Centrolateral Research Articles

The deep cerebellar nuclei to striatum disynaptic connection contributes to skilled forelimb movement

Cerebellar-thalamo-striatal synaptic communication has been implicated in a wide range of behaviors, including goal-directed actions, and is altered in cerebellar dystonia. However, its detailed connectivity through the thalamus and its contribution to the execution of forelimb movements is unclear. Here, we use trans-synaptic and retrograde tracing, exvivo slice recordings, and optogenetic inhibitions during the execution of unidirectional or sequential joystick displacements to demonstrate that the deep cerebellar nuclei (DCN) influence the dorsal striatum with a very high probability. We show that this mainly occurs through the centrolateral (CL), parafascicular (PF), and ventrolateral (VL) nuclei of the thalamus, observing that the DCN→VL and DCN→CL pathways contribute to the execution of unidirectional forelimb displacements while the DCN→PF and DCN→thalamo→striatal pathways contribute to the appropriate execution of forelimb reaching and sequential displacements. These findings highlight specific contributions of the different cerebellar-thalamo-striatal paths to the control of skilled forelimb movement.

Three-Dimensional Heterogeneity of Cerebellar Interposed Nucleus-Recipient Zones in the Thalamic Nuclei

The cerebellum is conceptualized as a processor of complex movements and is also endowed with roles in cognitive and emotional behaviors. Although the axons of deep cerebellar nuclei are known to project to primary thalamic nuclei, macroscopic investigation of the characteristics of these projections, such as the spatial distribution of recipient zones, is lacking. Here, we studied the output of the cerebellar interposed nucleus (IpN) to the ventrolateral (VL) and centrolateral (CL) thalamic nuclei using electrophysiological recording in vivo and trans-synaptic viral tracing. We found that IpN stimulation induced mono-synaptic evoked potentials (EPs) in the VL but not the CL region. Furthermore, both the EPs induced by the IpN and the innervation of IpN projections displayed substantial heterogeneity across the VL region in three-dimensional space. These findings indicate that the recipient zones of IpN inputs vary between and within thalamic nuclei and may differentially control thalamo-cortical networks.

Neural circuits of anxiolytic and antidepressant pherine molecules.

In this review, we describe proposed circuits mediating the mechanism of action of pherines, a new class of synthetic neuroactive steroids with demonstrated antianxiety and antidepressant properties, that engage nasal chemosensory receptors. We hypothesize that afferent signals triggered by activation of these peripheral receptors could reach subgroups of olfactory bulb neurons broadcasting information to gamma-aminobutyric acid (GABAergic) and corticotropin-releasing hormone (CRH) neurons in the limbic amygdala. We propose that chemosensory inputs triggered by pherines project to centrolateral (CeL) and centromedial (CeM) amygdala neurons, with downstream effects mediating behavioral actions. Anxiolytic pherines could activate the forward inhibitory GABAergic neurons that facilitate the release of neuropeptide S (NPS) in the locus coeruleus (LC) and GABA in the bed nucleus of the stria terminalis (BNST) and inhibit catecholamine release in the LC and ventral tegmental area (VTA) leading to rapid anxiolytic effect. Alternatively, antidepressant pherines could facilitate the CRH and GABAergic neurons that inhibit the release of NPS from the LC, increase glutamate release from the BNST, and increase norepinephrine (NE), dopamine (DA), and serotonin release from the LC, VTA, and raphe nucleus, respectively. Activation of these neural circuits leads to rapid antidepressant effect. The information provided is consistent with this model, but it should be noted that some steps on these pathways have not been demonstrated conclusively in the human brain.

Differentiating Cerebellar Impact on Thalamic Nuclei

SummaryThe cerebellum plays a role in coordination of movements and non-motor functions. Cerebellar nuclei (CN) axons connect to various parts of the thalamo-cortical network, but detailed information on the characteristics of cerebello-thalamic connections is lacking. Here, we assessed the cerebellar input to the ventrolateral (VL), ventromedial (VM), and centrolateral (CL) thalamus. Confocal and electron microscopy showed an increased density and size of CN axon terminals in VL compared to VM or CL. Electrophysiological recordings in vitro revealed that optogenetic CN stimulation resulted in enhanced charge transfer and action potential firing in VL neurons compared to VM or CL neurons, despite that the paired-pulse ratio was not significantly different. Together, these findings indicate that the impact of CN input onto neurons of different thalamic nuclei varies substantially, which highlights the possibility that cerebellar output differentially controls various parts of the thalamo-cortical network.

Increased GABAergic Efficacy of Central Amygdala Projections to Neuropeptide S Neurons in the Brainstem During Fear Memory Retrieval.

The canonical view on the central amygdala has evolved from a simple output station towards a highly organized microcircuitry, in which types of GABAergic neurons in centrolateral (CeL) and centromedial (CeM) subnuclei regulate fear expression and generalization. How these specific neuronal populations are connected to extra-amygdaloid target regions remains largely unknown. Here we show in mice that a subpopulation of GABAergic CeL and CeM neurons projects monosynaptically to brainstem neurons expressing neuropeptide S (NPS). The CeL neurons are PKCδ-negative and are activated during conditioned fear. During fear memory retrieval, the efficacy of this GABAergic influence on NPS neurons is enhanced. Moreover, a large proportion of these neurons (~50%) contain prodynorphin and somatostatin, two neuropeptides inhibiting NPS neurons. We conclude that CeL and CeM neurons inhibit NPS neurons in the brainstem by GABA release and that efficacy of this connection is strengthened upon fear memory retrieval. Thereby, this pathway provides a possible feedback mechanism between amygdala and brainstem routes involved in fear and stress coping.

Topographical connections of the substantia nigra pars reticulata to higher-order thalamic nuclei in the rat

The substantia nigra pars reticulata (SNR) is the ventral subdivision of the substantia nigra and contains mostly GABAergic neurons. The present study explores whether the SNR relates to all dorsal thalamic nuclei equally or just to a particular group of nuclei, such as first or higher-order nuclei. Injections of biotinylated dextran amine (BDA) were made into the SNR of 10 male adult rats. The distribution of anterogradely labelled axon terminals in the thalamic nuclei was documented. The projections of the SNR to the thalamic nuclei were exclusively to some motor higher-order, but not to first-order thalamic relays. There were bilateral projections to the ventromedial (VM), parafascicular (PF), centromedian (CM) and paracentral (PC) nuclei and unilateral projections to the centrolateral (CL), mediodorsal (MD) and thalamic reticular nucleus (Rt). Labelled axon terminals in the thalamic nuclei ranged from numerous to sparse in VM, PF, CM, CL, PC, MD and Rt. Further, injections into the SNR along its rostral-caudal axis showed specific topographical connections with the thalamic nuclei. The rostral SNR injections showed labelled axon terminals of VM, PF, CL, PC, CM, MD and Rt. Caudal SNR injections showed labelling of VM, PF, PC, CM and MD. All injections showed labelled axons and terminals in the zona incerta. The nigrothalamic GABAergic neurons can be regarded as an important system for the regulation of motor activities. The SNR is in a position to influence large areas of the neocortex by modulating some of the motor higher-order thalamic nuclei directly or indirectly via Rt.

Seizure-related activity of intralaminar thalamic neurons in a genetic model of absence epilepsy

Absence seizures are characterized by bilateral spike-and-wave discharges (SWDs) in thalamo-cortical circuits. In view of clinical studies indicating a critical involvement of intralaminar thalamic nuclei, we thought it timely to characterize the specific role and activity patterns of the respective neurons. Electrocorticographic (ECoG), intracellular, and unit activity recordings were performed in vivo from intralaminar thalamic neurons of the centrolateral (CL) and the paracentral (PC) thalamic nucleus in an established genetic rat model of absence epilepsy (WAG/Rij). Neurons in PC are depolarized to produce tonic series of action potentials at seizure-free episodes, and are rhythmically silenced concomitant with SWDs in a spike-locked manner. Rebound from spike-locked inhibition is associated with a transient increase in action potential activity. Neurons in CL possess a relatively negative membrane potential with overall low electrogenic activity at seizure-free episodes and generate burst-like discharges during SWDs that are locked to the decaying phase of the spike component on the ECoG. The SWD-locked membrane responses reverse close to the presumed chloride equilibrium potential, indicating GABAA receptor-mediated inhibitory postsynaptic potentials (IPSPs), with cell-type specific differences in polarity. In PC neurons, hyperpolarizing IPSPs result in spike-locked silencing of tonic firing and rebound burst discharges, while in CL neurons, IPSPs are depolarizing and trigger low-threshold burst firing likely mediated by a t-type Ca2+ conductance. These data show a unique pattern of rhythmic SWD-locked IPSPs in PC and CL associated with paroxysms apt to impose a transient dysfunctional state to thalamo-striato-prefrontocortical networks during absence seizures.

Bilateral phosphorylation of ERK in the lateral and centrolateral amygdala during unilateral storage of fear memories

We previously showed that when rats were trained to fear an auditory conditioned stimulus (CS) by pairing it with a mild unilateral shock to the eyelid (the unconditioned stimulus, or US), conditioned freezing depended upon the amygdala contralateral but not ipsilateral from the US. It was proposed that convergent activation of amygdala neurons by the CS and US occurred mainly in the amygdala contralateral from US delivery, causing memories of the CS–US association to be stored primarily by that hemisphere. In the present study, we further tested this interpretation by administering unilateral infusions of U0126 (in 50% dimethyl sulfoxide (DMSO) vehicle) to block phosphorylation of extracellular signal-responsive kinase (ERK) in the amygdala prior to CS–US pairings. Conditioned freezing was impaired 24 h after training when U0126 was infused contralaterally—but not ipsilaterally—from the US, suggesting that fear memories were consolidated mainly by the contralateral amygdala. However, immunostaining experiments revealed that ERK phosphorylation was elevated in both hemispheres of the amygdale's lateral (LA) and centrolateral (CeL) nuclei after paired (but not unpaired (UNP)) presentations of the CS and US. Thus, fear acquisition induced ERK phosphorylation bilaterally in the amygdala, even though the ipsilateral hemisphere did not appear to participate in conditioned freezing. These findings suggest that associative plasticity may occur in both amygdala hemispheres even when only one hemisphere is involved in freezing behavior. Conditioning-induced ERK phosphorylation was identical in both hemispheres of LA, but was slightly greater in the contralateral than ipsilateral hemisphere of CeL. Hence, asymmetric induction of plasticity in CeL might help to explain why conditioned freezing depends preferentially upon the amygdala contralateral from the US in our fear conditioning paradigm.

Effects of Acupuncture on c-Fos Expression in Brain After Noxious Tooth Stimulation of the Rat

Clinically, acupuncture therapy is useful for the control of acute or chronic pain. This study was designed to elucidate the antinociceptive mechanism of acupuncture and the mechanisms underlying cardiovascular reflex elicited by toothache. Expression of c-Fos, a neuronal activation marker, and the phenylethanalamine-N-methyltransferase (PNMT) were examined 1.5 hours after noxious intrapulpal tooth stimulation. Manual acupuncture was performed 20 min before noxious intrapulpal stimulation by 2 M KCl injection into upper or lower anterior tooth pulp. The acupuncture points were Li4 (Hegu) between the 1st and 2nd metacarpal bones or St36 (Zusanli) between the anterior crest of the tibial tuberosity and the fibula head below the patella. After noxious intrapulpal tooth stimulation, Fos-immunoreactive (IR) neurons were identified in the trigeminal subnucleus caudalis (Vc) and the transitional region between the subnucleus caudalis and the subnucleus interpolaris (Vi), in the inferior olivory nucleus (IO) connecting the cerebellum and other brain regions, and also the thalamic ventral posteromedial (VPM) nucleus and centrolateral (CL) nucleus, respectively. In addition, Fos-IR neurons were found in the central cardiovasuclar regulation centers, such as the hypothalamus supraoptic nucleus (SON) and paraventricular nucleus (PVN), and nucleus tractus solitarius (NTS) and rostral ventromedulla (RVLM). All acupuncture at St36 or Li4 significantly suppressed Fos-IR neurons in all Fos-expressed brain areas except the IO nucleus and attenuated the increases in arterial blood pressure (BP) and heart rate (HR) after noxious intrapulpal stimulation. Its Fos-suppressive effects were mostly blocked by naloxone, an opioid antagonist. In addition, acupuncture at St36 or Li4 significantly decreased Fos-containing PNMT, and this effect was also reversed by naloxone. These results suggest that: 1) tooth pulpal noxious signals transmit to the Vc and Vc/Vi transitional region and the 2nd afferent neuron synapse in the thalamic VPM and CL, 2) tooth pulpal pain elicits cardiovascular reflex mediated by NTS, VLM, hypothalamic SON and PVN, and 3) acupuncture reduces cardiovascular reflex elicited by toothache, is associated with the adrenergic system.

Differential projections from the mediodorsal and centrolateral thalamic nuclei to the frontal cortex in rats

The aim of the present study was to investigate afferent projections from the medial thalamic nuclei (MT) to the frontal cortical areas using a single small iontophoretic injection of biotinylated dextran amine (BDA) and analysis of the anterogradely labeled fibers and varicosities. Projections from the mediodorsal (MD) nuclei were found primarily and extensively in the anterior cingulate cortex (ACC), whereas those from the centrolateral (CL) thalamic nucleus were found in the frontal motor cortex. The density of terminals in the ACC was high in layers II and III and sparse in layer I. The majority of projected fibers from the CL were found at a high density in layer V, with a moderate density in the superficial layers. The differential projection patterns were topographically organized in the medial prefrontal cortex and sensory motor cortex. These findings support the results of our previous electrophysiological studies suggesting that neurons in the medial thalamic nuclei relay nociceptive information to the limbic or sensory motor cortical areas. The present results agree with the current notion that the medial thalamo-frontal cortical network circuitry plays an important role in processing the emotional aspect of nociception.

Contribution of intralaminar thalamic nuclei to spike-and-wave-discharges during spontaneous seizures in a genetic rat model of absence epilepsy.

In an epileptic rat model of generalized absence epilepsies, the genetic absence epilepsy rats from Strasbourg (GAERS), simultaneous recordings of bilateral epidural electroencephalogram (EEG) of the prefrontal cortex and unit activity of neurons in the intralaminar centrolateral (CL) and paracentral thalamic nucleus (PC) were performed under neurolept-anaesthesia (fentanyl-dehydrobenzperidol analgesia). Spike-and-wave (SW) seizures in these rats are characterized by generalized 7-10 Hz spike-and-wave discharges (SWDs) on the EEG. All neurons recorded in intralaminar thalamic nuclei during spontaneous SWDs showed high-frequency (average 368 Hz, range 200-500 Hz), burst-like activity, which occurred in a highly synchronized fashion with every SWD or with alternating SWD-complexes. Burst discharges in intralaminar neurons were delayed by 13.1 ms (CL) and 12.7 ms (PC), with respect to the spike component of a given SWD on the EEG, whereas burst discharges in the ventrobasal thalamus (VB) and in the rostral nucleus reticularis thalami (rRT) preceded the spike component by 17.8 ms and 8.3 ms, respectively. The onset of SWDs on the EEG was preceded by a tonic firing pattern (20-50 Hz) in about one third of CL and PC neurons. Microiontophoretic application of the gamma-aminobutyric acid (GABA)A receptor antagonist bicuculline aggravated, whereas, the glutamate receptor antagonists DNQX and APV dampened, SWD-related discharges in PC and CL; the GABAB receptor antagonist CGP 35347 had no measurable effect. These data indicate that intrathalamic nuclei are recruited rhythmically during SWDs, through mechanisms that seem to rely on a delayed glutamatergic excitation modulated by GABAergic influences, rather than a GABA-mediated rebound burst activity typical of relay cells. The finding of a temporal delay of SWD-related activity in intrathalamic, compared with "specific" thalamic relay nuclei, does not support the notion of a leading or pacemaker role in SWD generation. It is, however, rather suggestive of a function of intrathalamic neurons during synchronization and maintenance of neuronal oscillations, and these intrathalamic neurons may be recruited through glutamatergic corticofugal inputs.

Short-lasting nicotinic and long-lasting muscarinic depolarizing responses of thalamocortical neurons to stimulation of mesopontine cholinergic nuclei

1. The responses of thalamocortical neurons to stimulation of mesopontine [peribrachial (PB) and laterodorsal (LDT)] cholinergic nuclei were studied intracellularly in urethan-anesthetized cats. Neurons recorded from anterior thalamic (AT), ventroanterior-ventrolateral (VA-VL) and rostral intralaminar centrolateral (CL) nuclei were physiologically identified by their orthodromic responses to prethalamic stimulation and/or antidromic activation from the cerebral cortex. 2. Besides early excitatory and inhibitory postsynaptic potentials (EPSPs and IPSPs) that were not sensitive to cholinergic antagonists, two types of cholinergic responses were elicited by PB/LDT stimulation: a short-lasting and a late, long-lasting depolarization. All these components survived monoamine depletion by reserpine. 3. The latency of the short-lasting depolarizing response was 147.4 +/- 27.3 (SE) ms. The response lasted for 1.3 +/- 0.1 s and had a peak amplitude of 4.2 +/- 0.3 mV. This component was associated with 10-30% increase in membrane conductance and was abolished by systemic administration of the nicotinic antagonist mecamylamine. 4. The long-lasting depolarizing response had a latency of 1.2 +/- 0.1 s, a duration of 20.8 +/- 2.2 s, and a peak amplitude of 5.4 +/- 0.4 mV. Similar values were found in decorticated animals. The duration and amplitude of the late depolarizing component were dependent on stimulation parameters and membrane potential. This response increased under depolarizing current, decreased and eventually disappeared under hyperpolarizing current, and was associated on average with 40% increase in apparent input resistance. After systemic administration of the muscarinic antagonist scopolamine, the long-lasting depolarization disappeared; the surviving short-lasting depolarization was subsequently abolished by mecamylamine. 5. The prolonged depolarizing response of thalamocortical neurons to mesopontine cholinergic stimulation was accompanied by a desynchronization of the electroencephalogram (EEG). These two phenomena had a similar time course. Stimulation of deep cerebellar nuclei, whose axons traverse the PB area, did not induce a long-lasting depolarization of target thalamic cells, nor an EEG desynchronization. 6. These data demonstrate that, in addition to an initial nicotinic excitation, brain stem cholinergic stimulation elicits a late, long-lasting muscarinic depolarization of thalamocortical neurons. We suggest that the prolonged depolarization plays an important role in cortical activation.

Thalamic connectivity of rat somatic motor cortex

The purpose of this study was to investigate certain organizational features regarding the connectional relationships between the somatic motor cortex (SMI) and dorsal thalamus in the rat. This was accomplished by applying microiontophoretically horseradish peroxidase and tritiated amino acids into low threshold stimulation sites within hindlimb, forelimb and face representations of the SMI as defined by intracortical microstimulation. Injections into the SMI produced labeling in distinct sets of specific and non-specific thalamic nuclei. The former included the ventrolateral (VL), ventromedial (VM), posteromedial (Pom) and posterior (Po) nuclei, and the latter included the centrolateral (CL), paracentral (PC), centromedial (CeM) and parafascicular (PF) nuclei. The densest labeling, both retrograde and anterograde, was found in the VL, and to a slightly lesser extent, in the Pom nuclei. Labeling of specific nuclei was more extensive than in non-specific groups. Thalamic-SMI projections were reciprocal in nature with the exception of the reticular thalamic nucleus (R). The ventrobasal (VB) nucleus was labeled only after injections into the SMI representations of the hindlimb and forelimb. A topographic organization between the SMI and dorsal thalamic nuclei was indicated by the varied position of label following injections into different cortical representations. Injections into the hindlimb representation resulted in labeling in the rostrodorsolateral VL, ventrolateral VM, rostrodorsomedial Pom, dorsal Po, rostrodorsolateral R, dorsolateral PF, CL and PC. In contrast, injections into the face representation resulted in labeling in the caudoventromedial VL, dorsolateral VM, caudoventrolateral Pom, ventral Po, caudoventromedial R, ventrolateral PF, the PC, CeM and ventral CL. The position of thalamic labeling following injections into the forelimb representation was intermediate between that for hindlimb and face representations. In coronal section, distinct patterns of labeling were identified in all specific thalamic nuclei following injections into each topographic region of the SMI. In the VL, labeling appeared as an obliquely-oriented, longitudinal strip or band (more C-shaped following injections of the hindlimb representation); in the VM as a horizontal strip; in the Pom as an irregular V-shaped band; and in the Po as a circular-to-ovoid cluster. No distinct patterns of labeling were discerned in non-specific nuclei. Labeling in the anterior grouping of non-specific nuclei overlapped to a large extent, but this was not the case in either the specific thalamic nuclei or the PF nucleus. These findings are compared with those previously reported in the rat, and are discussed with regard to both the functional organization of the rat SMI and the interconnectional relations between the SMI and dorsal thalamus in other species.

Adult rat motor cortex connections to thalamus following neonatal and juvenile frontal cortical lesions: WGA-HRP and amino acid studies

Frontal cortex was removed in 1- and 30-day-old rats. When both groups reached 90 days of age, the forelimb motor/sensory cortex in the unlesioned hemisphere was injected with wheat germ agglutinin-horseradish peroxidase (WGA-HRP) or tritiated leucine. Thalamic neurons were retrogradely labeled only ipsilateral to the WGA-HRP injection site in both neonatally and juvenile-lesioned subjects. Ventrolateral (VL), ventromedial (VM), centromedial (CM), centrolateral (CL), parafascicular (PF), posteromedial (POm), and posterior (PO) thalamic nuclei were labeled. This and the demonstration of only ipsilateral thalamocortical connections at birth helped explain the marked thalamic atrophy which developed ipsilateral to neonatal frontal cortex lesions. Death of thalamic neurons after neonatal removal of their normal cortical target could be due to their failure to sprout into the opposite cortex because that cortex was already innervated by the opposite thalamus at birth. Leucine motor/sensory cortex injections in both neonatally and juvenile-lesioned subjects labeled the ipsilateral VL, VM, CM, CL, PF, POm, and PO thalamic nuclei; contralateral CM, CL, and PF thalamic nuclei; ipsilateral medial, ventral, and lateral pontine nuclei; and parts of the contralateral pontine nuclei. The ipsilateral connections were always more robust than the contralateral connections. The contralateral corticothalamic and corticopontine projections, however, were much more numerous and widespread in neonatally compared to juvenile-lesioned subjects. The greater sparing of some motor functions said to occur in neonatal compared to adult motor cortex-lesioned subjects could be due to the plasticity of corticothalamic, corticopontine, and other corticofugal pathways, but not to the plasticity of thalamocortical pathways.

Adult rat motor cortex connections to thalamus following neonatal and juvenile frontal cortical lesions: WGA-HRP and amino acid studies.

Frontal cortex was removed in 1- and 30-day-old rats. When both groups reached 90 days of age, the forelimb motor/sensory cortex in the unlesioned hemisphere was injected with wheat germ agglutinin-horseradish peroxidase (WGA-HRP) or tritiated leucine. Thalamic neurons were retrogradely labeled only ipsilateral to the WGA-HRP injection site in both neonatally and juvenile-lesioned subjects. Ventrolateral (VL), ventromedial (VM), centromedial (CM), centrolateral (CL), parafascicular (PF), posteromedial (POm), and posterior (PO) thalamic nuclei were labeled. This and the demonstration of only ipsilateral thalamocortical connections at birth helped explain the marked thalamic atrophy which developed ipsilateral to neonatal frontal cortex lesions. Death of thalamic neurons after neonatal removal of their normal cortical target could be due to their failure to sprout into the opposite cortex because that cortex was already innervated by the opposite thalamus at birth. Leucine motor/sensory cortex injections in both neonatally and juvenile-lesioned subjects labeled the ipsilateral VL, VM, CM, CL, PF, POm, and PO thalamic nuclei; contralateral CM, CL, and PF thalamic nuclei; ipsilateral medial, ventral, and lateral pontine nuclei; and parts of the contralateral pontine nuclei. The ipsilateral connections were always more robust than the contralateral connections. The contralateral corticothalamic and corticopontine projections, however, were much more numerous and widespread in neonatally compared to juvenile-lesioned subjects. The greater sparing of some motor functions said to occur in neonatal compared to adult motor cortex-lesioned subjects could be due to the plasticity of corticothalamic, corticopontine, and other corticofugal pathways, but not to the plasticity of thalamocortical pathways.

Convergence of the descending pathways of motor, visual and limbic cortex in the cat di- and mesencephalon

Comparisons of the descending pathways of the motor, visual and limbic cortex in the cat revealed a number of structures in di- and mesencephalon that receive projections from all these fields. They are centrolateral (CL), paracentral (Pc), central medial (CeM) and centre median (CM), nuclei of the thalamus, zona incerta (ZI) and Forel's field H 1 of the subthalamus, nucleus of the posterior commissure and anterior and posterior nuclei of the pretectum (Prt), stratum griseum intermedial and profundum of superior colliculus (CS), periaqueductal gray matter (GC) and pontine nuclei (NP). The projections from the striate field of the visual cortex to ventrobasal complex of the thalamus (VB) are shown. The results are discussed with recent data on the anatomy and physiology. A possible role of corticocortical and corticofugal fiber connections is dealt with.