Desensitizing glutamate receptors shape excitatory synaptic inputs to tiger salamander retinal ganglion cells

AMPA/kainate (KA) receptors mediate a component of ganglion cell excitatory postsynaptic currents (EPSCs). We investigated whether desensitization at these receptors contribute to the shape of transient EPSCs in ON-OFF ganglion cells. Whole-cell, voltage-clamp recordings were made from ganglion cells in the retinal slice or in isolation. EPSCs were evoked by either stimulating the slice with light or puffing K+ at the outer plexiform layer (OPL). The AMPA/KA receptor-mediated component of the EPSCs was isolated by including NMDA receptor antagonists in the bath. Strychnine and picrotoxin blocked inhibitory inputs. In isolated ganglion cells, cyclothiazide (10 microM), which blocks desensitization in non-NMDA receptors, enhanced both the amplitude and the duration of currents evoked by puffs of AMPA or glutamate. EPSCs evoked by K(+)-puffs in the OPL were also enhanced by cyclothiazide (30 microM). When AMPA/KA receptors were blocked with NBQX (10 microM), no enhancement of the EPSCs by cyclothiazide was observed, indicating that cyclothiazide did not act presynaptically. Cyclothiazide also enhanced the amplitude and duration of both the ON and OFF light-evoked (L-) EPSCs recorded in ON-OFF ganglion cells. Current-voltage relationships showed the enhancement was not voltage dependent. When control and enhanced responses where normalized, it was observed that the rate of desensitization of both the ON and OFF L-EPSCs was decreased by cyclothiazide. Cyclothiazide selectively enhanced the AMPA/KA receptor-mediated component of ganglion cells EPSCs, suggesting that desensitization of AMPA/KA receptors shape transient L-EPSCs.     

The functional influence of burst and tonic firing mode on synaptic interactions in the thalamus

Thalamocortical and perigeniculate (PGN) neurons can generate action potentials either as Ca2+ spike-mediated high-frequency bursts or as tonic trains. Using dual intracellular recordings in vitro in monosynaptically connected pairs of PGN and dorsal lateral geniculate nucleus (LGNd) neurons, we found that the functional effect of synaptic transmission between these cell types was strongly influenced by the membrane potential and hence the firing mode of both the pre- and postsynaptic neurons. Activation of single action potentials or low-frequency spike trains in PGN or thalamocortical neurons resulted in the generation of PSPs that were 0.5-2.0 mV in amplitude. In contrast, the generation of Ca2+ spike-mediated bursts of action potentials in the presynaptic cell increased these PSPs to an average of 4.4 mV for the IPSP and 3.0 mV for the EPSP barrage, because of temporal summation and/or facilitation. If the postsynaptic neuron was at a resting membrane potential (e.g., -65 mV), these PSP barrages could result in the activation of a low-threshold Ca2+ spike and burst of action potentials. These results demonstrate that the burst firing mode of action potential generation is a particularly effective means by which perigeniculate and thalamocortical neurons may influence one another. We propose that the activation of burst discharges in these cell types is essential for the generation of some forms of synchronized rhythmic oscillations of sleep and of epileptic seizures.     

Context-dependent synaptic action of glycinergic and GABAergic inputs in the dorsal cochlear nucleus

Cartwheel cells are prominent interneurons in the dorsal cochlear nucleus (DCN) that bear considerable homology to cerebellar Purkinje cells. They contact other cartwheel cells as well as fusiform cells, the principal cells of the DCN. In fusiform cells, the inhibition from cartwheel cells interacts with excitation mediated by granule cells and auditory nerve fibers, and shapes the output of the DCN in its ascent to the inferior colliculi. With intracellular recordings from anatomically identified cells in slices, synaptic inputs to fusiform and cartwheel cells were analyzed pharmacologically. Shocks to the auditory nerve and granule cell domains evoked glutamatergic, glycinergic, and GABA(A)ergic postsynaptic potentials (PSPs) in both cartwheel and fusiform cells. The temporal patterns of spontaneous and evoked glycinergic PSPs in fusiform and cartwheel cells were similar and mirrored the pattern of firing of cartwheel cells, probably reflecting the anatomical connections between these cell types and supporting the conclusion that cartwheel cells are glycinergic. In fusiform cells, glycinergic and GABA(A)ergic IPSPs evoked with shocks reversed at -68 mV on average. In marked contrast, glycinergic and GABA(A)ergic PSPs in cartwheel cells, as well as responses to exogenous application of 50-100 mM glycine or 100 microns muscimol, were depolarizing. Reversal potentials of PSPs and responses to glycine and muscimol were similar and averaged -52 mV. Glycinergic and GABA(A)ergic PSPs could elicit firing from cartwheel cells at their resting potentials, but could also reduce rapid firing during strong depolarizations. Thus, the action of glycinergic and GABA(A)ergic inputs on cartwheel cells depends on the electrophysiological context in which they occur.     

Pallidal afferent territory of the Macaca mulatta thalamus: neuronal and synaptic organization of the VAdc

Ventral anterior thalamic nucleus pars densicellularis (VAdc) as delineated earlier (Ilinsky and Kultas-Ilinsky [1987] J. Comp. Neurol. 262:331-364) was analyzed by using qualitative and quantitative neuroanatomical techniques. Projection neurons (PN), retrogradely labeled with wheat germ agglutinin conjugated horseradish peroxidase from the cortex, were small to medium in size (mean area, 312 microm2) with numerous primary dendrites displaying a tufted branching pattern. Local circuit neurons (LCN), immunoreactive for gamma-aminobutyric acid (GABA) and glutamic acid decarboxylase, were small (mean area, 110 microm2), and gave off few dendrites. Two subpopulations of GABA positive boutons (F1 type) were distinguished: large (mean area, 2.6 microm2) terminals with symmetric synapses containing few pleomorphic vesicles and numerous mitochondria densely covered proximal PN sites; smaller F1 boutons with a slightly different morphology contacted mostly distal PN dendrites. Two subpopulations of terminals containing round vesicles and forming asymmetric synapses were distinguished by bouton size (mean areas, 0.4 microm2 and 1.6 microm2, respectively). These targeted mainly distal PN dendrites, but some synapsed proximally next to large F1 boutons. On distal dendrites, representatives of both types were labeled from the cortex. The density of boutons with symmetric and asymmetric synapses (the number of boutons per 100 microm of PN membrane length) was 3.3:0.2 on primary, 2.5:1.2 on secondary, and 0.8:12 on distal dendrites. The numerical density of synapses formed by presynaptic LCN dendrites on all PN levels was 20 to 40 times less than that of axon terminals at the same sites. Afferent input to LCN from boutons of all types, including that from 50% of labeled cortical boutons, mainly targeted distal dendrites. Overall, the findings suggest that PN in VAdc receive massive inhibitory input proximally intermingled with some presumably excitatory input, and that LCN contribution to PN inhibition is modest.     

Modulation of spike frequency by regions of special axonal geometry and by synaptic inputs

1. Spike propagation across the nonhomogeneous section of the giant axon in ganglion T3 of the cockroach was analyzed by intracellular microelectrodes recording at the posterior and anterior ends of T3. Ascending and descending potentials were evoked by stimulation of A5-A6 and T2-T3 connectives. 2. At high frequencies, descending and ascending impulses exhibit the following: a) consecutive reduction in the spike amplitude, b) a decrease in the afterhyperpolarization; c) gradual appearance of a prepotential together with an increase in delay of spike initiation; d) failure of full spike invasion into the recording area, showing only a decremental potential. 3. The duration of a train required to block spike propagation when the whole connective is stimulated is much shorter (about 6 times) than that required when a single giant axon is stimulated. 4. The conduction block is associated with a marked decrease in effective membrane resistance, greater than that expected from depolarization and delayed rectification. 5. Synaptic potentials could be recorded in the giant axons in the caudal base of ganglion T3 after stimulation of either the ipsilateral or contralateral connectives at both ends of the ganglion. These synaptic potentials could be blocked by d-tubocurarine (d-TC) or low Ca2+-high Mg2+. 6. Activation of these synapses produces a marked increase in membrane conductance, blocking propagation of spike trains through the ganglion. 7. After these synapses are blocked by d-TC or low Ca2+-high Mg2+, high-frequency stimulation still produces a conduction block. 8. It seems that conduction of spike during repetitive stimulation is affected both by accumulation of extracellular potassium, which depolarizes the membrane and causes sodium inactivation, and by activation of synaptic inputs to shunt the membrane in this region. 8. Each of these two mechanisms by itself can produce conduction block along the giant axons in ganglion T3.     

Indirect synaptic inputs from filiform hair sensory neurons contribute to the receptive fields of giant interneurons in the first-instar cockroach

The purpose of this study was to assess peripheral quantitative computed tomography (pQCT) imaging for measurement of volumetric bone mineral density (BMD) in vivo in mouse tibia following ovariectomy, and following treatment with 17 beta-oestradiol (E2). Two studies were undertaken. In study 1, three groups (n = 10) of mature mice were ovariectomized (OVX) or sham operated (SHAM); one of the OVX groups was dosed weekly with E2 (OVX.E2). Images of the proximal tibia were acquired on the day of surgery and at intervals following surgery until week 6. In study 2, four groups (OVX, SHAM, OVX.E2 and a SHAM group dosed with E2, SHAM.E2) of immature mice (n = 10) were imaged weekly up to 10 weeks post-surgery. Precision of pQCT for measurement of total (trabecular plus cortical) BMD was 2.4%, trabecular 5.2% and cortical 2.6%. In mature animals, significantly slower net bone formation was seen in OVX compared with SHAM animals using paired analysis with each animal as its own control. Group analysis detected no significant difference in BMD between SHAM and OVX at any time point. In immature animals, using paired analysis, with each animal as its own control, a significant difference between SHAM and OVX animals was detectable 3 weeks post-surgery (P < 0.05). As in study 1, group analysis of total BMD failed to detect any significant difference between SHAM and OVX at any time point. Treatment with E2 caused an easily-detected increase in BMD and led to osteopetrosis in both groups. The statistical power of this technique is adequate for testing antiresorptive or bone-forming therapies in the mouse.     

Continuous vesicle cycling in the synaptic terminal of retinal bipolar cells

Endocytosis and exocytosis were investigated in the synaptic terminal of retinal bipolar cells by monitoring the uptake and loss of the fluorescent dye FM1-43. Depolarization in the presence of Ca2+ stimulated a continuous cycle of exocytosis and endocytosis that was approximately balanced at rates up to 3800 vesicles per s. Vesicles became available for exocytosis within 1 min of endocytosis, and about 700,000 releasable vesicles were specifically localized to a region within 2 microm of the plasma membrane. Release of caged Ca2+ using NP-EGTA while simultaneously monitoring cytosolic Ca2+ with Fura-2 indicated that continuous exocytosis was stimulated by sub-micromolar levels of Ca2+. It has been suggested that the ribbon synapse of bipolar cells only supports transient exocytosis, but our results demonstrate that this synapse is specialized for the continuous secretion of neurotransmitter.     

Activity-dependent plasticity of synaptic efficacy at inhibitory junctions

Despite a considerable amount of investigation on long-term potentiation, the question of whether this process occurs at inhibitory synapses has remained controversial until studies of these junctions have been achieved in the Mauthner cell of Teleosts. In this preparation, inhibitory long-term potentiation similar to that occurring at hippocampal excitatory synapses has been demonstrated.     

Neurochemistry and pharmacology of the major hippocampal transmitter systems: synaptic and nonsynaptic interactions

Hippocampus plays a crucial role in important brain functions (e.g. memory, learning) thus in the past two decades this brain region became a major objective of neuroscience research. During this period large number of anatomical, neurochemical and electrophysiological data have been accumulated. While excellent reviews have been published on the anatomy and electrophysiology of hippocampal formation, the neurochemistry of this area has not been thoroughly surveyed. Therefore the aim of this review is to summarize the neurochemical and pharmacological data on the release of the major neurotransmitters found in the hippocampal region: glutamate (GLU), gamma-amino butyric acid (GABA), acetylcholine (ACh), noradrenaline (NA) and serotonin (5-HT). In addition, this review analyzes the synaptic and nonsynaptic interactions between hippocampal neuronal elements and overviews how auto- and heteroreceptors are involved in the presynaptic modulation of transmitter release. The presented data clearly show that transmitters released from axon terminals without synaptic contact play an important role in the fine tuning of communication between neurons within a neuronal circuit.     

Simulated responses of cerebellar Purkinje cells are independent of the dendritic location of granule cell synaptic inputs

Cerebellar Purkinje cell responses to granule cell synaptic inputs were examined with a computer model including active dendritic conductances. Dendritic P-type Ca2+ channels amplified postsynaptic responses when the model was firing at a physiological rate. Small synchronous excitatory inputs applied distally on the large dendritic tree resulted in somatic responses of similar size to those generated by more proximal inputs. In contrast, in a passive model the somatic postsynaptic potentials to distal inputs were 76% smaller. The model predicts that the somatic firing response of Purkinje cells is relatively insensitive to the exact dendritic location of synaptic inputs. We describe a mechanism of Ca2+-mediated synaptic amplification, based on the subspiking threshold recruitment of P-type Ca2+ channels in the dendritic branches surrounding the input site.     

Synapse-specific control of synaptic efficacy at the terminals of a single neuron

The regulation of synaptic efficacy is essential for the proper functioning of neural circuits. If synaptic gain is set too high or too low, cells are either activated inappropriately or remain silent. There is extra complexity because synapses are not static, but form, retract, expand, strengthen, and weaken throughout life. Homeostatic regulatory mechanisms that control synaptic efficacy presumably exist to ensure that neurons remain functional within a meaningful physiological range. One of the best defined systems for analysis of the mechanisms that regulate synaptic efficacy is the neuromuscular junction. It has been shown, in organisms ranging from insects to humans, that changes in synaptic efficacy are tightly coupled to changes in muscle size during development. It has been proposed that a signal from muscle to motor neuron maintains this coupling. Here we show, by genetically manipulating muscle innervation, that there are two independent mechanisms by which muscle regulates synaptic efficacy at the terminals of single motor neurons. Increased muscle innervation results in a compensatory, target-specific decrease in presynaptic transmitter release, implying a retrograde regulation of presynaptic release. Decreased muscle innervation results in a compensatory increase in quantal size.     

Characterization of spontaneous inhibitory synaptic currents in salamander retinal ganglion cells

Spontaneous and light-evoked postsynaptic currents (sPSCs and lePSCs, respectively) in retinal ganglion cells of the larval tiger salamander were recorded under voltage-clamp conditions from living retinal slices. The focus of this study is to characterize the spontaneous inhibitory PSCs (sIPSCs) and their contribution to the light-evoked inhibitory PSCs (leIPSCs) in ON-OFF ganglion cells. sIPSCs were isolated from spontaneous excitatory PSCs (sEPSCs) by application of 10 microM 6,7-dinitroquinoxaline-2,3-dione (DNQX) + 50 microM 2-amino-5-phosphonopentanoic acid (AP5). In approximately 70% of ON-OFF ganglion cells, bicuculline (or picrotoxin) completely blocks sIPSCs, suggesting all sIPSCs in these cells are mediated by GABAergic synaptic vesicles and gamma-aminobutyric acid-A (GABAA) receptors (GABAergic sIPSCs, or GABAsIPSCs). In the remaining 30% of - ganglion cells, bicuculline (or picrotoxin) blocks 70-98% of the sIPSCs, and the remaining 2-30% are blocked by strychnine (glycinergic sIPSCs, or GLYsIPSCs). GABAsIPSCs occur randomly with an exponentially distributed interval probability density function, and they persist without noticeable rundown over time. The GABAsIPSC frequency is greatly reduced by cobalt, consistent with the idea that they are largely mediated by calcium-dependent vesicular release. GABAsIPSCs in DNQX + AP5 are tetrodotoxin (TTX) insensitive, suggesting that amacrine cells that release GABA under these conditions do not generate spontaneous action potentials. The average GABAsIPSCs exhibited linear current-voltage relation with a reversal potential near the chloride equilibrium potential, and an average peak conductance of 319.67 +/- 252.83 (SD) pS. For GLYsIPSCs, the average peak conductance increase is 301.68 +/- 94.34 pS. These parameters are of the same order of magnitude as those measured in inhibitory miniature postsynaptic currents (mIPSCs) associated with single synaptic vesicles in the CNS. The amplitude histograms of GABAsIPSCs did not exhibit multiple peaks, suggesting that the larger events are not discrete multiples of elementary events (or quanta). We propose that each GABAsIPSC or GLYsIPSC in retinal ganglion cells is mediated by a single or synchronized multiple of synaptic vesicles with variable neurotransmitter contents. In a sample of 16 ON-OFF ganglion cells, the average peak leIPSC (held at 0 mV) at the light onset is 509.0 +/- 233.85 pA and that at the light offset is 529.0 +/- 339.88 pA. The approximate number of GABAsIPSCs and GLYsIPSCs required to generate the average light responses, calculated by the ratio of the charge (area under current traces) of the leIPSCs to that of the average single sIPSCs, is 118 +/- 52 for the light onset, and 132 +/- 76 for the light offset.     

Sprouting of the visual corticocollicular terminal field after removal of contralateral retinal inputs in neonatal rabbits

Lentinan (LNT), a beta-glucan derived from Lentinus edodes (Berk.) Sign., is known to work positively against cachexia in patients with malignant tumors. Because the cachectin/tumor necrosis factor (TNF) is supposed to be one of the factors that mediate cancer cachexia, we tested the effects of LNT on TNF-induced cachexia in rats. First, we analyzed in detail the cachectic actions of TNF (0.2 mg/kg/day, 5 days, IV) on food and water intake, body weight, and locomotor activity. The day after the first administration of TNF (acute phase), food and water intake, as well as body weight, of all rats decreased. However, over the next few days of treatment (chronic phase), the rats gradually developed a tolerance to the cachectic actions of TNF. Specifically, after the third administration, the rats treated with TNF had a higher amount of water intake than the control rats. This was mainly due to an increase in daytime water intake. We also analyzed the effects of LNT (0.1 or 1.0 mg/kg, twice/wk. IV) on TNF-induced cachexia, and compared the data with those from the rats treated with TNF alone. The higher dosage of LNT significantly suppressed TNF-induced daytime polydipsia and increased the amount of nighttime water intake, as well as the meal size of nighttime food intake. These results suggest that LNT partially normalizes TNF-induced cachexia in rats.     

Corticotrophin-releasing factor produces a long-lasting enhancement of synaptic efficacy in the hippocampus

We have previously demonstrated that intra-hippocampal injection of corticotrophin-releasing factor improved memory retention of an inhibitory avoidance learning in rats; while the electrophysiological effects corticotrophin-releasing factor produces on hippocampal neurons are largely uncharacterized. In the present study, we found that corticotrophin-releasing factor injected into the dentate gyrus of hippocampus produced a dose-dependent and long-lasting enhancement in synaptic efficacy of these neurons, as measured by an increase in the amplitude and slope of population excitatory postsynaptic potentials, as well as the amplitude of population spike. The onset of corticotrophin-releasing factor-induced potentiation was slow. It was observed approximately 40-60 min after corticotrophin-releasing factor administration and lasted for more than 5 h. This effect of corticotrophin-releasing factor was blocked by pretreatment with the cyclase-adenosine-3,5-monophosphate (cAMP) inhibitor Rp-adenosine-3,5-cyclic monophosphothiolate triethylamine (Rp-cAMPS) and partially blocked by the N-methyl-D-aspartate receptor antagonist MK-801. Further, pretreatment with corticotrophin-releasing factor receptor antagonist dose-dependently diminished tetanization-induced long-term potentiation, and corticotrophin-releasing factor and tetanic stimuli had an additive effect on hippocampal neuron excitation. Moreover, direct injection of corticotrophin-releasing factor increased cAMP level in the dentate gyrus. These results together suggest that corticotrophin-releasing factor-induced potentiation simulates the late phase of tetanization-induced long-term potentiation and cAMP seems to be the messenger mediating this effect. Moreover, corticotrophin-releasing factor-induced potentiation and long-term potentiation may share some similar mechanisms, and corticotrophin-releasing factor is probably involved in the neural circuits underlying long-term potentiation. Thus, corticotrophin-releasing factor may play an important role in modulating synaptic plasticity in the hippocampus.     

Ethanol modulation of excitatory and inhibitory synaptic interactions in cultured cortical neurons

The effects of ethanol on spontaneous excitatory and inhibitory postsynaptic currents (EPSCs and IPSCs) were studied in a culture of embryonic rat cortical neurons. In these experiments, EPSCs and IPSCs were recorded concurrently as inward and outward currents, respectively. These spontaneous currents were dominated by a slow (<1 Hz) repetitive pattern of prolonged N-methyl D-aspartate (NMDA)-EPSCs and co-occurring IPSCs when Mg2+ was left out of the perfusate. A 3- to 5-min bath perfusion of 100 mM ethanol reduced the average integrated EPSC by 65%, while simultaneously potentiating IPSCs by about 3-fold. EPSC frequency was also reduced by about one-third. NMDA-mediated EPSCs were inhibited more than non-NMDA currents. A perfusion of 30 mM ethanol was less effective and probably represents a threshold concentration for these effects. The ethanol inhibition of currents evoked by directly applied glutamate or NMDA to these cells was much less than that observed for spontaneous EPSCs. Currents evoked by exogenous gamma-aminobutyric acid (GABA) application were never potentiated by ethanol. When spontaneous NMDA-EPSCs were blocked with an NMDA antagonist, ethanol no longer potentiated the IPSCs. However, benzodiazepine treatment increased these IPSCs 2-fold. In other experiments, spontaneous IPSCs were blocked by a GABA(A) antagonist. Here, the EPSCs occurred as groups of repetitive bursts. Ethanol decreased the total number of EPSCs per burst but did not decrease their overall amplitude, as in the control recordings. Thus, the way in which ethanol affects concurrently recorded spontaneous EPSCs and IPSCs appears different from the way in which it affects isolated GABA- and NMDA-evoked currents. In addition, the antagonist studies show that concurrently activated NMDA and GABA channels each tend to limit the responses of the other. Thus, the overall effect of ethanol on spontaneous activity may result, in part, by a modification of this synaptic interaction.     

Calcium and protein kinase C regulate the actin cytoskeleton in the synaptic terminal of retinal bipolar cells

The organization of filamentous actin (F-actin) in the synaptic pedicle of depolarizing bipolar cells from the goldfish retina was studied using fluorescently labeled phalloidin. The amount of F-actin in the synaptic pedicle relative to the cell body increased from a ratio of 1.6 +/- 0.1 in the dark to 2.1 +/- 0.1 after exposure to light. Light also caused the retraction of spinules and processes elaborated by the synaptic pedicle in the dark. Isolated bipolar cells were used to characterize the factors affecting the actin cytoskeleton. When the electrical effect of light was mimicked by depolarization in 50 mM K+, the actin network in the synaptic pedicle extended up to 2.5 micrometer from the plasma membrane. Formation of F-actin occurred on the time scale of minutes and required Ca2+ influx through L-type Ca2+ channels. Phorbol esters that activate protein kinase C (PKC) accelerated growth of F-actin. Agents that inhibit PKC hindered F-actin growth in response to Ca2+ influx and accelerated F-actin breakdown on removal of Ca2+. To test whether activity-dependent changes in the organization of F-actin might regulate exocytosis or endocytosis, vesicles were labeled with the fluorescent membrane marker FM1-43. Disruption of F-actin with cytochalasin D did not affect the continuous cycle of exocytosis and endocytosis that was stimulated by maintained depolarization, nor the spatial distribution of recycled vesicles within the synaptic terminal. We suggest that the actions of Ca2+ and PKC on the organization of F-actin regulate the morphology of the synaptic pedicle under varying light conditions.     

Trigeminal projections to thalamus and subthalamus in the hedgehog tenrec

The objective of the present study was the identification and characterization of the trigemino-diencephalic target areas in the Madagascan lesser hedgehog tenrec in order to get a more comprehensive view on the mammalian somatosensory thalamus, its evolution and representation in different species. Such an analysis has been considered important because in lower mammals the head and face are relatively well represented, but their ascending trigeminal projections have scarcely been analysed. Following injections of different tracer substances into the rostral and caudal portions of the trigeminal nuclear complex the most prominent area of termination was found in the medial ventroposterior nucleus. These projections were patchy and scarcely overlapped the region previously shown to receive spinal and dorsal column nuclear afferents. On the basis of the laterality and the intensity of the projections, two subdivisions were distinguished, the principal portion and the accessory portion receiving a dense contralateral and a weak bilateral input, respectively. They were considered equivalents to the magnocellular and parvocellular subdivisions of the medial ventroposterior nucleus in more differentiated mammals. In the latter species, however, the overlap between trigeminal and parabrachial fibres appears less extensive than in the tenrec. In addition, a weak bilateral projection was shown from the caudal trigeminal nucleus to the caudal and dorsal subdivision of the nucleus submedius. There was little, if any evidence for a trigeminal projection to the intralaminar nuclei and we failed to identify a correlate to the posterior nuclear complex of higher mammals. On the other hand, there was a distinct contralateral projection to the ventral portion of the zona incerta. This projection was of similar strength as the projection to the medial ventroposterior nucleus; it supports the notion that the zona incerta may play a crucial role in relaying trigeminal information.