Anteroventral Thalamic Nucleus Research Articles

Effects of MK-801 upon local cerebral glucose utilisation in conscious rats following unilateral lesion of caudal entorhinal cortex

Local cerebral glucose utilisation was examined in 62 discrete regions of conscious rats following unilateral ibotenic acid lesion of the caudal entorhinal cortex, and subsequent pharmacological challenge with (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5, 10-imine maleate (MK-801), a non-competitive N-methyl- d-aspartate (NMDA) receptor antagonist. Fourteen days after unilateral lesion of the entorhinal cortex, there were no significant alterations in local cerebral glucose use except within the lesioned entorhinal cortex (reduced by 31% compared to sham-operated control animals). In sham-operated animals, systemic administration of MK-801 (0.5 mg/kg, i.v.) induced anatomically organised alterations in glucose use with increases in olfactory areas, subicular complex and some limbic areas (posterior cingulate cortex, mammillary body and anteroventral thalamic nucleus), and decreases in the inferior colliculus and neocortex (auditory, sensory-motor, somatosensory and frontal cortices). In animals with unilateral entorhinal cortex lesions, the metabolic response to MK-801 differed significantly from the response to the drug in sham-lesioned animals in a number of regions, viz. hippocampus, molecular layer (ipsilateral to lesion), entorhinal cortex (ipsilateral), dentate gyrus (ipsilateral), presubiculum (bilateral), parasubiculum (bilateral) and nucleus accumbens (bilateral). The ability of MK-801 to reduce glucose use in the neocortex was not altered by entorhinal cortex lesion. These data suggest that the functional consequences of non-competitive NMDA receptor blockade are dependent in some areas upon the integrity of the perforant pathway from the entorhinal cortex to the hippocampus.

Corticotropin-releasing factor receptors in the rabbit brain visualized by in vitro autoradiography

Corticotropin-releasing factor (CRF) binding sites were visualized in the rabbit brain by in vitro autoradiography using the radioligand 125I-[Tyr 0]ovine CRF. The radioligand binding to sections of rabbit cingulate cortex were competed for by ovine and rat CRF with inhibitory constants (K i) of 26 and 37 nM, respectively, whereas sauvagine and alpha-helical CRF 9–41 were approximately 10-fold less potent. In the rabbit brain, the highest densities of binding sites for CRF are found in the pineal gland and the choroid plexus. The cerebral cortex is labelled throughout, with the highest concentration of binding sites in the piriform and primary olfactory divisions. In the cerebellar cortex, the granular layer is more intensely labelled than the molecular layer. The distribution of CRF binding sites in the hippocampus follows a laminar pattern; the molecular layer of the dentate gyrus is intensely labelled, the oriens, radiatum and lacunosum moleculare layers of Ammon's horn contain moderate densities of binding and no binding is observed in the granular layer of the dentate gyrus and the pyramidal cell layer. The ventral subnucleus of the lateral septum, the zonal and superficial layers of the superior colliculus contain high densities of receptors. A moderate concentration of binding sites is observed in the caudate nucleus, putamen, bed nucleus of the stria terminalis, paraventricular, anterodorsal and anteroventral thalamic nuclei and the medial nucleus of the mammillary body. The fundus striati, the dorsal subnucleus of the lateral septum, the lateral dorsal thalamic, lateral and medial geniculate nuclei, the lateral and anterior cortical amygdaloid nuclei, central and posterior interpeduncular nuclei all contain low but significant levels of CRF binding sites. No detectable binding is observed in the pons, medulla oblongata or fibre tracts. The high densities of CRF binding sites found in the cortex, hippocampus and structures associated with the limbic system supports a role for CRF in the modulation of behavioural and physiological responses associated with stress. However, the extremely high density of CRF binding sites found in the pineal gland and choroid plexus suggest a more extensive role for CRF in the rabbit central nervous system.

Effects of NMDA antagonists, MK-801 and CPP, upon local cerebral glucose use

The effects upon cerebral glucose utilisation of (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine (MK-801, a non-competitive N-methyl- D-aspartate (NMDA, receptor antagonist) and 3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP, a competitive NMDA receptor antagonist) were examined in conscious, lightly restrained rats. Cerebral glucose utilisation was assessed quantitatively in 74 brain regions with [ 14C]2-deoxyglucose autoradiography. The intravenous (i.v.) administration of MK-801 (0.05–5 mg/kg) induced heterogeneous patterns of altered cerebral glucose utilisation with statistically significant increased being observed in 21 brain areas and statistically significant decreases in 8 brain regions. Pronounced dose-related increases in glucose use were observed after MK-801 in the subicular complex, hippocampus molecular layer, dentate gyrus, limbic system (posterior cingulate cortex; mamillary body; anteroventral thalamic nucleus), olfactory areas and substantia nigra (pars reticulata). Glucose use in the neocortex and inferior colliculus was particularly sensitive to reduction by MK-801 administration. The pattern of altered glucose use after administration of CPP (3–30 mg/kg, i.v.) differed markedly from that observed after MK-801 treatment. Statistically significant increases in glucose use after CPP were noted in 11 brain areas and statistically significant decreases in 5 of the regions examined. Regions in which increases were noted after CPP included hippocampus molecular layer, olfactory areas, cochlear nucleus, vestibular nucleus, cerebellar nucleus, superior olives and substantia nigra (pars reticulata). These data indicate that widespread, anatomically organised alterations in cerebral function are associated with the administration of NMDA receptor antagonists despite the minor role normally ascribed to these receptors in conventional fast synaptic transmission. The distinct patterns of response to competitive and non-competitive antagonists may be a reflection of the differential responses of the two modes of receptor blockade to increased glutaminergic transmission.

Retrograde double‐labeling study of the marnmillothalamic and the mammillotegmental projections in the rat

Collateral axonal branching from the medial or lateral mammillary nuclei to the anterior thalamus, Gudden's tegmental nuclei, the nucleus reticularis tegmenti pontis, and the medial pontine nucleus was studied using the fluorescent retrograde double-labeling method. One day after injection of Fast Blue into the anterior thalamic nuclei or Gudden's tegmental nuclei, Nuclear Yellow was injected into Gudden's tegmental nuclei or the nucleus reticularis tegmenti pontis and the medial pontine nucleus. Following 1 day survival, single- and double-labeled neurons were examined in the mammillary nuclei. The lateral mammillary nucleus contains neurons whose collateral fibers project to both the dorsal tegmental nucleus of Gudden and the ipsilateral or contralateral anterodorsal thalamic nucleus, to both the medial pontine nucleus and the anterodorsal thalamic nucleus, and to both the dorsal tegmental nucleus of Gudden and the medial pontine nucleus. The pars medianus and pars medialis of the medial mammillary nucleus contain neurons whose collateral fibers project to both the anteromedial thalamic nucleus and the ventral tegmental nucleus of Gudden, to both the anteromedial thalamic nucleus and the medial part of the nucleus reticularis tegmenti pontis, and to both the ventral tegmental nucleus of Gudden and the medial part of the nucleus reticularis tegmenti pontis. The dorsal half of the pars posterior of the medial mammillary nucleus contains a few neurons whose collateral fibers project to both the anteromedial thalamic nucleus and the rostral part of the ventral tegmental nucleus of Gudden, and to both the caudal part of the anteroventral thalamic nucleus and the rostral part of the ventral tegmental nucleus of Gudden, while the pars lateralis of the medial mammillary nucleus contains no double-labeled neurons and projects only to the anteroventral thalamic nucleus.

Neurons containing cholecystokinin mRNA in the mammillary region: ontogeny and adult distribution in the rat

1. The ontogeny and adult distribution of neurons containing cholecystokinin (CCK) mRNA in the premammillary and mammillary nuclei and supramammillary region of the rat brain were studied using hybridization histochemistry. 2. The earliest detection of CCK mRNA in the mammillary region was on E14, followed by a marked increase in transcript levels during the next 4 days, a time during which neurons in this region still divide. During the first 2 weeks of life, few changes in the levels of CCK transcripts were seen, and an adult-like pattern of expression was seen on the twenty-first day of life. 3. Low levels of transcripts were present in numerous neurons located in all divisions of the medial nucleus and in the posterior nucleus known to project ipsilaterally to the anteroventral and anteromedial thalamic nuclei. In contrast, none of the neurons in the lateral nucleus (projecting bilaterally to the anterodorsal thalamic nucleus) had detectable transcripts. 4. Many neurons in the supramammillary nucleus had low, moderate, or high levels of transcripts. Some nearby nuclei (such as the dorsal premammillary nucleus) had smaller numbers of neurons with low levels of CCK mRNA, whereas others (such as the ventral premammillary nucleus) had none.

Cerebral Glucose Utilization in Rats is Not Altered by Hindlimb Restraint or by Femoral Artery and Vein Cannulation

The effects of immobilization and femoral artery and vein cannulation on resting rates of local cerebral glucose utilization (LCGU) were measured in 35 brain regions of awake rats by using the quantitative, autoradiographic [14C]2-deoxy-D-glucose [( 14C]DG) technique. Three groups of rats were cannulated on the previous day, and LCGU was measured under conditions of no restraint, 4 h of hindlimb restraint, or acute, four-limb immobilization. A fourth group represented the conventional preparation for [14C]DG experiments, with same-day cannulation followed immediately by 4 h of hindlimb restraint. Plasma catecholamines, corticosterone, and glucose concentrations were measured in all groups; all were elevated significantly above values in unrestrained animals only during four-limb immobilization. LCGU was unchanged by same-day surgery, hindlimb restraint, or both. During four-limb immobilization, LCGU was reduced by 25% in the dorsal hippocampus, and to a lesser extent in the anteroventral thalamic nucleus. It was increased only in the lateral habenula (42%). We conclude that two stressors of the experimental preparation (same-day surgery and hindlimb restraint) do not influence LCGU measurements by the [14C]DG method. More severe, acute stress selectively alters LCGU in a few rat brain regions.

Effects of nicotine on local cerebral glucose utilization in the rat

We used the autoradiographic 2-deoxy-D-[1-14C]glucose (14C-DG) method of Sokoloff to identify brain areas with altered rates of local cerebral glucose utilization (LCGU) in vivo in response to peripheral I-nicotine administration (0.1, 0.3, 1.0, and 1.75 mg/kg, s.c.). Nicotine stimulated LCGU primarily in areas reported to contain nicotine binding sites, indicating that the sites are true receptors. Increases in LCGU of 100% or more over control were obtained in the medial habenula, fasciculus retroflexus, superior colliculus, and median eminence. Substantial stimulation (50-100% increases) also was obtained in the cerebellar vermis, interpeduncular nucleus, and anteroventral and interanteromedial thalamic nuclei. Moderate increases (20-50%) were observed in the reticular nucleus of the medulla, paramedian lobule, nucleus of the spinal tract of the trigeminal nerve, presubiculum, subiculum, red nucleus, ventral tegmental area, substantia nigra, nucleus ambiguus, nucleus tractus solitarius, dorsal lateral geniculate nucleus, mammillothalamic tract, and fornix. The greatest stimulation in most affected areas was obtained with 0.3 mg/kg nicotine administered at 2 min, but not longer, before 14C-DG. Effects of nicotine on LCGU were antagonized by mecamylamine. The findings indicate that the interaction of nicotine with specific binding sites is coupled to cerebral energy metabolism. The distribution of in vivo cerebral metabolic effects of nicotine implicates various brain regions in the behavioral and physiological effects of nicotine.

Physiological characteristics of anterior thalamic nuclei, a group devoid of inputs from reticular thalamic nucleus.

This study tested the hypothesis that neurons of thalamic nuclei, which are normally devoid of inputs from the reticular thalamic nucleus, do not display spindle oscillations and related rhythmic spike bursts. This proposal derived from our recent studies indicating that the reticular nucleus is the generator of spindling rhythmicity. We used retrograde tracing methods, intracellular recordings in barbiturized cats, and extracellular recordings of single neurons and field potentials in anteroventral (AV), anteromedial (AM), ventroanterior (VA), ventrolateral (VL), and central lateral (CL) thalamic nuclei in cats with rostral brain stem transections (cerveau isolé preparations), before and after administration of barbiturates. The observation that AV and AM nuclei do not receive inputs from the reticular nucleus was confirmed by using injections of horseradish peroxidase conjugated to wheat germ agglutinin confined within the limits of anterior nuclei. Such injections led to massive retrograde labeling in mammillary nuclei and layer VI of the retrosplenial cortex but left free of labeling the neurons of the reticular thalamic nucleus. Intracellular recordings showed that AV-AM neurons discharge tonically in response to a depolarizing current applied at rest, whereas they give rise to a slow spike that underlies a burst of fast action potentials when the membrane is hyperpolarized by 5-12 mV. Despite the fact that they share similar properties with other thalamic neurons, intracellularly recorded AV-AM neurons do not exhibit spindle waves under barbiturate anesthesia, whereas VA-VL, CL, and other thalamocortical neurons that receive afferents from the reticular nucleus commonly display such oscillations. With extracellular recordings performed simultaneously in CL and AV or AM nuclei of the unanesthetized cerveau isolé preparation, focal spindle oscillations and related rhythmic high-frequency spike bursts of single CL cells contrasted with absence of spindles and spike bursts in AV or AM neurons. Spindling could be induced in AV-AM nuclei only after administration of barbiturates at doses exceeding 3 mg/kg, and it appeared approximately 35-40 s after the barbiturate effect was detected in the simultaneously recorded CL nucleus. Moreover, the spike bursts that were elicited in AV-AM neurons after barbiturate administration were not temporally related with focal spindles. Since spindle oscillations did not appear intracellularly in AV-AM neurons, the possibility was envisaged that barbiturate-induced spindles were the passive reflection of field potentials actively generated in neighboring thalamic nuclei.(ABSTRACT TRUNCATED AT 400 WORDS)

Mammillothalamic enkephalinergic pathway in the rat: an immunocytochemical analysis

We studied the afferent sources of Leu-enkephalin (ENK) -like immunoreactive (ENKI) fibers in the anteroventral thalamic nucleus (AV) of the rat using experimental immunohistochemistry. These fibers were markedly fewer on the operated side after the destruction of the medial mammillary nucleus pars medialis where a number of ENKI cells were observed. This strongly suggests that these ENKI cells project ipsilaterally to the AV. ENKI fibers seemed to reach the AV via the mammillothalamic tract.

Cholinergic neurons of the laterodorsal tegmental nucleus: Efferent and afferent connections

The ascending projections of cholinergic neurons in the laterodorsal tegmental nucleus (TLD) were investigated in the rat by using Phaseolus vulgaris leucoagglutinin (PHA-L) and wheat germ agglutinin-conjugated horseradish peroxidase (WGA-HRP) anterograde tracing techniques. Two ascending pathways were identified after iontophoretic injections of PHA-L into the TLD. A long projection system courses through the dorsomedial tegmentum, caudal diencephalon, medial forebrain bundle, and diagonal band. Different branches of this system innervate the midbrain (superior colliculus, interstitial magnocellular nucleus of the posterior commissure, and anterior pretectal nucleus), the diencephalon (lateral habenular nucleus, parafascicular, anteroventral, anterodorsal, mediodorsal, and intralaminar thalamic nuclei), and the telencephalon (lateral septum and medial prefrontal cortex). The second system is shorter and more diffuse and innervates the median raphe, interpeduncular, and lateral mammillary nuclei. Retrograde tracing with WGA-HRP, combined with choline acetyltransferase immunohistochemistry, revealed that most of the TLD projections to the tectum, pretectum, thalamus, lateral septum, and medial prefrontal cortex are cholinergic. Afferents to the TLD were studied by anterograde and retrograde tracing techniques. Injection of tracers into the TLD retrogradely labelled neurons bilaterally in the midbrain reticular formation, the periaqueductal gray, the medial preoptic nucleus, the anterior hypothalamic nucleus, and the perifornical and lateral hypothalamic areas. Retrogradely labelled cells were also located bilaterally in the premammillary nucleus, paraventricular hypothalamic nucleus, zona incerta, and lateral habenular nucleus. In the telencephalon, the nucleus of the diagonal band and the medial prefrontal cortex contained retrogradely labelled neurons ipsilateral to the TLD injection site. The projections of the medial prefrontal cortex, the bed nucleus of the stria terminalis, and the lateral habenular nucleus to the TLD were confirmed in anterograde tracing studies. These findings indicate that the TLD gives rise to several ascending cholinergic projections that innervate diverse regions of the forebrain. Afferents to the TLD arise in hypothalamic and limbic forebrain regions, some of which appear to have reciprocal connections with the TLD. The latter include the lateral habenular nucleus and medial prefrontal cortex.

Autoradiographic distribution of high affinity muscarinic and nicotinic cholinergic receptors labeled with [ 3H]acetylcholine in rat brain

The relative distribution of muscarinic and nicotinic cholinergic receptors labeled with [ 3H]acetylcholine was determined using autoradiography. [ 3H]acetylcholine binding to high affinity muscarinic receptors was similar to what has been described for an M-2 distribution: highest levels of binding occurred in the pontine and brainstem nuclei, anterior pretectal area and anteroventral thalamic nucleus, while lower levels occurred in the caudate-putamen, accumbens nucleus and primary olfactory cortex. Nicotinic receptors were labeled with [ 3H]acetylcholine to the greatest extent in the interpeduncular nucleus, several thalamic nuclei, medial habenula, presubiculum and superior colliculus, and to the least extent in the hippocampus and inferior colliculus. By using autoradiography to localize cholinergic binding sites throughout the brain it was observed that the distributions of high affinity muscarinic and nicotinic sites labeled with the endogenous ligand, [ 3H]acetylcholine are different from each other and are different from distributions of muscarinic and nicotinic sites labeled with muscarinic and nicotinic antagonists.

Quantitative autoradiography of 3H-nomifensine binding sites in rat brain.

The distribution of 3H-nomifensine binding sites in the rat brain has been studied by quantitative autoradiography. The binding of 3H-nomifensine to caudate putamen sections was saturable, specific, of a high affinity (Kd = 56 nM) and sodium-dependent. The dopamine uptake inhibitors benztropine, nomifensine, cocaine, bupropion and amfonelic acid were the most potent competitors of 3H-nomifensine binding to striatal sections. The highest levels of (benztropine-displaceable) 3H-nomifensine binding sites were found in the caudate-putamen, the olfactory tubercle and the nucleus accumbens. 6-Hydroxydopamine-induced lesion of the ascending dopaminergic bundle resulted in a marked decrease in the 3H-ligand binding in these areas. Moderately high concentrations of the 3H-ligand were observed in the bed nucleus of the stria terminalis, the anteroventral thalamic nucleus, the cingulate cortex, the lateral septum, the hippocampus, the amygdala, the zona incerta and some hypothalamic nuclei. There were low levels of the binding sites in the habenula, the dorsolateral geniculate body, the substantia nigra, the ventral tegmental area and the periaqueductal gray matter. These autoradiographic data are consistent with the hypothesis that 3H-nomifensine binds primarily to the presynaptic uptake site for dopamine but also labels the norepinephrine uptake site.

Anterior thalamic afferents from the mamillary body and the limbic cortex in the rat.

Anterior thalamic afferents from the mamillary body and the limbic cortex were studied by using single and double retrograde transport methods in the rat. The medial mamillary nucleus was divided on the basis of the cytoarchitecture into four subnuclei: the pars medialis centralis, pars medialis dorsalis, pars lateralis, and pars basalis. Extensive connections were seen between each of these subdivisions of the mamillary body and the anterior thalamic nuclei, topographically organized so that the anteromedial thalamic nucleus receives projections exclusively from the pars medialis centralis, while the anteroventral thalamic nucleus receives projections from the pars medialis dorsalis and pars lateralis. Nuclei in the dorsal half of these two mamillary subdivisions project predominantly to the medial half of the anteroventral thalamic nucleus, and those in the ventral half to the lateral half of the nucleus. The pars basalis was found to have numerous projections to the magnocellular part of the anteroventral nucleus. All limbic cortical areas send projections bilaterally to all regions of the anteromedial nucleus as well as to the parvicellular parts of the anteroventral thalamic nucleus, while the anterodorsal nucleus receives ipsilateral projections originating exclusively from the preagranular, anterior limbic, and cingular regions. The magnocellular part of the anteroventral nucleus, however, receives only ipsilateral projections from all of the limbic cortex. Some neurons in the infralimbic region also project bilaterally to all of the anterior thalamic nuclei except the anterodorsal nucleus. All of these cortical projections to the anterior thalamus originate in layers V and VI of the limbic cortex.

Nucleus locus ceruleus: new evidence of anatomical and physiological specificity.

Nucleus locus ceruleus: new evidence of anatomical and physiological specificity.

Multiple-unit activity of the prefrontal cortex and mediodorsal thalamic nucleus during acquisition of discriminative avoidance behavior in rabbits

Multiple-unit activity of the prefrontal cortex (PFC) and the mediodorsal (MD) thalamic nucleus was recorded during discriminative conditioning of a locomotory avoidance response in rabbits. A major objective was to compare the results with those previously obtained from the posterior limbic (cingulate) cortex, and the anteroventral (AV) thalamic nucleus. The results indicated the development, with training, of discriminative neuronal activity, i.e., greater neuronal discharges to presentation of the positive conditional stimulus (CS+, a tone paired with a footshock unconditional stimulus), relative to the negative conditional stimulus (CS—, a tone not paired with the footshock). The rostral-sulcal subfield of the PFC developed the discriminative activity during the first session of conditioning, prior to the acquisition of discriminative behavioral responding. This effect persisted throughout training to the asymptote of behavioral acquisition. The medial subdivision of the MD nucleus, with which the rostral-sulcal PFC is interconnected, did not develop discriminative effects. The caudal (supragenual) subfield of the PFC also developed discriminative activity in the first session of training but the effect declined progressively in the remaining acquisition sessions. The lateral subdivision of the MD nucleus, with which the caudal PFC is interconnected, manifested robust discriminative activity in the late acquisition sessions, concomitant with acquisition of significant behavioral discrimination. Thus, as in the cingulate cortical-AV nuclear system, a corticothalamic sequential progression of discriminative activity occured in the PFC-MD nuclear system during behavioral acquisition. However, the effect was confined to one subsystem: the caudal subfield of the PFC and the lateral subdivision of the MD nucleus. Also, discriminative activity developed more rapidly in the PFC than in the cingulate cortex, and it developed more rapidly in the MD nucleus than in the AV nucleus. Implications are considered concerning the contributions to learning and memory processes, of the PFC-MD thalamic system.

Anterior thalamic lesions and neuronal activity in the cingulate and retrosplenial cortices during discriminative avoidance behavior in rabbits.

Bilateral electrolytic lesions of the anteroventral (AV) nucleus of the thalamus given after training impaired retention performance (extinction and reacquisition) of rabbits in a differential avoidance conditioning task. In addition, the lesions abolished the excitatory, discriminative multiple-unit discharges that had developed in the cingulate and retrosplenial cortices to the auditory conditional stimuli (CSs) during the course of behavioral acquisition, prior to the induction of the lesions. The excitatory discharges were supplanted in the subjects with lesions by CS-elicited reduction of neuronal firing to levels below the prestimulus baseline. Lesions given before training did not disrupt behavioral acquisition, but they did eliminate the excitatory tone-elicited neuronal discharges that normally occur in the cortex before and during training. The CS-elicited reduction of neuronal firing did not occur at the beginning of training in the subjects given lesions before training, but it developed during the course of training. The lesions did not eliminate the excitatory and discriminative neuronal activity of the prefrontal cortex. These results demonstrate that excitatory and discriminative neuronal discharges in the cingulate and retrosplenial cortices are critically dependent on the connections of these areas with the anterior thalamic nuclei. Also the lesion-induced disruption of performance during extinction and reacquisition but not during original learning confirms a prediction from past electrophysiological studies, that the AV thalamic nucleus is involved in the mediation of the maintenance and retention of the conditioned avoidance behavior, but not in its original acquisition.

Parallel and serial processes of the prefrontal and cingulate cortical systems during behavioral learning

GABRIEL, M. AND E. ORONA. Parallel and serial processes of the prefronlal and cingulate cortical systems during behavioral learning. BRAIN RES. BULL. 8(6) 781–785, 1982.—Multiple unit activity of the prefrontal cortex (PFC) and the mediodorsal (MD) nucleus of the thalamus was recorded during differential conditioning of a locomotory (wheel-rotation) avoidance response. The positive and negative conditional stimuli (CS+ and CS−) were pure tones (1 kHz and 8 kHz), and the unconditional stimulus was a footshock (1.5-2.0 mA) delivered through the grid floor of the wheel apparatus. A principal objective was to compare the development during training of CS-related neuronal activity in the PFC and MD nucleus, to that obtained in past studies of the adjacent limbic mesocorticothalamic system (the cingulate cortex and the anteroventral (AV) thalamic nucleus). The results indicated that these systems perform associative processing of task-related stimuli in parallel: as in the cingulate cortex, discriminative neuronal discharges (greater discharges to the CS+ than to the CS−) developed in the PFC in the earliest training stage, before incipient discriminative behavior, and as in the AV nucleus, discriminative discharges in the MD nucleus developed in a later training stage. Nevertheless the possibilities of serial processing and intercausality in these systems was suggested by the finding that discriminative activity in the PFC and MD nucleus developed at briefer latencies and earlier in the course of trials than in the cingulate cortex and the AV nucleus.

Direct retinal input to the limbic system of the rat

Retinal projections in rats were studied using anterograde horseradish peroxidase (HRP) tracing and electron microscopic (EM) degeneration. HRP-labeled axons were observed to leave the optic tract in the vicinity of the lateral geniculate nucleus and enter the stria terminalis where they coursed anteriorly to the bed nucleus of the stria terminalis (BNST), and the anterodorsal (TAD) and anteroventral (TAV) thalamic nuclei. After enucleation, selected areas studied with EM confirmed that retinal presynaptic terminals are located in the BNST and TAV. These results support the finding of Conrad and Stumpf that the retina has a direct link to the limbic system 2.

Responses of the cingulate cortex to dorsal hippocampal stimulation in cats

Responses of the cingulate gyrus to stimulation of the dorsal hippocampus were studied in unanesthetized cats. Both short and long polysynaptic projections were found to participate in their genesis. It is postulated on the basis of the results of experiments with stimulation of and injury to the limbic nuclei of the thalamus that responses of the posterior zone of the cingulate gyrus to dorsal hippocampal stimulation arise as a result of activation of the anteroventral thalamic nucleus.

Localization of putative cholinergic neurons innervating the anteroventral thalamus

The brainstem localization of acetylcholinesterase (AChE)-containing neurons projecting to the anteroventral thalamic nucleus (AVN) was studied in rats. The AVN is one of several forebrain regions innervated by the AChE-containing dorsal tegmental pathway described by Shute and Lewis. In the present study, horseradish peroxidase (HRP) was injected into the region of the AVN to determine the brainstem origin of afferent projections. Alternate sections of tissue were stained for HRP or AChE. HRP-labeled neurons were found in the laterodorsal tegmental nucleus (LTN) and the locus coeruleus. Examination of adjacent sections revealed AChE-containing neurons in both of these nuclear regions. Combined HRP/AChE histochemistry demonstrated that transported HRP and AChE were in the same cells. In further experiments, unilateral lesions of the LTN were found to cause a decrease in AChE staining of the ipsilateral AVN. Destruction of the locus coeruleus had no effect. In combination with available evidence, the present findings suggest that cholinergic neurons in the LTN innervate the AVN.