 and L152,806 had no significant effect. Expression of NPY is limited to neurons in the reticular thalamic nucleus (nRt), but Y 1 receptors are expressed in both nRt and adjacent thalamic relay nuclei. Thus, intra-nRt or nRt to relay nucleus NPY release could cause Y 1 receptor mediated inhibition of thalamic oscillations.

Neurochemical organization of reptilian thalamus. Comparative analysis of amniote optical centers

Study of neurochemical characteristics of the turtle thalamus was performed using antibodies against several biologically active compounds; monoamines (5-HT, TH), neuropeptides (SP, m-Enk, NPY), against ChAT and by histochemical detection of NADPH-d. Based on our own results and literature data obtained on other representatives of reptiles, birds, and mammals, a comparative analysis was carried out of neurochemical organization of two thalamic optical centers—relay nuclei of thalamofugal (GLd) and tectofugal (Rot/LP-Pulv) systems of amniotes. Features of similarities and differences of these centers in representatives of non-mammalian and mammalian amniotes are revealed. GLd has a great similarity of the studied neurochemical characteristics in all amniotes. It receives innervation from all studied transmitter-modulatory systems with predominance of serotonin-, choline- and NPY-ergic projections. Neurochemical organization of Rot comparable with the tectorecipient part of mammalian LP-Pulv has a great resemblance in reptiles and birds, with considerable interspecies differences inside each class. In the majority of the studied systems, Rot is characterized by scant innervation. On the contrary, LP-Pulv receives sufficiently massive innervation from these systems. The most characteristic of this complex are rich SP- and cholinergic projections that are scant in Rot of reptiles and birds. The similar feature of Rot and LP-Pulv is the presence of massive serotonin- and NO-ergic (NADPH-positive) projections. The revealed similarities and differences of the neurochemical characteristics of thalamic optical centers among amniotes seem to reflect various transformations of thalamo- and tectofugal visual systems in the course of phylogenetic and adaptive evolution.

Contact-call driven and tone-driven zenk expression in the nucleus ovoidalis of the budgerigar (Melopsittacus undulatus)

The effectiveness of species-typical contact calls and a 3-kHz pure tone to induce zenk gene protein expression in the primary thalamic auditory relay nucleus ovoidalis was compared in budgerigars (Melopsittacus undulatus), a parrot species capable of lifelong vocal learning. Ovoidalis consists of a core which projects topographically to field L of the telencephalon and a ventromedial shell containing many calcitonin-gene-related peptide neurons that project throughout field L as well as to an adjacent field receiving visual input. Tone-induced and call-induced zenk expression in the ovoidalis core were similar; however, call-induced zenk expression in ventromedial ovoidalis shell was significantly greater than tone-induced expression. These results support the idea that the ovoidalis shell may contain neurons specialized to process complex sounds including species-typical communication sounds.