Ventrobasal Thalamus Research Articles

Acute thrombotic infarction suppresses metabolic activation of ipsilateral somatosensory cortex: evidence for functional diaschisis.

To study the effects of focal infarction on the capacity for functional activation of an ipsilateral somatosensory system remote from the lesion, we produced a small thrombotic infarct in the left frontal pole of male Wistar rats by a photochemical method. Five days later, the awake, restrained rats received tactile stimulation of the large whiskers (vibrissae) of the right side of the face, while a double-label 14C-autoradiographic study of local CMRglc (lCMRglc) and local CBF (lCBF) was performed. Unlesioned and unstimulated animals served as controls. In rats without frontal infarct, vibrissae stimulation led to activation of lCMRglc in the three synaptic relay stations of the barrel-field pathway (ipsilateral trigeminal medullary nucleus, contralateral ventrobasal thalamus, and contralateral barrel-field cortex). The mean increment in lCMRglc was 42% in lamina IV of barrel-field cortex and 49% in ventrobasal thalamus. Normalized lCBF tended to increase in superficial cortical laminae. In unstimulated animals with frontal infarct, lCMRglc was reduced by 20-30% throughout the ipsilateral barrel-field cortex as well as other ipsilateral cortical regions, but not in ventrobasal thalamus or other subcortical areas. In animals with frontal infarct subjected to contralateral vibrissae stimulation, a remarkable suppression of activation was observed throughout the barrel-field cortex so that left-less-than-right hemispheral lCMRglc asymmetry persisted despite stimulation. The ventrobasal thalamus, similarly, failed to increment its lCMRglc with vibrissae stimulation, whereas activation of the trigeminal nucleus was not suppressed. Similar trends were observed in the normalized lCBF data. These observations, which establish that a small frontal infarct is capable of suppressing normal physiological activation in remote ipsilateral brain structures, may have important implications with respect to suppression and recovery of function in human ischemic stroke.

Modulation of NMDA receptor-mediated responses by glycine and d-serine in the rat thalamus in vivo

The effects of iontophoretically applied glycine and d-serine upon responses of rat ventrobasal thalamus neurones to excitatory amino acids and sensory stimulation were investigated. Glycine inhibited excitatory responses to kainate, quisqualate and N-methylaspartate (NMA). Strychnine antagonised inhibitory responses to glycine, but in only a small number ( 2 7 ) of cases did such an antagonism reveal a facilitatory action of glycine on NMA responses. d-Serine inhibited responses of almost all neurones to either kainate or quisqualate, but enhanced responses to NMA on nearly half of the tested neurones, whilst having a weaker inhibitory action on the remainder. It is thus possible that d-serine has a dual action: (i) a facilitation of N- methyl- d-aspartate (NMDA) receptor-mediated responses and (ii) a non-selective inhibitory action.

Modulatory effects of serotonin on excitatory amino acid responses and sensory synaptic transmission in the ventrobasal thalamus

Excitatory amino acid receptors are thought to mediate sensory input to the ventrobasal thalamus. There is evidence for a brainstem serotonergic projection to the ventrobasal thalamus which may have a modulatory role. The possibility that serotonin may selectively modulate responses to excitatory amino acid receptor agonists and its effects on sensory synaptic transmission has been examined in the rat ventrobasal thalamus in vivo. Iontophoretic ejection of serotonin at low currents produced a marked facilitation of responses to excitatory amino acids. In contrast, excitatory responses to cholinomimetic agonists were attenuated. Synaptic transmission was concomitantly enhanced or unchanged in these circumstances. Higher serotonin ejection currents reversed the facilitation, or inhibited excitatory amino acid responses and synaptic transmission. It is concluded that serotonin can modulate responses to excitatory amino acids relatively selectively and that synaptic transmission of somatosensory information through the ventrobasal thalamus may be susceptible to brainstem serotonergic modulation.

Synaptic substrates for enkephalinergic and serotoninergic interactions with dental primary afferent terminals in trigeminal subnucleus interpolaris: an immunocytochemical study using peroxidase and colloidal gold.

Pain processing in the trigeminal complex has been thought to reside primarily in the spinal subnucleus caudalis (Vc). However, trigeminal tractotomies eliminating primary afferent input to Vc and severance of secondary trigemino-thalamic fibers from Vc do not disturb pain perception from the central face and oral cavity. Furthermore, large numbers of neurons that are highly responsive to noxious stimuli and suppressed by inputs from the periaqueductal gray and raphe complex have been identified in subnuclei interpolaris (Vi) and oralis (Vo). Therefore, the purpose of this study was to assess the distribution and spatial arrangements of nociceptive modulatory transmitters with nociceptive afferents and trigemino-thalamic relay cells in the rostral portion of the spinal trigeminal nuclear complex. The dental pulp contains predominantly nociceptors that project to all three subdivisions of the trigeminal spinal complex. These projections were visualized by anterograde transganglionic transport of horseradish peroxidase or by degeneration following administration of toxic ricin to the pulp chambers. The spatial arrangements of dental primary afferents with enkephalinergic (ENK) and serotoninergic (5HT) inputs was then assessed by employing avidin-biotin peroxidase and protein-A colloidal gold double-labeling immunocytochemistry. Trigemino-thalamic relay cells were also labeled by retrograde transport of HRP after stereotaxic injections into the ventrobasal thalamus. ENK and 5HT immunoreactivity was found in the ventrolateral quadrant and lateral margin of Vi, together with the adjacent interstitial nucleus (IN). This activity extended from the caudal pole of Vi and the periobex region, where it was most dense, rostrally to a position approximately 2.9 mm from the Obex. Neither ENK nor 5HT immunoreactivity was observed in Vo. Primary dental afferents projected into the ventromedial quadrant of rostral Vi and were found in the ventrolateral quadrant and dorsal aspect of the subnucleus farther caudally. They appeared as simple boutons with single contacts or as larger, sometimes scalloped terminals that formed multiple contacts. Postsynaptic elements were usually small dendritic profiles, although relay cell somata rarely received primary afferent inputs. Many primary afferents entered areas of synaptic clustering and contacted enkephalinergic dendrites, some of which were also postsynaptic to serotoninergic synapses. Alternatively, primary afferents contacted unlabeled processes that were also postsynaptic to the enkephalinergic element to form a triad arrangement. The least common occurrence was axo-axonic contacts in which enkephalinergic synapses were presynaptic to primary afferents. Both enkephalinergic and serotoninergic synaptic categories displayed round vesicles and generally formed asymmetric junctions.(ABSTRACT TRUNCATED AT 400 WORDS)

Multiple inputs to a population of thalamocortical neurons projecting to cat somatosensory cortex.

Ninety thalamocortical (TC) neurons were recorded extracellularly in ventrobasal thalamus of halothane-anesthetized cats. Projections of all of these neurons to specific subdivisions of somatosensory cortex were identified by their antidromic invasion following intracortical microstimulation restricted to these subdivisions. Collision-extinction tests were used to document excitatory inputs to TC neurons from afferent fibers of forelimb nerves stimulated electrically. Thirty-nine TC neurons (43% of sample) were excited from at least one forelimb nerve. Fifteen TC neurons were activated from two or more forelimb nerves. Combinations of effective nerves included ones innervating topographically different regions of forelimb. Neurons projecting to area 1-2 were least likely to be activated from more than one nerve. Seven TC neurons activated by electrical stimulation of nerve trunks were tested also with two distinct forms of mechanical somatic stimuli, i.e., hair bending and vibration, and with intradermal electrical stimuli. These tests revealed convergent inputs from hairy and glabrous skin. We conclude that there is a population of neurons, located in ventrobasal thalamus, which is capable of conveying multiple inputs to each of the subdivisions of primary somatosensory cortex. These neurons could be involved in forming properties of feature-extracting neurons of somatosensory cortex.

Gamma-aminobutyric acid and afferent inhibition in the cat and rat ventrobasal thalamus

Extracellular single neuron recordings were made in the ventrobasal thalami of anaesthetized rats and cats. Physiological stimulation of vibrissa and hair follicle afferents was performed with an air jet (10–20 ms duration) directed at a single vibrissa or small area of hairy skin. Paired conditioning and test air jets delivered to the excitatory portion of receptive fields revealed inhibition of the response of ventrobasal thalamic neurons to test stimuli following the excitatory response to the conditioning stimulus. Such inhibitions could last up to 500 ms. An increase in neuronal excitability was sometimes observed following this inhibitory period. In addition, it was possible to produce inhibition without an excitatory response using conditioning stimuli delivered adjacent to the excitatory receptive field. Iontophoretic application of bicuculline methochloride, with currents that were adequate to antagonize iontophoretically applied GABA, was found to reduce the inhibition of test responses evoked by conditioning stimuli in almost all of the neurons studied. In most cases, no excitatory responses to conditioning stimuli directed outside the original excitatory receptive field were revealed by application of the GABA antagonist. In rats, bicuculline also led to a decrease in the post-inhibitory excitation, whereas in cats the converse appeared to be the case. These results suggest that GABAergic transmission may underlie inhibitory responses of cat and rat ventrobasal thalamus neurons to physiological stimulation of somatosensory afferents. Furthermore, removal of such inhibition does not appear to reveal excitatory inputs from outside of the original excitatory receptive field.

The effects of N-acetylaspartylglutamate and distribution of N-acetylaspartylglutamate-like immunoreactivity in the rat somatosensory thalamus

The ventrobasal thalamus and adjacent regions were stained for the presence of N-acetylaspartylglutamate-like immunoreactivity. Immunoreactive axonal terminals were observed in this area and also in certain non-specific thalamic nuclei, the reticular thalamic nucleus and the lateral geniculate nucleus. Stained somata were found in the habenula, centrolateral thalamic nucleus and reticular thalamic nucleus. Iontophoretically applied N-acetylaspartylglutamate had variable, although predominantly inhibitory, actions on ventrobasal thalamus neurons. These results indicate that N-acetylaspartylglutamate is unlikely to be the neurotransmitter of ascending somatosensory afferents, but do not rule out the possibility that it has some other neurotransmitter or neuromodulator role in the ventrobasal thalamus.

Antagonism of N-methylaspartate and synaptic responses of neurones in the rat ventrobasal thalamus by ketamine and MK-801.

1. Extracellular single neurone recordings were made in the ventrobasal thalamus of urethane-anaesthetized rats. 2. Iontophoretically and intravenously administered ketamine and MK-801 were found to be selective antagonists of responses of neurones to iontophoretically applied N-methylaspartate. 3. Both antagonists, administered in N-methylaspartate-selective quantities, reduced the synaptic responses of ventrobasal thalamus neurones to a two-second air jet directed at the peripheral receptive field.

The effect of thiamine deficiency on the structure and physiology of the rat forebrain

Dietary thiamine deficiency, enhanced by pyrithiamine administration in adult rats, produces overt lesions in the brain that are especially prominent in the thalamus. The present study was undertaken to determine whether the thalamic lesions could be correlated with alterations in the physiological properties of neurons in the thalamus and somatosensory cortex. The regimen for experimentally inducing thiamine deficiency produced large lesions in the thalamus of every case; the lesions included most, if not all, of the neurons in the intralaminar thalamic nuclei. The extent of the lesion in the intralaminar thalamus was highly correlated with the loss of bilaterally synchronous spontaneous activity in the cerebral cortex. This correlation was seen in animals analyzed as early as 1-18 hr after the appearance of opisthotonus, the crisis state of thiamine deficiency, and as late as 2-9 weeks of recovery following thiamine replacement therapy. The loss of bilateral synchronous bursting neuronal activity following intralaminar thalamic lesions is consistent with the proposed role of the intralaminar thalamus as a pacemaker for rhythmic cortical activity (Armstrong-James et al., Exp. Brain Res., 1985; Fox and Armstrong-James, Exp. Brain Res. 63: 505-518, 1986). The location and size of the central lesions within the thalamus suggest that the observed neuronal loss could result from a nonhemorrhagic infarction in the ventromedial branches of the superior cerebellar arteries. Experimental thiamine deficiency also produced alterations in the receptive field properties of the somatosensory cortex neurons in all animals examined. Changes in cortical receptive field properties were correlated with the destruction of sensory relay neurons in the thalamic ventrobasal complex. The loss of the central lateral thalamic input to the cortex and the loss of somatosensory relay neurons in the ventrobasal thalamus in experimental thiamine deficiency produce alterations in cortical function which may contribute to deficits in memory and cognition analogous to those which characterize Korsakoff's psychosis in humans.

Inhibition of rat spinothalamic tract neuronal responses to noxious skin heating by stimulation in midbrain periaqueductal gray or lateral reticular formation

The descending inhibitory effects of electrical midbrain stimulation on identified lumbar spinothalamic tract (STT) neurons were investigated in rats anesthetized with sodium pentobarbital. STT units were identified by their antidromic response to stimulation in the contralateral ventrobasal thalamus or medial lemniscus (mean conduction velocity: 18–20 m/sec). Thirty-two of 43 dorsal horn multireceptive STT units gave reproducible responses to noxious heat stimuli (42–56°C, 10 sec) applied to the ventral hind paw. All STT units' responses were suppressed during stimulation (100 msec trains at 100 Hz, 3/sec, 15–300 μA) in PAG or LRF bilaterally. On- and offset of inhibition was rapid ( < 1 sec). STT unit responses to noxious heat were more effectively suppressed by LRF than PAG stimulation, based on statistically significant differences in mean thresholds for inhibition, slopes of current-inhibition plots, and mean current intensities evoking 50% inhibition. Mapping experiments revealed lowest-threshold ( < 25 μA) sites for inhibition to be in ventral PAG, subjacent tegmentum, and LRF bilaterally. STT unit responses increased with graded increases in stimulus temperature from threshold (mean: 46°C) to 56°C. Slopes of temperature-response functions were significantly reduced with little change in threshold during PAG stimulation, whereas these functions were shifted in a parallel manner toward higher temperatures during LRF stimulation. The serotonin antagonist methysergide reduced or blocked PAG- or LRF-evoked inhibition in 3 5 and 5 12 STT units, respectively. These results indicate that STT units are subject to different inhibitory controls from PAG and LRF.

A common somaesthetic pathway to red nucleus and motor cortex

Comparable short latency somaesthetic responses have been observed in the red nucleus and the motor cortex. Since previous experiments showed that a ventral spinal ascending pathway could account for red nucleus responses, the present experiments were designed to establish whether the same pathway could also transmit the short latency peripheral inputs to motor cortex. Two experimental data argue in favour of a such organization: (1) Using the collision technique, it was demonstrated that somaesthetic responses recorded in red nucleus cells are transmitted by collaterals of ascending fibres ending in the ventrobasal thalamus. (2) Intracellular recordings from identified corticospinal cells were performed on cats acutely prepared on section of the brachium conjunctivum and the dorsal columns of the spinal cord. Cortico-cortical connections to motor cortex were also eliminated by lesions of the ipsilateral sensory cortex and contralateral motor cortex. With this preparation it is still possible to record postsynaptic potentials after stimulation of primary afferent fibres in the dorsal columns, caudally to their section. The existence of these somaesthetic parallel inputs to rubro- and corticospinal cells suggests that the ongoing movement might be corrected on-line by these two pathways.

Collaterals of spinothalamic tract cells to the periaqueductal gray: a fluorescent double-labeling study in the rat

Spinothalamic tract (STT) cells were investigated in the rat to determine the distribution of STT cells with terminals in both the ventrobasal (VB) thalamus and the lateral periaqueductal gray (PAG). Two retrogradely transported fluorescent dyes (Diamidino yellow and Granular blue) were injected into each animal. The distribution of single- and double-labeled cells was mapped in the cervical, thoracic, lumbar and sacral spinal cord. An average of 1.4% of all STT cells and 6.2% of PAG cells projected to both VB thalamus and PAG. Double-labeled cells were observed only in cervical and lumbar levels of the spinal cord, with the greatest number found in the cervical enlargement. The double-labeled cells were located in laminae I and V and also in the lateral spinal nucleus (LSN). The number of double-labeled cells found in each of these 3 areas varied depending on the spinal cord level. This population of neurons exhibiting collaterals provide an anatomical mechanism by which noxious stimuli activate neurons not only in the thalamus but also in the PAG, which is an area involved in stimulation-produced analgesia (SPA).

Medullary sources of projections to the kinesthetic thalamus in raccoons: external and basal cuneate nuclei and cell groups x and z.

In raccoons and other mammals, a pathway for kinesthetic sensation (from muscles, fascia, tendons, and joints) reaches the anterodorsal cap of the ventrobasal thalamus and the anteriormost part of the somatic sensory cerebral cortex. To find the medullary component of this kinesthetic pathway in raccoons, small injections of horseradish peroxidase were made in the thalamus under guidance of simultaneous electrophysiological recording from kinesthetic projections. As determined by retrograde labeling following these injections, kinesthetic thalamic subregions receive projections as follows: caudomedial from cells in the external cuneate nucleus and its medial tongue, rostromedial from cells in basal cuneate nucleus, and rostrolateral from cells in cell group z and the reticular division of cell group x. Electrophysiological recording showed kinesthetic representations in each of these medullary regions. Labeled cells were also observed in the infratrigeminal subnucleus of the lateral reticular nucleus. Cats have kinesthetic projections to the thalamus from the basal cuneate and cell group z; raccoons (and monkeys) have these plus projections from the external cuneate and cell group x. This suggests that the kinesthetic projection system in raccoons and monkeys is expanded in correlation with their more dextrous use of the hand.

Excitatory amino acid receptor-mediated transmission of somatosensory evoked potentials in the rat thalamus.

1. To examine the role of excitatory amino acid receptors in the rat ventrobasal thalamic nucleus (v.b.t.n.) for the transmission of cortical somatosensory evoked potentials (s.e.p.s), potentials were recorded from the somatosensory cortex of barbiturate-anaesthetized and of unanaesthetized awake rats. The effects of microapplications of the selective N-methyl-D-aspartate (NMDA) antagonist (-)-2-amino-7-phosphono-heptanoate ((-)AP7) and the broad-spectrum excitatory amino acid antagonist 1-(p-chlorobenzoyl)-piperazine-2,3-dicarboxylate (pCB-PzDA) into the thalamus on the amplitudes and latencies of cortical potentials were measured. 2. To define the receptor specificity of local microinjections of (-)AP7 and pCB-PzDA electroencephalogram (e.e.g.) recordings were made from the immediate vicinity of the injection cannula within the thalamus. (-)AP7 selectively antagonized epileptic discharges induced by NMDA, but not those by kainate, whereas pCB-PzDA antagonized epileptic discharges induced by both. 3. In both anaesthetized and unanaesthetized rats, microapplications of pCB-PzDA into the thalamus suppressed transmission of cortical potentials as indicated by a decrease of their amplitudes and an increase of their peak latencies. Further experiments in anaesthetized rats showed that pCB-PzDA exerted its effects in a dose-dependent and site-specific way. 4. In both anaesthetized and unanaesthetized rats, microapplications of (-)AP7 into the ventrobasal thalamus did not affect cortical potentials. 5. These results are consistent with the assumption that an excitatory amino acid serves as transmitter at thalamic synapses mediating transmission of cortical potentials, and that this transmitter interacts preferentially with non-NMDA receptors.

Effects of repeated noxious thermal stimuli on the responses of neurons in the lateral cervical nucleus of cats: evidence for an input from A-nociceptors to the spinocervicothalamic pathway

Recent findings indicate that the lateral cervical nucleus (LCN) in cats is capable of transmitting to the ventrobasal thalamus information that may contribute to nociception. In the present study, we examined the effects of repeated noxious thermal stimulation on the responses of LCN neurons in unanesthetized cats that were decerebrated and partially spinalized. Seventeen LCN neurons were recorded that responded to noxious mechanical stimuli. The most responsive area of the receptive field of each neuron was exposed to repeated and sustained thermal stimuli of up to 55 °C. Such stimulation decreased the thermal thresholds of all 17 LCN neurons and increased the frequencies of their responses to identical thermal stimuli. The characteristics of this sensitization suggest that the spino-cervicothalamic pathway receives a prominent input from A-nociceptors.

Chronic sensory deprivation affects cytochrome oxidase staining and glutamic acid decar☐ylase immunoreactivity in adult rat ventrobasal thalamus

The rodent ventrobasal thalamus (VB) contains groups of vibrissa-related neurons (barreloids) that are highly reactive for the enzyme cytochrome oxidase. The present experiments show that each barreloid also contains a dense accumulation of glutamic acid decar☐ylase (GAD) immunoreactive terminals. Chronic vibrissa trimming results in parallel declines in staining for both cytochrome oxidase (CO) and GAD in barreloids associated with the trimmed hairs. Thus, thalamic metabolism like that in the cortex is dependent upon normal sensory input. This includes projection neurons as well as neurons in the reticular nucleus, which are the major source of γ-aminobutyric acid (GABA)ergic input to the rat VB.

Thresholds and encoding of neuronal responses to mechanical stimuli in the ventro-basal thalamus during carrageenin-induced hyperalgesic inflammation in the rat

Neuronal response thresholds and the encoding of mechanical stimulus intensity in the ventro-basal (VB) thalamus was analyzed in anaesthetized rats before and during the first two hours following induction of hyperalgesic inflammation. This inflammation was induced by the intra-plantar injection of carrageenin in the hindpaw contralateral to the recorded neurones. Only neurones exclusively driven by noxious stimuli and with a receptive field on or including the injected paw were considered. In this early phase of the inflammatory process, there was no significant modification of the response threshold to the mechanical stimulus (indentation of about 300 micron). This suggests the involvement of additional neuronal population(s) to account for the decrease in the vocalisation threshold to pressure observed in the freely moving animal at this time of the inflammation. A liner encoding of the indentation depth was observed before and after the carrageenin injection although the slope of the stimulus response-curve was steeper after the injection. The data emphasize that the carrageenin-sensitization acts differentially on the liminal and supra-liminal responses of the same neurone to a skin indentation, since in the first hour following the initiation of the inflammation the sensitization is essentially observed for responses obtained with stimulus intensity largely above the threshold value. With regard to previous observations using thermal stimulation, the results also illustrate that the carrageenin induced sensitization of responses differs depending on the stimulus intensity and modality used.

Excitatory amino acid receptors and synaptic transmission in the rat ventrobasal thalamus.

1. Extracellular single-neurone recordings were made in the ventrobasal thalamus (v.b.t.) of urethane-anaesthetized rats with multi-barrel ionophoretic electrodes in order to test the hypothesis that excitatory amino acid receptors are involved in the responses of these neurones to stimulation of sensory afferents. 2. Responses of neurones to either physiological stimulation of hair and vibrissa follicle sensory afferents and to ionophoretically applied excitatory amino acids were challenged with the antagonists D-2-amino-5-phosphonovalerate (APV), kynurenate and gamma-D-glutamylaminomethyl sulphonate (GAMS). 3. In agreement with previous findings in other brain areas, ionophoretically applied APV was found to selectively antagonize responses of v.b.t. neurones to N-methylaspartate (NMA), whereas GAMS was found to be moderately kainate selective. Kynurenate was found to be relatively non-selective. 4. Responses of neurones to short-duration (10-20 ms) physiological stimulation of afferents were resistant to APV when this antagonist was applied with NMA-selective ionophoretic currents. In contrast, these APV currents were adequate to antagonize responses to maintained physiological stimulation. 5. The broad spectrum excitatory amino acid antagonist kynurenate was found to block synaptic responses of v.b.t. neurones to both short-duration and maintained stimuli when it was applied with currents which were sufficient to reduce responses to ionophoretic quisqualate. 6. GAMS was found to selectively block kainate responses in a proportion of the neurones tested. In such cases, there was little effect of the antagonist on the responses evoked by either short-duration or maintained sensory stimuli. 7. It is concluded that excitatory amino acid receptors of both the NMDA and non-NMDA type are involved in the synaptic responses of v.b.t. neurones to sensory afferent stimulation, and that the apparent synaptic pharmacology depends on the mode of stimulation of the afferent pathway.

The differential synaptic organization of the spinal and lemniscal projections to the ventrobasal complex of the rat thalamus. Evidence for convergence of the two systems upon single thalamic neurons

The synaptic organization of terminals originating either from the spinal cord (spinothalamic) or from the dorsal column nuclei (lemniscal) was investigated in the ventrobasal complex of the rat thalamus. Wheatgerm agglutinin conjugated to horseradish peroxidase was used as an anterogradely transported axonal tracer, using benzidine dihydrochloride as a chromogen for the identification by electron microscopy of spinal and lemniscal projections to the ventrobasal thalamus. A double anterograde tract tracing strategy, based upon labeling by wheatgerm agglutinin conjugated to horseradish peroxidase of spinal terminals and simultaneous visualization of lemniscal terminals identified by Wallerian degeneration induced by lesion of the neurons of origin in the dorsal column nuclei, was used to compare the postsynaptic elements contacted by the two pathways and to look for a possible convergence of the two pathways onto single thalamic neurons. Spinal and lemniscal terminals are large (2–2.5 μm mean average diameter) terminals containing several mitochondria and numerous rounded vesicles. A quantitative analysis of the mean average diameters of the terminals revealed that one could not differentiate between synapses formed by the two pathways on a morphological basis. Terminals of the two pathways make asymmetrical contacts (Gray type I) with dendrites of varying diameter, dendritic protrusions, and cell somata. A quantitative analysis of the least diameter of the postsynaptic elements demonstrates projections of the two systems to different, partially overlapping regions of thalamic neurons. Lemniscal terminals originating from the dorsal column nuclei frequently contact cell somata; axosomatic spinothalamic contacts are uncommon. In addition, lemniscal projections tend to contact more proximal dendrites than do spinal projections, and this differential synaptic organization is statistically significant. From a functional point of view, this differential synaptic organization might indicate that lemniscal inputs have greater influence than spinal inputs in affecting the activity of thalamic neurons. Labeled spinothalamic terminals contact the same dendritic profile as do degenerating lemniscal terminals in about 10% of single sections. Because the present study did not include a complete reconstruction of ventrobasal complex neurons of the thalamus or even regions of dendritic arbors, the degree of convergence is likely to be significantly underestimated. These findings indicate that the anatomical basis exists for an interaction between nociceptive and non-nociceptive somesthetic systems at the level of single ventrobasal neurons of the thalamus of the rat.

Evidence for a viscerotopic sensory representation in the cortex and thalamus in the rat

The functional organization of the insular cortex was studied by recording neuronal responses to visceral sensory stimuli. Horseradish peroxidase (HRP) was then iontophoresed at the recording sites to identify afferents from the ventrobasal thalamus to specific visceroceptive sites in the insular cortex. The relationship of the ventrobasal thalamus to the insular cortex and to brainstem relay nuclei for the ascending visceral projections was then examined by using the axonal transport of HRP, wheat germ agglutinin conjugated to HRP (WGA-HRP), and fluorescent dyes. Of a total of 55 neurons that were tested for responses to visceral sensory stimuli, 33 units responded to at least one visceral sensory modality: 6 received gastric mechanoreceptor input, 8 responded to taste inputs, 13 were activated by arterial chemoreceptors and/or showed respiratory related activity, and 6 responded to cardiovascular baroreceptor stimulation. On the basis of its cytoarchitecture and connections with the thalamus, the insular cortex was divided into a dorsal granular area, an intermediate dysgranular region, and a ventral agranular strip. Taste-responsive neurons were located anteriorly, primarily in the dysgranular region, whereas unit responses to general visceral modalities were distributed dorsally and posteriorly in the granular insular cortex. Gastric mechanoreceptor-responsive units were situated more dorsally and anteriorly in the granular insular cortex, while cardiopulmonary inputs were located more ventrally and posteriorly. Injections of HRP into the gustatory insular cortex resulted in retrograde labeling of neurons in the parvicellular part of the ventroposterior medial thalamic nucleus (VPMpc). Injections into the general visceral insular cortex retrogradely labeled neurons lateral to VPMpc in the ventroposterior lateral parvicellular thalamic nucleus (VPLpc). Injections of HRP, WGA-HRP, and fluorescent dyes into VPMpc and VPLpc verified that their projection to the insular cortex is topographically organized. In the same experiments, retrogradely labeled neurons in the parabrachial nucleus identified the likely subnuclei within this nucleus for relay of visceral sensory information to the thalamus. Injections of WGA-HRP into the parabrachial nucleus demonstrated that its projection to the ventrobasal thalamus is also topographically organized. These results demonstrate the relationship of general visceral and special visceral (taste) representations in the insular cortex. The ascending pathway for visceral sensory information appears to be viscerotopically organized at all levels of the neuraxis, including the insular cortex.