Characteristics of small neurons in the reticular thalamic nucleus of WAG/Rij rat

The aim of this investigation was to study the ultrastructure of small neurons in the reticular thalamic nucleus (RTN) in rats of the WAG/Rij strain, which is a recognized model for human absence epilepsy. 24 rats were used in these studies. The paraffin sections of the brain taken from 10 rats were stained with Nissl's cresyl violet and were used for the study of neuronal cytoarchitecture and cytological characteristics. For electron microscopic study, RTN was dissected under microscopic control and fixed in cooled 2.5% glutaraldehyde solution in 0.1 M sodium phosphate buffer (pH 7.4). Small neurons were found to constitute 5-8% of the total number of RTN neurons. They had ovoid cell body, scanty pale-staining cytoplasm, often were seen in pairs. The ultrastructure of these neurons was characterized by poor development of membranes, axonal branching close to the cell body, multiple contacts of axon with cell body and dendrites. It is suggested that the neurons described are short-axonal.     

Cholinergic stimulation of the nucleus basalis of Meynert and reticular thalamic nucleus affects spike-and-wave discharges in WAG/Rij rats

The role of the cholinergic innervated nucleus basalis of Meynert (NB) and reticular thalamic nucleus (RT) in the generation or modulation of spontaneously occurring spike-and-wave discharges (SWDs) was investigated in the WAG/Rij rat model of absence epilepsy. The cholinergic agonist carbachol and the muscarinic antagonist scopolamine were injected in the NB and RT in the doses of 0.55 and 5.5 nmol while the EEG was recorded. Carbachol injected in the NB decreased the number and the mean duration of SWDs. Scopolamine alone had no influence on SWDs, but could antagonize the effects of carbachol if administered simultaneously in NB. Injections of carbachol in the RT inhibited the occurrence of SWDs, but did not affect the mean duration. Scopolamine administered in the RT had no influence on seizure activity. It is concluded that cholinergic stimulation of the NB or the RT inhibits the cortical synchronous activity characterizing SWDs.     

Dual effect of pyrilamine on absence seizures in WAG/Rij rats

Inflammation Research - .     

Projections to the rostral reticular thalamic nucleus in the rat

Summary Afferent pathways to the rostral reticular thalamic nucleus (Rt) in the rat were studied using anterograde and retrograde lectin tracing techniques, with sensitive immunocytochemical methods. The analysis was carried out to further investigate previously described subregions of the reticular thalamic nucleus, which are related to subdivisions of the dorsal thalamus, in the paraventricular and midline nuclei and three segments of the mediodorsal thalamic nucleus. Cortical inputs to the rostral reticular nucleus were found from lamina VI of cingulate, orbital and infralimbic cortex. These projected with a clear topography to lateral, intermediate and medial reticular nucleus respectively. Thalamic inputs were found from lateral and central segments of the mediodorsal nucleus to the lateral and intermediate rostral reticular nucleus respectively and heavy paraventricular thalamic inputs were found to the medial reticular nucleus. In the basal forebrain, afferents were found from the vertical and horizontal limbs of the diagonal band, substantia innominata, ventral pallidum and medial globus pallidus. Brainstem projections were identified from ventrolateral periaqueductal grey and adjacent sites in the mesencephalic reticular formation, laterodorsal tegmental nucleus, pedunculopontine nucleus, medial pretectum and ventral tegmental area. The results suggest a general similarity in the organisation of some brainstem Rt afferents in rat and cat, but also show previously unsuspected inputs. Furthermore, there appear to be at least two functional subdivisions of rostral Rt which is reflected by their connections with cortex and thalamus. The studies also extend recent findings that the ventral striatum, via inputs from the paraventricular thalamic nucleus, is included in the circuitry of the rostral Rt, providing further evidence that basal ganglia may function in concert with Rt. Evidence is also outlined with regard to the possibility that rostral Rt plays a significant role in visuomotor functions.Abbreviations ac anterior commissure - aca anterior commissure, anterior - Acb accumbens nucleus - AI agranular insular cortex - AM anteromedial thalamic nucleus - AV anteroventral thalamic nucleus - BST bed nucleus of stria terminalis - Cg cingulate cortex - CG central gray - CL centrolateral thalamic nucleus - CM central medial thalamic nucleus - CPu caudate putamen - DR dorsal raphe nucleus - DTg dorsal tegmental nucleus - EP entopeduncular nucleus - f fornix - Fr2 Frontal cortex, area 2 - G gelatinosus thalamic nucleus - GP globus pallidus - Hb habenula - HDB horizontal limb of diagonal band - IAM interanterodorsal thalamic nucleus - ic internal capsule - INC interstitial nucleus of Cajal - IF interfascicular nucleus - IL infralimbic cortex - IP interpeduncular nucleus - LC locus coeruleus - LDTg laterodorsal tegmental nucleus - LH lateral hypothalamus - LHb lateral habenular nucleus - ll lateral lemniscus - LO lateral orbital cortex - LPB lateral parabrachial nucleus - MD mediodorsal thalamic nucleus - MDL mediodorsal thalamic nucleus, lateral segment - Me5 mesencephalic trigeminal nucleus - MHb medial habenular nucleus - mlf medial longitudinal fasciculus - MnR median raphe nucleus - MO medial orbital cortex - mt mammillothalamic tract - OPT olivary pretectal nucleus - pc posterior commissure - PC paracentral thalamic nucleus - PF parafascicular thalamic nucleus - PPTg pedunculopontine tegmental nucleus - PrC precommissural nucleus - PT paratenial thalamic nucleus - PV paraventricular thalamic nucleus - PVA paraventricular thalamic nucleus, anterior - R red nucleus - Re reuniens thalamic nucleus - RRF retrorubral field - Rt reticular thalamic nucleus - Scp superior cerebellar peduncle - SI substantia innominata - sm stria medullaris - SNR substantia nigra, reticular - st stria terminalis - TT tenia tecta - VL ventrolateral thalamic nucleus - VO ventral orbital cortex - VP ventral pallidum - VPL ventral posterolateral thalamic nucleus - VTA ventral tegmental area - 3 oculomotor nucleus - 3V 3rd ventricle - 4 trochlear nucleus     

Dopamine-dependent nature of depression-like behavior in WAG/Rij rats with genetic absence epilepsy

WAG/Rij rats given placebo showed a depression-like state as compared with normal Wistar rats (lacking convulsive pathology); this was analogous to the state previously seen in rats of this line, with decreased investigative activity in the open field test, increased immobility in the forced swimming test, and decreased consumption and preference for sucrose solution (anhedonia). Chronic administration of the tricyclic antidepressant imipramine (15 mg/kg, i.p., 15 days) had therapeutic (antidepressant) effects on depression-like behavior in WAG/Rij rats. After withdrawal of antidepressant therapy, the behavior of WAG/Rij rats was not significantly different from that of Wistar rats. Acute (single-dose) administration of the selective dopamine D₂/D₃ receptor antagonist raclopride (100 μg/kg, i.p., 15 min before the start of behavioral testing) increased the symptoms of depression-like behavior and suppressed the antidepressant effect of chronic administration of imipramine in WAG/Rij rats. Raclopride had no significant effect on behavior in Wistar rats. Administration of the dopamine D₂/D₃ receptor agonist parlodel (a therapeutic form of bromocriptine) cured the depression-like behavior of WAG/Rij rats and had no significant effect on behavior in Wistar rats, with the exception of a reduction in the duration of immobility in the forced swimming test. Imipramine and raclopride had no significant effect on the levels of total movement activity and anxiety in either WAG/Rij or Wistar rats. These results demonstrate the dopamine-dependent nature of depression-like behavior in WAG/Rij rats and show the possible involvement of dopamine D₂ receptors in mediating the antidepressant effect of imipramine on genetically determined depression-like behavior in WAG/Rij rats. __________ Translated from Zhurnal Vysshei Nervnoi Deyatel’nosti imeni I. P. Pavlova, Vol. 57, No. 1, pp. 91–102, January–February, 2007.     

Absence seizures during pregnancy in WAG/Rij rats

Spontaneously occurring spike-wave discharges (SWDs) and serum concentrations of ovarian steroid hormones were investigated before, during and after pregnancy in WAG/Rij rats, a rat strain with genetically determined absence seizures. Eight groups of rats were included in the assays of progesterone and estradiol: rats at diestrus, at various days of pregnancy and at lactating days. The number of SWDs in cortical EEG of WAG/Rij rats was decreased from the 3rd up to the 18th day of pregnancy and subsequently increased to control level. Thereafter, a new decrease was found 2-3 days after parturition. Serum concentration of progesterone was threefold increased at the 3rd day of pregnancy, remained elevated until the 18th day of pregnancy and returned to control values before delivery. Over measured days, estradiol was significantly elevated only at the 18th day of pregnancy. Results demonstrate that physiological conditions induced by the state of pregnancy lead to suppression of occurrence of SWDs. Changes in plasma progesterone concentration correspond to the changes in number of SWDs: an increased level of progesterone during pregnancy is accompanied by a decreased number of SWDs, while a decrease in circulating progesterone before parturition is paralleled by an increase of SWDs. Of interest, the relationship between SWDs and concentration of progesterone found during pregnancy is diametrically opposite to results obtained in acute administration studies of progesterone in nonpregnant animals.     

Brain histamine in the WAG/Rij rat,an animal model of absence epilepsy

Inflammation Research -     

Propagation of spike and wave activity to the medial prefrontal cortex and dorsal raphe nucleus of WAG/Rij rats

Although there is pharmacological evidence for the involvement of the serotonergic system in the expression of spike and wave discharges (SWDs) in experimental absence epilepsy, no direct investigation of this paroxysm in the dorsal raphe nucleus (DRN), one of the main serotonergic nuclei, has been carried out. We have now recorded the EEG simultaneously with local field potentials and unit activity in DRN from WAG/Rij rats, one of the best established models of absence epilepsy during spontaneous SWDs. We have also compared this activity to that in the thalamocortical networks, where SWDs are generated, and in the medial prefrontal cortex (mPFC), as this brain area is reciprocally connected to the DRN. We have found that SWDs propagate to the DRN with a short delay, and that the firing rate of its neurons changes during this type of paroxysm. These results provide the first direct evidence for clear alterations in the firing properties of mPFC and DRN neurons during spontaneous SWDs.     

Corticothalamic inhibition in the thalamic reticular nucleus

Mutual inhibition between the GABAergic cells of the thalamic reticular nucleus (RTN) is important in regulating oscillations in the thalamocortical network, promoting those in the spindle range of frequencies over those at lower frequencies. Excitatory inputs to the RTN from the cerebral cortex are numerically large and particularly powerful in inducing spindles. However, the extent to which corticothalamic influences can engage the inhibitory network of the RTN has not been fully explored. Focal electrical stimulation of layer VI in the barrel cortex of the mouse thalamocortical slice in vitro resulted in prominent di- or polysynaptic inhibitory postsynaptic currents (IPSCs) in RTN cells under the experimental conditions used. The majority of cortically induced responses consisted of mixed PSCs in which the inhibitory component predominated or of large IPSCs alone, implying inhibition of neighboring cells by other, cortically excited RTN cells. Within the mixed PSCs, fixed and variable latency components could commonly be identified. IPSCs could be blocked by application of ionotropic glutamate receptor antagonists or of GABA(A) receptor antagonists, also indicating their dependence on corticothalamic excitation triggering disynaptic or polysynaptic inhibition. Spontaneous GABA(A) receptor-dependent IPSCs were routinely observed in the RTN and, taken together with the results of cortical stimulation, indicate the existence of a substantial network of intrareticular inhibitory connections that can be effectively recruited by the corticothalamic system. These results suggest activation of cortical excitatory inputs triggers the propagation of inhibitory currents within the RTN and support the view that activation of the RTN from the somatosensory cortex, although focused by the topography of the corticothalamic projection, is capable of disynaptically engaging the whole inhibitory network of the RTN, by local and probably by reentrant GABA(A) receptor-based synapses, thus spreading the corticothalamic influence throughout the RTN.     

Auditory neurons in the rat thalamic reticular nucleus

Summary In the thalamic reticular nucleus (TR) of the rat a cluster of neurons has been located which receives auditory inputs and acts as a source of inhibition for relay neurons of the medial geniculate nucleus (MG). These TR neurons (auditory thalamic reticular neurons; A-TR neurons) showed a repetitive burst of grouped discharge upon electrical stimulation of the inferior colliculus (IC) or of the auditory cortex. Many of them responded to tonal stimuli such as clicks or pips.Adjacent to the cluster of A-TR neurons there were the cluster of TR neurons receiving visual inputs (V-TR neurons) and that receiving somatosensory inputs (S-TR neurons). The cluster of A-TR neurons was situated ventrally to the cluster of V-TR neurons, both extending caudally from the level of the rostral tip of the dorsal lateral geniculate nucleus. The S-TR neurons distributed rostrally to the clusters of A- and V-TR neurons. Some of the sensory TR neurons, usually found around the boundaries between the clusters of different sensory modalities, were activated from stimulation of different central sensory pathways.Single electric shocks directly applied to the cluster of A-TR neurons suppressed discharges of relay neurons of the MG, either spontaneous or evoked by click stimuli or by electric shocks to the IC. The postexcitatory suppression of MG relay neurons was similar in time course to the suppression following electrical stimulation of A-TR neurons.Response latencies of the A-TR neurons to IC shocks were found to be 1.0–1.5 ms longer than those of the MG relay cells with respect to the modal and shortest values. It is suggested that A-TR neurons are intercalated in the axon collateral circuit of the thalamocortical projection arising from relay neurons of the MG.Dedicated to Dr. Kitsuya Iwama, Emeritus Professor of Osaka University Medical School, on the occasion of his retirement     

Morphometric Golgi study of cortical locations in WAG/Rij rats: the cortical focus theory

Recently it was demonstrated that for the absence epilepsy characteristic spike-wave discharges initially emerge from the somatosensory cortex and quickly involve the rest of the cortex and cortico-thalamic network. This has led to the development of the focal theory of absence epilepsy. In this experiment, this theory was further investigated by studying the neuronal organization of the cortical focal zone, a non-focal zone in genetic epileptic WAG/Rij rats and functional related areas in non-epileptic age matched control rats. A classical Golgi staining technique was used to visualize whole cortical neurons with dendritic and axon arborisation. Apical dendrites of pyramidal cells in epileptic rats were often split, declined and were running in non-perpendicular directions. Quantitative differences between the strains were found for the length of neurons, between focal and control areas mainly for dendritic arborization. A significant "strain-zone" interaction was found for the maximal distance between two points of dendritic arborization, the mean length of a dendritic segment and the number of free terminations of apical dendrites. All this demonstrates that properties of dendrites in the cortical focal area of WAG/Rij rats were at variance with dendritic characteristics outside the focal area and with functional similar areas in non-epileptic controls. These features might reflect the hyperexcitability of somatosensory neurons, which underlie the initiation and spreading of spike-wave discharges in WAG/Rij rats. Finally, these results are in line with the cortical focus theory of absence epilepsy.     

The deafferented reticular thalamic nucleus generates spindle rhythmicity

The hypothesis that nucleus reticularis thalami (RE) is the generator of spindle rhythmicity during electroencephalogram (EEG) synchronization was tested in acutely prepared cats. Unit discharges and focal waves were extracellularly recorded in the rostral pole of RE nucleus, which was completely disconnected by transections from all other thalamic nuclei. In some experiments, additional transections through corona radiata created a triangular island in which the rostral RE pole survived with the caudate nucleus, putamen, basal forebrain nuclei, prepyriform area, and the adjacent cortex. Similar results were obtained in two types of experiments: brain stem-transected preparations that exhibited spontaneous spindle sequences, and animals under ketamine anesthesia in which transient spindling was repeatedly precipitated during recording by very low doses of a short-acting barbiturate. Both spindle-related rhythms (7- to 16-Hz waves grouped in sequences that recur with a rhythm of 0.1-0.3 Hz) are seen in focal recordings of the deafferented RE nucleus. The presence of spindling rhythmicity in the disconnected RE nucleus contrasts with total absence of spindles in cortical EEG leads and in thalamic recordings behind the transection. Oscillations within the same frequency range as that of spontaneous spindles can be evoked in the deafferented RE nucleus by subcortical white matter stimulation. In deafferented RE cells, the burst structure consists of an initially biphasic acceleration-deceleration pattern, eventually leading to a long-lasting tonic tail. Quantitative group data show that the burst parameters of disconnected RE cells are very similar to those of RE neurons with intact connections. In the deafferented RE nucleus, spike bursts of RE neurons recur periodically (0.1-0.3 Hz) in close time-relation with simultaneously recorded focal spindle sequences. The burst occurrence of deafferented RE cells is greatly reduced after systemic administration of bicuculline. The preservation of both spindle-related rhythms in the disconnected RE nucleus, together with our recent experiments showing abolition of spindle oscillations in thalamic nuclei after lesions of RE nucleus (24), demonstrate that RE nucleus is the generator of spindle rhythms.     

The turtle thalamic anterior entopeduncular nucleus shares connectional and neurochemical characteristics with the mammalian thalamic reticular nucleus

Neurochemical and key connectional characteristics of the anterior entopeduncular nucleus (Enta) of the turtle (Testudo horsfieldi) were studied by axonal tracing techniques and immunohistochemistry of parvalbumin, gamma-aminobutyric acid (GABA) and glutamic acid decarboxylase (GAD). We showed that the Enta, which is located within the dorsal peduncle of the lateral forebrain bundle (Pedd), has roughly topographically organized reciprocal connections with the dorsal thalamic visual nuclei, the nucleus rotundus (Rot) and dorsal lateral geniculate nucleus (GLd). The Enta receives projections from visual telencephalic areas, the anterior dorsal ventricular ridge and dorsolateral cortex/pallial thickening. Most Enta neurons contained GABA and parvalbumin, and some of them were retrogradely labeled when the tracer was injected into the visual dorsal thalamic nuclei. Further experiments using double immunofluorescence revealed colocalization of GAD and parvalbumin in the vast majority of Enta neurons, and many of these cells showed retrograde labeling with Fluoro-gold injected into the Rot and/or GLd. According to these data, the Enta may be considered as a structural substrate for recurrent inhibition of the visual thalamic nuclei. Based on morphological and neurochemical similarity of the turtle Enta, caiman Pedd nucleus, the superior reticular nucleus in birds, and the thalamic reticular nucleus in mammals, we suggest that these structures represent a characteristic component which is common to the thalamic organization in amniotes.     

Does the reticular thalamic nucleus project to the midbrain?

In this study, we investigated whether the reticular thalamic nucleus has a projection to major centres of the midbrain in rats, rabbits and cats. Various tracers (biotinylated dextran, cholera toxin B subunit, fluorescent latex beads) were injected either into the midbrain tectum (deep layers of the superior colliculus) or tegmentum (midbrain reticular and pedunculopontine nuclei). In other experiments, different coloured latex beads (red and green) were injected into the deep layers of the superior colliculus and into the midbrain reticular nucleus of the same animal (rabbits). Our major finding is that in rats, rabbits and cats, there are no retrogradely labelled cells in the reticular thalamic nucleus after tracer injections into the abovementioned midbrain centres. In rabbits and cats, however, there are retrogradely labelled cells lying close to the ventromedial edge of the reticular thalamic nucleus after such injections. We show, by means of immunocytochemical double-labelling, that these retrogradely labelled cells do not lie in the reticular thalamic nucleus as suggested by previous studies, but in the inner small-celled region, a group of small cells that forms part of the zona incerta. Although there appears to be no clear topography of projection of the inner small-celled region, our tracer double-labelling experiments show that separate cells in the inner small-celled region project to individual centres of the midbrain (i.e., there are very few double-labelled cells after double injections). In rats, unlike in rabbits and cats, there is no clearly defined inner small-celled region and there are no retrogradely labelled cells seen along the ventromedial edge of the reticular thalamic nucleus. Our results suggest that in rats, rabbits and cats, there is no projection of the reticular thalamic nucleus to major centres of the midbrain, suggesting that the nucleus may not have a very strong influence on midbrain function, as it does on dorsal thalamic function.     

Absence seizures are reduced by the enhancement of GABA-ergic inhibition in the hippocampus in WAG/Rij rats

Classical theories on absence epilepsy suggest that spike-wave discharge (SWDs) represent thalamo-cortical oscillations, where an abnormally excitable cortex interacts with thalamus and brain stem reticular formation. The limbic system is generally not included in any theory about the pathogenesis of absence seizures. However, some data demonstrated that the alterations in the limbic system attribute to the expression of absence epileptic phenotype in genetic models of absence epilepsy. The present study investigated whether local intrahippocampal administration of progesterone (a GABA_A-mimetic) and tiagabine (an inhibitor of GABA (re)uptake) might affect the occurrence of SWDs. Male WAG/Rij rats were implanted with permanent electroencephalograph (EEG) electrodes and bilateral cannulas in the CA1-CA3 region of the dorsal hippocampus. Control rats had bilateral cannulas in the cortical area above the hippocampus. Rats received intracerebral injections of progesterone (5 mg/ml), 45% β-cyclodextrin (CD), saline, or tiagabine (2 mg/ml). EEG recordings were made before and after injection. Progesterone, CD, and tiagabine administration to the hippocampus reduced SWDs for 60 min following administration without behavioral or electroencephalographic side-effects. Both progesterone administration into the cortex and saline injection into the hippocampus yielded no changes in the occurrence of SWDs. These data suggest that activation of GABA-ergic transmission in the hippocampus has an inhibitory effect on cortico-thalamo-cortical circuits underlying the generation of SWDs and might be critically involved in the regulation of absence seizures.     

Giant spontaneous depolarizing potentials in the developing thalamic reticular nucleus

The thalamic reticular nucleus (nRt) provides a major source of inhibition in the thalamo-cortical circuit and is critically involved in the generation of spindle oscillations. Here we describe the properties of thalamic giant depolarizing potentials (tGDPs) that were observed in nRt during early development. tGDPs persisted in presence of ionotropic glutamate antagonists but were completely abolished by GABA(A)R antagonist SR 35591. tGDPs occurred primarily between p3 and p8 (in 30-50% of cells) and occasionally up until p15. tGDPs lasted 0.4-3 s with peak conductances of 2-13 nS and occurred at frequencies between 0.02 and 0.06 Hz. We used mice with a benzodiazepine-insensitive alpha3 subunit [alpha3(H126R)] to probe for the identity of the GABA receptors responsible for tGDP generation. Benzodiazepine enhancement of tGDP amplitude and duration persisted in nRt neurons in alpha3(H126R) mice, indicating that the GABA(A)Rs containing alpha3 are not critical for tGDP generation and suggesting that tGDPs are mediated by GABA(A)Rs containing the alpha5 subunit, which is transiently expressed in nRt neurons in early postnatal development. Furthermore we found that exogenous GABA application depolarized nRt neurons younger than p8, indicating elevated [Cl(-)](i) at this developmental stage. Taken together, these data suggest that in immature nRt, long-lasting depolarizing responses mediated by GABA receptors could trigger Ca(2+) entry and play a role in functional development of the spindle-generating circuitry.     

Selective optical drive of thalamic reticular nucleus generates thalamic bursts and cortical spindles

The thalamic reticular nucleus (TRN) is hypothesized to regulate neocortical rhythms and behavioral states. Using optogenetics and multi-electrode recording in behaving mice, we found that brief selective drive of TRN switched the thalamocortical firing mode from tonic to bursting and generated state-dependent neocortical spindles. These findings provide causal support for the involvement of the TRN in state regulation in vivo and introduce a new model for addressing the role of this structure in behavior.     

The pathways connecting the hippocampal formation, the thalamic reuniens nucleus and the thalamic reticular nucleus in the rat

Most dorsal thalamic nuclei send axons to specific areas of the neocortex and to specific sectors of the thalamic reticular nucleus; the neocortex then sends reciprocal connections back to the same thalamic nucleus, directly as well indirectly through a relay in the thalamic reticular nucleus. This can be regarded as a 'canonical' circuit of the sensory thalamus. For the pathways that link the thalamus and the hippocampal formation, only a few comparable connections have been described. The reuniens nucleus of the thalamus sends some of its major cortical efferents to the hippocampal formation. The present study shows that cells of the hippocampal formation as well as cells in the reuniens nucleus are retrogradely labelled following injections of horseradish peroxidase or fluoro-gold into the rostral part of the thalamic reticular nucleus in the rat. Within the hippocampal formation, labelled neurons were localized in the subiculum, predominantly on the ipsilateral side, with fewer neurons labelled contralaterally. Labelled neurons were seen in the hippocampal formation and nucleus reuniens only after injections made in the rostral thalamic reticular nucleus (1.6-1.8 mm caudal to bregma). In addition, the present study confirmed the presence of afferent connections to the rostral thalamic reticular nucleus from cortical (cingulate, orbital and infralimbic, retrosplenial and frontal), midline thalamic (paraventricular, anteromedial, centromedial and mediodorsal thalamic nuclei) and brainstem structures (substantia nigra pars reticularis, ventral tegmental area, periaqueductal grey, superior vestibular and pontine reticular nuclei). These results demonstrate a potential for the thalamo-hippocampal circuitry to influence the functional roles of the thalamic reticular nucleus, and show that thalamo-hippocampal connections resemble the circuitry that links the sensory thalamus and neocortex.