Midline Thalamus Research Articles

The effects of transient functional depression of the thalamus on spindles and on bilateral synchronous epileptic discharges of feline generalized penicillin epilepsy.

A transient functional depression of thalamic activity (TFDTA) was induced in acute experiments in cats by the microinjection of 25% KCl into the thalamus. Spontaneous and evoked thalamic electrical activity was markedly depressed at the site of KCl microinjection. Spread of this depression to other thalamic areas often occurred, mainly when KCl was injected into the midline thalamus. In normal cats both spontaneous and evoked cortical spindle bursts as well as other evoked thalamocortical responses were reduced or abolished during the KCl-induced TFDTA. The generalized spike-and-wave discharges of feline generalized epilepsy were also suppressed for the duration of TFDTA, while incidental focal cortical interictal and ictal epileptic discharges, as well as generalized tonic-clonic seizure discharge, remained unaffected. The same effects were observed in animals with lesions of the mesencephalic reticular formation, indicating that the suppression of spindles and spike-and-wave discharges cannot be attributed to a release of the activity of the reticular formation by the TFDTA. An unexplained occurrence of generalized tonic-clonic EEG seizure was observed in most cases late after thalamic KCl microinjection, usually after the spike-and-wave discharges had recovered. These data are consistent with the hypothesis that the spontaneous bilaterally synchronous epileptic bursts of feline generalized penicillin epilepsy are not only closely related to spindles but are crucially dependent on thalamic inputs to the cerebral cortex.

Dorsal midline thalamus, pretectum and responses to diffuse light in the rat

The present study examined dorsal midline thalamic and pretectal lesion effects on visual task performance, and tested current sensory interpretations of these effects. The first three experiments supported a previous claim that the pretectal area plays a role in diffuse light perception. Experiments 1 and 2 showed that dorsal midline thalamic lesions disrupt choice of the correct illuminated goal box over the incorrect, dark goal box in a “simultaneous” two-choice discrimination task, but only when the rats wear light diffusing translucent eye masks. Experiment 3 showed that the deficit following a unilateral lesion is greatest when the animals are forced to use the diffusely occluded contralateral eye, which in the rat projects strongly to the damaged hemisphere. Despite this seemingly substantial support for an impairment in diffuse light perception, certain observations made during these experiments led to formulation of an alternative, nonvisual description of the lesion deficit. According to this new hypothesis, thalamic lesions undermine the ability to inhibit position responding, which in the diffuse light condition is critical for successful discrimination performance in such paradigms. Experiments 4–6 validated this new interpretation. First, Experiment 4 substantiated the literature indicating that thalamic lesions impair the animal's capacity to inhibit prepotent responses. Next, Experiments 5 and 6 showed that in a “successive” version of the two-choice task and in a task involving conditioned suppression of lever pressing to a light stimulus—two paradigms which probably make identical response demands in both the diffuse light and normal visual states—the lesion deficit registered is the same under both visual conditions. The study was judged to have undermined the view that dorsal midline and pretectal structures contribute directly to visual perception in the intact mammal.

A neurophysiological approach to the identification, connections and pharmacology of the hypothalamic tuberoinfundibular system.

Hypothalamic hypophysiotropic or 'tuberoinfundibular' neurons can be identified by antidromic activation following electrical stimulation on the surface of the median eminence. These neurons appear to be localized within the medial hypothalamic and preoptic areas. Both the source and the nature (i.e. excitatory or inhibitory) of connections of these identified neurons can be examined with electrophysiological methods. Afferent pathways appear to originate in the medial preoptic area, amygdala, hippocampus, lateral septum and retina. Axon collaterals of some tuberoinfundibular neurons engage recurrent excitatory and inhibitory pathways and/or project to the anterior hypothalamic area, medial preoptic area, paraventricular nucleus, amygdala, lateral septum and midline thalamus. Neuropharmacological studies indicate that gamma-aminobutyric acid, catecholamines and possibly some hypothalamic peptides may participate in synaptic transmission in afferent or efferent connections in the tuberoinfundibular system.

Periventricular system lesions and stimulation-produced analgesia

Three areas within the periventricular system were studied: caudal periaqueductal gray (PAG), rostral PAG, and caudal midline thalamus. Rats were chronically prepared with a bipolar stimulating electrode in one of these areas and two lesion electrodes in another. Current thresholds for stimulation-produced analgesia in the tail-flick test were assessed. Then, lesions were made and thresholds for analgesia re-assessed. Destruction of the caudal PAG consistently produced large increases in thresholds for analgesia at rostral stimulation sites; however, destruction of the rostral areas did not affect thresholds at caudal PAG sites. Lesions in all 3 areas yielded significant reductions in baseline (pre-brain stimulation) tail-flick latencies. Both sham lesioned control animals and animals with small lesions maintained stable baseline latencies and analgesia thresholds. The data support the view that all 3 brain areas studied contribute to the same pain-inhibitory system. They further suggest that stimulation at rostral sites activates elements which connect to or pass through the caudal PAG.

Role of the periaqueductal grey in vocal expression of emotion

In 32 squirrel monkeys (Saimiri sciureus) the role of the periaqueductal grey has been investigated by combined stimulation/lesioning and by neuroanatomical experiments. The results are as follows. Firstly, periaqueductal lesions invading the laterally adjacent tegmentum abolish species-specific calls elicitable by electrical brain stimulation. This holds for stimulation sites rostral as well as caudal to this area. The only vocalizations which survive are phonations of an artificial character which can be evoked from the lateral medulla. Spontaneous vocalizations also seem to be abolished. Secondly, vocalizations elicited from the periaqueductal grey are not affected by bilateral lesions in vocalization-eliciting areas rostral to it, but are abolished by lesions in the dorsolateral pons and ventrolateral medulla. Thirdly, the periaqueductal grey receives direct projections from all vocalization-eliciting areas tested, viz. the precallosal cingulate gyrus, gyrus rectus, medial amygdata, central amygdaloid nucleus/substantia innominata, nucleus striae terminalis, dorsal hypothalamus, midline thalamus, periventricular grey, dorsolateral and ventrolateral midbrain tegmentum. Fourthly, the periaqueductal grey projects directly to the nucleus ambiguus, the site of the laryngeal motoneurones. The course of the main bulk of fibres corresponds to the lesion sites effective in abolishing periaqueductally elicited vocalizations. From these results, it was concluded that the caudal periaqueductal-lateral tegmental area is a necessary relay station for all external and internal stimuli capable of inducing species-specific calls. Its position within the stimulus-response loop seems to be on the output side, immediately above the level of motor-corrdination but below that of stimulus recognition.

Influence of thalamic cooling on sensory responses in association cortex

O'BRIEN, J. H. AND S. M. ROSENBLUM. Influence of thalamic cooling on sensory responses in association cortex. BRAIN RES. BULL. 4(1) 91–98, 1979.—Evoked responses to light flash, click, and paw stimuli were recorded in the four cortical association areas in the acutely prepared cat. Average evoked responses (AEP) for 100 trials were formed before, during, and after localized cooling in the midline thalamus. Cooling of the midline thalamus reduced the magnitude of responses to click and paw stimuli, and increased or did not change the responses to light flash. There was very little similarity in trial-to-trial fluctuations of EP magnitude across cortical areas, and cooling did not reduce the similarity that existed. Waveform similarity was reduced by cooling for responses across the cortex to a single stimulus modality, whereas similarity of responses in a single cortical area to all three stimuli was not changed. The temporal components of the AEP influenced by thalamic cooling were different for different stimuli and cortical locations. It was concluded that the midline thalamo-cortical projection through the centromedian area to association cortices is particularly well-differentiated for multisensory responses in a single cortical region, and that the system should not be thought of as nonspecific but as convergent or multisensory.

Drinking and haemodynamic changes induced in the dog by intracranial injection of components of the renin-angiotensin system.

1. Intracranial injections of the individual components of the renin-angiotensin system caused drinking in water-replete dogs. 2. Angiotensin II was the most reliable, potent and rapidly acting intracranial dipsogen and elicited drinking in the absence of peripheral circulatory changes. After the highest dose of angiotensin II (10(-9) mole) five dogs drank a mean amount of 380.0 +/- 88.6 ml. For the other components, the order of dipsogenic effectiveness was angiotensin I, synthetic renin substrate, and angiotensin III. 3. Isotonic saline, bradykinin (10(-10) mole), eledosin-hexapeptide (10(-10) mole), oxytocin (10(-10) mole) and prostaglandin F2alpha (1-200 X 10(-12) mole) were ineffective. 4. Intracranial renin (10 m-u.) produced a mean intake of 445 +/- 152 ml. of water in eight dogs. 5. Dog renin substrate and synthetic renin substrate, injected intracranially in a dose of 10(-10) mole, produced similar intakes of water but these amounts were very much less than the volume drunk in response to the same dose of angiotensin II. 6. None of the components injected into dipsogenically responsive sites in the brain caused changes in blood pressure, although the act of drinking itself produced a small rise. 7. Angiotensin II at the highest dose produced drinking when injected into the subfornical organ, preoptic region, anterior hypothalamus, lateral ventricle, third ventricle, ventral hippocampus and mid-line thalamus. Negative sites were found in the caudate nucleus, fourth ventricle, mid-brain, posterior thalamus, dorsal hippocampus, lateral hypothalamus and posterior hypothalamus. 8. After the lowest dose of intracranial angiotensin II (10(-12) mole) only the preoptic region and subfornical orgal were responsive. These two sites were equally sensitive in terms of latency and amounts drunk at all doses injected. 9. Angiotensin did not necessarily have to reach a cerebral ventricle in order to cause drinking. 10. The dog resembles the rat in its responsiveness to the dipsogenic action of intracranial angiotensin II. The regions of the brain from which drinking can be elicited are more widespread than has been claimed by some in the rat.

Convergent projections of different limbic vocalization areas in the squirrel monkey

The projections of four different sub-areas within the anterior limbic cortex, all yielding vocalization when electrically stimulated, were compared in six squirrel monkeys by the autoradiographic tracing technique. Areas of convergence of the projections from all four vocalization loci were the cortex within the anterior cingulate sulcus, a zone following the inferior thalamic peduncle from the central amygdaloid nucleus through the substantia innominata into the midline thalamus, a second zone following the periventricular fibre system from the anterior diencephalon to the caudal midbrain and dorsolateral pontine tegmentum and, finally, the tail of the caudate nucleus. Except for the latter, all of these brain structures produce vocalization when electrically stimulated. The call types elicitable from these projection areas are sometimes different from those elicitable from the anterior limbic cortex. It is hypothesized that the anterior limbic cortex controls vocalization directly, independently of the specific motivational state underlying it.

Efferent connections of the septal area in the rat: An analysis utilizing retrograde and anterograde transport methods

Experiments were performed by either retrograde (horseradish peroxidase histochemistry) or anterograde ([3H]leucine radioautography) transport methods to determine the efferent connections of the septum in the rat. It was observed that the dorsal septum projects to the lateral preoptic area, lateral hypothalamus, periventricular hypothalamus and midline thalamus. Fibers from the ventral half of the septum project topographically to the hippocampal formation, thalamus, hypothalamus and midbrain. Specifically, neurons located along the midline in the vertical limb of the diagonal band project through the dorsal fornix to all CA fields of the dorsal hippo campus and adjacent subicular cortex. Other fibers from this region project through the stria medullaris to the medial habenular nucleus and anteromedial nuclhe pars posterior of the medial mammillary nucleus. Cells located immediately lateral to the midline in the vertical limb of the diagonal band project through the medial part of the fimbria to all CA fields of the posterior hippocampus and adjacent subicular cortex. Other fibers which originate from this region project through the stria medullaris to both the medial and lateral habenular nuclei and the paratenial nucleus of the thalamus, and through the medial forebrain bundle to the pars posterior of the medial mammillary nucleus. Cells located in the intermediolateral septum project through the lateral part of the fimbria to all CA fields of the ventral hippocampus and adjacent subicular and entorhinal cortices. These cells also send fibers through the stria medullaris to the lateral habenular nucleus and mediodorsal thalamic nucleus. Other axons arising from these cells descend through the medial forebrain bundle to terminate in a region dorsal to the interpeduncular nucleus. Fibers from the most lateral part of the ventrl septum (i.e., bed nucleus of the anterior commissure) project through the stria terminalis to the ventral subiculum. In addition, cells located in the horizontal limb of the diagonal band project massively to the pars posterior of the medial mammillary nucleus and the ventral tegmental area, and amygdala.

Reinforcing concomitants of electrically elicited vocalizations.

In 38 squirrel monkeys 251 vocalization-producing electrode positions were tested for their positive and negative reinforcing properties. Two groups of vocalization-producing brain areas could be distinguished: One group in which the electrically elicited vocalization was independent of the accompanying reinforcement effect, and a second group in which vocalization and reinforcement effect were correlated. The first group included the anterior cingulate gyrus, the adjacent supplementary motor area, gyrus rectus, ventromedial edge of the capsula interna, caudal periaqueductal gray and adjacent parabrachial region. The second group consited of the caudatum, septum, substantia innominata, amygdala, inferior thalamic peduncle, stria terminalis, midline thalamus, ventral and periventricular hypothalamus, substantia nigra, rostral periaqueductal gray, dorsolateral midbrain tegmentum and lateral medulla. It is hypothesized that the first group contains predominantly or exclusively "primary" vocalization substrates; the second group is thought to be composed mainly of structures whose stimulation yields vocalization secondarily due to stimulus induced motivational changes.

Ontogenetic development of somatosensory thalamus: II. Electrogenesis

Electrodes were implanted into the brains of newborn kittens to study chronically the ontogenesis of unit spike and slow-wave phenomena in the somatosensory thalamus and adjacent structures. In general, the upper brain stem and midline (nonspecific) thalamus showed evidences of functional maturation appreciably sooner than the more laterally lying sensory nuclei. State-dependent changes in single-unit behavior began to develop relatively early (fourth postnatal day) and occasional, scattered spike bursts could be seen by the tenth to 14th day, especially during slow wave sleep. However, this scattered, low-density burst pattern, with total absence of synchrony across leads from the same electrode cluster, at a time when runs of thalamic slow waves or spindles are already very obvious, casts considerable doubt on any obligatory relationship between these two phenomena. Alternative functional models for the production of thalamic wave trains are considered.

Projections from the ‘Cingular’ vocalization area in the squirrel monkey

In 5 squirrel monkeys the anatomical projections from the 'cingular' vocalization area were studied by the autoradiographic tracing technique. The 'cingular' vocalization area lies around the sulcus cinguli at the level of the genu of the corpus callosum; its electrical stimulation yields purring and cackling calls. The following efferent connections were found: corticocortical fibers could be traced into the orbital cortex (areas 10 and 11), dorsomedial frontal cortex (areas 9, 8 and 6), limbic cortex (areas 25, 24 and 23), Broca's area (area 44), frontal operculum (area 50), insula (areas 13 and 14), and auditory association cortex (area 22). Subcortical terminal fields within the telencephalon were found in the nucleus caudatus, putamen, claustrum, globus pallidus, olfactory tubercle, preoptic region and nucleus centralis and basolateralis amygdalae. Fibers reached most of these structures along different trajectories. In the diencephalon terminal fields lay in the dorsal hypothalamus, the subthalamus, lateral habenular nucleus, and the following thalamic nuclei: nucleus reticularis, ventralis anterior, centralis medialis, centralis superior lateralis, centralis inferior, submedius, medialis dorsalis and centrum medianum. In the midbrain, the periaqueductal gray was the only projection area, extending into the parabrachial nuclei at the pontomesencephalic transition. The most caudal terminal field was found in the medial pontine gray. No terminals were detected in the nucleus ambiguus, nucleus n. hypoglossi or in any other cranial motor nucleus involved in phonation processes. A comparison of this projection system with the whole of structures producing vocalization when electrically stimulated yielded only partial overlap. Not all vocalization areas lie within the 'cingular' projection system, and inversely, not the whole projection system yielded vocalization. Overlap took place in the anterior limbic cortex, preoptic region, central amygdaloid nucleus, midline thalamus, dorsal hypothalamus, periaqueductal gray and parabrachial nuclei. These structures are considered to compose a functionally coherent vocalization system. The projections into Broca's area, nucleus ventralis anterior thalami, frontoopercular cortex within the lateral fissure, pontine nuclei and superior temporal gyrus are discussed in their possible relationship to vocalization processes.

Projections of the locus coeruleus and adjacent pontine tegmentum in the cat.

The projections of the locus coeruleus and adjacent pontine tegmentum have been studied using anatomical and physiological methods in the cat. Axonal trajectories were traced using either the Fink-Heimer I method following electrolytic lesions, or the autoradiographic method after injection of tritiated proline into the nucleus. Results with both methods were similar. Axons of locus noeruleus neurons ascended ipsilaterally through the mesencephalon lateral to the medial longitudinal fasiculus, ventrolateral to the central gray. In the caudal diencephalon, the ascending fibers entered the centrum medianum-parafascicular complex where they diverged into two fascicles: a dorsal fascicle which terminated in the intralaminar nuclei of the thalamus, and a ventral fascicle which gave off fibers to the ventrobasal complex and reticular nucleus of the thalamus while continuing centrolaterally into the lateral hypothalamus medial to the internal capsule. Fibers of the ventral fascicle ascended in the lateral hypothalamus and zona incerta and were traced through the preoptic region into the septum. Fibers could not be consistently traced to the cerebral cortex, and were not seen at all in the cerebellum. Throughout the ascending course of the path from the locus coeruleus, axons were given off to the pretectal area, the medial and lateral geniculate nuclei and the amygdala; fibers passed contralaterally through the posterior commissure, the midline thalamus, and the supraoptic commissure. Fibers descending from the locus coeruleus surrounded the intramedullary portion of the facial nerve and further caudally were observed ventrolateral to the hypoglossal and dorsal vagal nuclei. The axonal trajectories visualized with degeneration and autoradiographic methods followed closely those previously shown for reticular formation neurons, but were also similar to locus coeruleus projections revealed by histofluorescence methods. After injections of horseradish peroxidase into the centrum medianum-parafascicular complex, lateral hypothalamus or preoptic region, labeled neurons were located in the locus coeruleus, nucleus subcoeruleus, and lateral parabrachial nucleus. Reticular formation neurons were not labeled. Neurons in locus coeruleus and adjacent pontine tegmentum could be antidromically activated by stimulation in the rostral midbrain or caudal diencephalon. Our data indicate that both adrenergic and non-adrenergic neurons of the dorsolateral pontine tegmentum have similar projections.

Neuroanatomic Projections Related to Biting Attack Elicited from Ventral Midbrain in Cats

A single electrode was implanted in each of ten cats at a point in the ventral midbrain from which nonaffective biting attack on a rat could be elicited by electrical stimulation. A lesion was then made which was just large enough to eliminate the elicitation of attack at suprathreshold intensities from that electrode. After post-lesion survival times of 3-14 days the cats were sacrificed, and the degeneration resulting from the lesions was followed with the use of modified Nauta silver stains. Four additional cats were used as anatomic controls. Degenerating fibers were observed to descend bilaterally through the midbrain, pontine, and medullary tegmentum to the vicinity of the principal sensory and motor nuclei of the trigeminal nerve. There was, in addition, evidence of degenerating terminals within the nucleus of the facial nerve and the spinal nucleus of the trigeminal nerve. Of particular note was the observation that the degenerating fibers in the region of the nucleus of the spinal tract of the trigeminal nerve terminated in glomeruli in the rostral portion of the nucleus. Degenerating fibers ascending from the lesion were found to course along the medial forebrain bundle into the hypothalamus and the midline thalamus in a pattern very similar to that previously demonstrated after lesions of biting attack sites in the hypothalamus. The role that the neural pathways associated with ventral midbrain attack sites might play in the mediation of behavior patterns which are elicited during attack stimulation was discussed and it was concluded that the demonstrated neural pathway could provide a cogent explanation for some of the properties of centrally elicited attack behavior.

The ascending and descending connections of the hypothalamus in the cat

The ascending and descending projections of the lateral preopticohypothalamus were studied with radioautographic methods. Injections of [ −3H]leucine were placed throughout the rostral to caudal extent of the lateral preopticohypothalamic zone in adult cats. Ascending fibers of the rostral two-thirds of the lateral preopticohypothalamus terminate primarily in a nonspecific manner within the lateral and intermediolateral parts of septum and to a limited extent in the medial septum. Fibers from the rostral two-thirds of the lateral preopticohypothalamus also project to the lateral habenular nucleus via the stria medullaris. The caudal third of lateral hypothalamus appears to provide little or no contribution to the septum and habenular complex. Neurons from all parts of the lateral hypothalamus contribute to the total projection to both the ventral tegmental region and lateral preoptic region and adjacent structures. Projections from the lateral hypothalamus to midline thalamus could not be identified in the present study.

Mediodorsal nucleus and behavior regulation in the rat

Twelve electrodes aimed at the mediodorsal thalamic nucleus were implanted in 6 rats. In 5 of these animals intracranial stimulation was effective in punishing a bar press response on a baseline schedule of water reinforcement. The sixth animal was not tested. In all 6 animals lesions produced through these electrodes disrupted response suppression to punishing electric shock superimposed on the same baseline. Those animals in which both parts of the mediodorsal thalamic nucleus were damaged showed a more marked and graded punishment effect of intracranial stimulation and a more profound disruption of the quantitative shock intensity-response relationship than those in which only the rostromedial part of the nucleus was damaged. Three other animals had electrodes implanted in the rostromedial hypothalamus or the midline thalamus. They showed neither the punishing effect of intracranial stimulation nor the disruptive effect on response suppression of electrocoagulative lesions.

Alcohol withdrawal in mice: Electroencephalographic and behavioral correlates

Chronic bipolar electrodes were implanted in forebrain structures of mice including dorsal hippocampus, dorsal-frontal cortex, dorsal-lateral thalamus and septum. Two weeks after surgery, the mice were reduced to 85–90% of free-feeding weight, and physical dependence on alcohol was established by maintaining the mice on an alcohol-containing liquid diet for 6 days. A control group was pair-fed an identical liquid diet except sucrose was substituted isocalorically for alcohol. Following 6 days of consumption alcohol was withdrawn and the development of both EEG and behavioral sequelae of withdrawal was monitored for 6–8h. Only mice withdrawn from alcohol exhibited behavioral signs of withdrawal which included hyperactivity, severe tremor, ataxia, sudden sprawling movements, and clonic-tonic convulsions. No abnormal behavior and no abnormal EEG activity resulted from the withdrawal of the sucrose control diet. EEG recordings during withdrawal from alcohol, however, indicated a progressive development of widespread neural epileptiform activity beginning with EEG slowing and increased amplitudes, followed by single spike events and often leading to sustained epileptic seizure discharge. Similar abnormal EEG patterns were observed throughout the forebrain including cortex, thalamus, hippocampus and septal area. The development of abnormal EEG activity was more severe during the second alcohol withdrawal period following 4 days of alcohol exposure than during the first alcohol withdrawal period following 6 days of alcohol exposure. It is hypothesized that the widespread forebrain epileptiform activity originates in, or is organized from, a central pacemaking region such as midline thalamus or reticular formation.

Effects of thalamic midline nuclei stimulation upon lateral geniculate transmission in rats: inhibition of principal cells and excitation of internuncial cells.

Effects of low-frequency stimulation of thalamic midline nuclei (MID) upon unitary activities of principal (P) and internuncial (I) cells of the lateral geniculate body were examined in urethane-anesthetized rats. P-cells responsed to single shocks to the optic tract (OT) with single spikes at short latencies (initial spike, IS), followed by a phase of inhibition which lasted for more than 150 msec and ended with a burst of grouped discharges (late discharge, LD). Excitability of P-cells, assessed with the response probability of IS to testing OT shocks, was reduced for about 300 msec after single shock stimulation of MID. Usually this excitability depression became evident about 20 msec after MID shocks and was maximum from 50 to 100 msec. LDs were made more vigorous when MID shocks were given almost simultaneously with testing OT shocks. This was interpreted that MID stimulation induced an inhibition in P-cells and it summed with that induced by OT stimulation. That the MID-induced inhibition of P-cells was due to IPSPs was proved by the quasi-intracellular recording. I-cells, the units fired repetitively by single OT shocks and have been presumed to be inhibitory neurons acting upon P-cells, were found to receive from MID stimulation an excitatory effect followed by an inhibitory one of long duration. It was suggested that the primary inhibition of P-cells by low-frequency stimulation of MID would be a direct consequence of the primary excitation of I-cells.

Effect of subcortical aluminum cream lesions on attentive behavior and the electroencephalogram in monkeys

Seven monkeys were prepared with aluminum hydroxide cream implants in subcortical loci; three implants were aimed at the midline thalamus and four at the upper brain stem-mesencephalic region. Prior to surgery, the animals had been trained in the performance of a sustained attention (successive color discrimination) task, some for water reinforcement and others for shock avoidance. All monkeys had implanted electrodes to permit monitoring of EEG. The animals with thalamic lesions showed little or no impairment in various measures of task performance, whereas every animal with a brain stem lesion showed substantial deficits that were interpreted as impairment in attention, coupled with some motor impairment. The impairment in the monkeys with brain stem implants was associated with hypersynchronous, slow-wave bursts in the EEG, which tended to diminish over time in the two animals which showed substantial recovery. Convulsive activity was seen in one animal with a brain stem lesion, and this appeared to be associated with the extensive invasion of aluminum hydroxide cream into the ventricular system. The brain stem lesions were large and unilateral and in every case destroyed portions of the superior and inferior colliculi, lateral lemniscus, and reticular nuclei. The thalamic lesions produced bilateral damage to midline and medial thalamic structures, as well as large areas of patchy cell loss in surrounding regions. The results are discussed in relation to research designed to model petit mal epilepsy in animals, and that aimed at exploring the role of brain structures in visually guided behavior.

Fiber projections of the non-specific midline nuclei to the anterior dorsal nucleus of the thalamus in the cat.

Fiber degenerations following stereotactic lesions in the midline nuclei of the cat thalamus, especially in the nucleus centralis medialis, rhomboidalis and reuniens (after perpendicular and oblique electrode approach) were investigated by the Fink-Heimer method of terminal degeneration. These nuclei fail to send direct fibers to all checked cortex regions; they are therefore trunco-thalamic. The midline nuclei of the thalamus, however, have besides very few degenerated fibers to the rostral pole of the thalamus (VA nucleus) strong direct connections to both anterior dorsal nuclei (A.d). This suggests a new additional path of non-specific cortical activation from the thalamic midline nuclei through the anterior dorsal nucleus to the retrosplenial cortex, and hence to the surrounding cortical fields.