A direct projection from the retina to the hypothalamus was demonstrated in the rat. Following injection of tritiated leucine or proline into the posterior chamber of the eye, labelled protein was shown autoradiographically in the suprachiasmatic nuclei of the medial hypothalamus, both ipsilateral and contralateral to the injected eye. The labelling of the nucleus was heaviest in its ventral portion but extended throughout the nucleus. No evidence for a projection to the supraoptic nucleus or any other hypothalamic nucleus was observed. All of the known terminal nuclei of the primary and accessory optic tracts were heavily labelled. The projection to the suprachiasmatic nucleus could not be clearly confirmed in material prepared using the Fink-Heimer method for the demonstration of degenerating axon terminals. Electron microscopic study of the suprachiasmatic nucleus following orbital enucleation showed degenerating endings making synaptic contacts with small dendrites of the suprachiasmatic nucleus cells. These first appeared at three days after operation and were nearly gone by seven days. Thus, the retinohypothalamic tract in the rat appears to arise from the ganglion cells of the retina and to terminate on the smaller dendritic branches of the neurons of the suprachiasmatic nucleus.It is now well-established that environmental light plays an important role in regulating hypothalamic-anterior pituitary function in the adult mammal (cf. Harris, '55; Wurtman, '67; Szentagothai et al., '68, for reviews). Yet, despite the extensive information available on these neuroendocrine effects of light, the component of the central retinal projection responsible for mediating the effects has not been identified. The simplest pathway by which light might affect hypothalamo-hypophyseal function would be a direct projection from the retina to the medial hypothalamus. There is substantial evidence for such a projection in submammalian vertebrates (Herrick, '42; Riss et al., '63; Knapp et al., '65; Ebbesson, '68; Ebbesson and Ramsey, '68; Bons and Assenmacher, '69) but in mammals the literature concerning a direct retinohypothalamic projection, while large, is contradictory (cf. Hayhow et al., '60; Kiernan, '67; Szentagothai et al., '68, pg. 59; '70, for reviews). In a previous study we failed to find convincing evidence for a retinohypothalamic projection in the rat (Moore, J. COMP. NEUR., 146: 1-14.'69) when applying the Fink-Heimer methods (Fink and Heimer, '67) at several postoperative survival periods following unilateral enucleation. The present study was undertaken to re-investigate this problem using a new method for tracing central pathways. Recent reports have demonstrated that labelled amino acids injected into the posterior chamber of the eye are incorporated into protein by ganglion cells and transported along the axons of the optic nerve by axoplasmic flow to the terminal nuclei of the optic system (Taylor and Weiss, '65; Grafstein, '67; Sjostrand and Karlsson, '69). In the lateral geniculate bod...

Summary: Purpose:We assessed rates of symptoms of anxiety and depression among pediatric patients with epilepsy.Methods: We administered the Revised Child Manifest Anxiety Scale (RCMAS), and Child Depression Inventory (CDI) to 44 epilepsy patients aged 7-18 years (mean age 12.4 years). Demographic, socioeconomic, and epilepsy-related information was examined in relation to depression and anxiety scores.Results: No patients had been previously identified to have depression or anxiety. However, 26% had significantly increased depression scores and 16% met critieria for significant anxiety symptomatology. Conclusions: Symptoms of depression and anxiety are common among pediatric patients with epilepsy and appear to be overlooked by care providafs. Key Words: AnxietyDepression-Epilepsy-Seizures-Pediatric.Many controversial studies suggest that patients with epilepsy are at high risk for psychiatric disturbances (1-3) including depression (43) and anxiety (6-8). Most such studies are based on adults; there are far fewer studies of psychiatric symptoms in children and adolescents with seizures. Although depression in childhood has been reported to occur with administration of barbiturates (9), very little is known about overall rates and determinants of depression and anxiety in pediatric patients with epilepsy.Rutter et al. (10) reported psychiatric disturbances in as many as 33% of children with epilepsy but did not specifically delineate affective disorders. Hoare (1 1) noted higher rates of behavioral difficulties in children with epilepsy than in children with diabetes mellitus, but did not determine rates of anxiety and depression. The present study was therefore designed to (a) determine the degree to which the affective disorders (depression and anxiety) had been detected and treated in previous clinical care, (b) determine the frequency of depressive and anxiety-related symptoms among children and adolescents with epilepsy at present, and (c) examine the relationship between self-reported anxiety and depression symptoms with demographic and seizure-related factors. METHODSInclusion and exclusion criteria were as follows: Study entry was offered consecutively to outpatients (aged 7-18 years) with epilepsy (defined as recurrent unprovoked seizures) attending the Pediatric Neurology Department at the University at Stony Brook. Patients with mental retardation were excluded. Patients and their parents completed several self-report measures that examined the following variables:1. Demograptiic variables. Patient ages and sex were recorded. Ages were divided into groups aged 7-12 and 13-18 years. For each child, 1 parent completed the Hollingshead Index, a measure of socioeconomic status (SES) which contains questions about family income, marital and occupational status, and education (12). Scores from the Hollingshead Index were divided into scores of ~2 9 , 2 9 4 8 , and >48 to define lower, middle, and upper SES groups.

Hippocampal neurons are highly plastic in their excitable properties, both during development and in the adult brain. As voltage-sensitive K+ channels are major determinants of membrane excitability, one mechanism for generating plasticity is through regulation of K+ channel activity. To gain insights into the regulation of K+ channels in the hippocampus, we have analyzed the spatiotemporal expression patterns of five K+ channel polypeptides in rat hippocampal neurons developing in situ and in vitro. Delayed rectifier-type channels (Kv1.5, Kv2.1, and Kv2.2) are expressed on all neuronal somata and proximal dendrites, while A-type channels (Kv1.4 and Kv4.2) are present distally on distinct subpopulations of neurons. The development of these patterns in situ is monotonic; that is, while the time and spatial development varies among the channels, each K+ channel subtype initially appears in its adult pattern, suggesting that the mechanisms underlying spatial patterning operate through development. Immunoblots confirm the differential temporal expression of K+ channels in the developing hippocampus, and demonstrate developmentally regulated changes in the microheterogeneity of some K+ channel polypeptide species. Temporal expression patterns of all five K+ channels observed in situ are retained in vitro, while certain aspects of cellular and subcellular localization are altered for some of the K+ channel polypeptides studied. Similarities in K+ channel polypeptide expression in situ and in vitro indicate that the same regulatory mechanisms are controlling spatiotemporal patterning in both situations. However, differences between levels of expression for all subtypes studied except Kv2.1 indicate additional mechanisms operating in situ but absent in vitro that are important in determining polypeptide abundance.

Stroke in children is rarely diagnosed in the time frame of 3 to 6 hours. Given the causes and outcome of stroke in children, this age group might benefit from thrombolysis and from neuroprotective therapy, yet the long delay in diagnosis in this age group excludes most cases from being considered for such treatments. This situation should encourage attempts to increase public and professional awareness of stroke in children and of the potential value of early diagnosis and treatment, preferably by broadening current educational efforts to all age groups.

NGF acts as a neurotrophic factor by binding and activating its receptor on certain neuronal populations in the CNS and PNS. TrkA is a receptor for NGF. Recent findings in vitro indicate that this NGF- activated receptor tyrosine kinase transduces the NGF signal. To further define NGF actions in the CNS, we examined trkA expression in the adult rat brain. We found that trkA mRNA and immunoreactivity (IR) coincided in specific, defined neuronal populations in the forebrain and brainstem. In addition to cholinergic neurons in the basal forebrain and neostriatum, trkA expression was found in noncholinergic neurons in (1) the paraventricular anterior and reuniens thalamic nuclei, (2) the rostral and intermediate subnuclei of the interpeduncular nucleus (IPN), (3) scattered neurons in the ventrolateral and paramedian medulla, (4) the prepositus hypoglossal nucleus, and (5) the area postrema. NGF responsiveness was demonstrated for each of these populations. In contrast to trkA, p75NGFR was found only in a minority of NGF-responsive populations. Our data provide further evidence that expression of trkA marks NGF-responsive CNS neurons and suggests novel roles for NGF in the brain.

Large, calyciform axonal endings, as well as typical terminal boutons, have been previously described in the ventral cochlear nucleus and the nucleus of the trapezoid body by light microscopists. In the present study, these endings were examined with the electron microscope in chinchillas, rats, and a cat after perfusion fixation with osmium tetroxide. The calyces were found to consist of elongated processes arising from myelinated axons and making multiple synaptic contacts with perikarya and dendrites. This finding suggests that an important property of calyces is the large amount of synaptic activity that they can bring to bear on a single postsynaptic structure. Adjacent to the calyciform endings were variable numbers of boutons that made synaptic contacts with the same perikarya and dendrites. The majority of boutons contained smaller synaptic vesicles than those present in the calyces, implying both anatomical and functional differences between these two types of ending. It is suggested that many of these boutons in the ventral cochlear nucleus are endings of centrifugal, inhibitory fibers described by previous workers.Held (1893) and others (e.g., Ram6n y Cajal, '34; Harrison and Irving, '65) have described calyciform terminations of axons in mammalian auditory nuclei. When impregnated with the Golgi method, these calyces of Held appear at the terminations of axons as expansions of variable size from which arise processes of variable shape. These elongated processes provide for large areas of apposition between a single axonal ending and a perikaryon or dendrite. It has been shown that similar calyciform axonal endings in chick ciliary ganglia are electrically coupled with ganglion cells (Martin and Pilar, '63a, b, '64), and thorough cytological studies of these calyces are available (e.g., Takahashi and Hama, '65). It therefore seemed of interest to examine the auditory calyces with the electron microscope, and to compare their structure to that of the chick ciliary ganglion calyces.Among the calyciform endings in mammalian auditory nuclei are other axonal endings which appear as typical terminal boutons in Golgi preparations (Ram6n y Cajal, '09). They are distinguished from calyces by their smaller size and simple shape. In the cochlear nucleus, many of these appear to be endings of axons from AM. J. ANAT., 1 1 8 : 375-390.higher auditory centers (Rasmussen, '60), which are probably inhibitory (Pfalz, '62). A second objective of this study was to identify these endings and to determine their synaptic relationships with the calyces and adjacent neurons. MATERIALS AND METHODSThe material for the present report consisted of four adult rats, three adult chinchillas, and one adult cat. The regions studied most intensively were the nucleus of the trapezoid body in rat, and the ventral cochlear nucleus in chinchilla.Animals were first anesthetized with chloral hydrate, and the body temperature lowered to 26°C (Wolfe, '65). The brains were fixed by perfusion through the aorta with balanced salt solution...

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The effect of intermittent seizures on the pyramidal neurons of the hippocampus is largely unknown. To determine whether recurrent seizures centered in the hippocampus can produce neuronal loss in this region, a morphometric analysis was performed from standardized sections of hippocampus using 5 groups of animals: (1) surgical control subjects, (2) rats kindled by the rapidly recurring hippocampal seizure (RRHS) paradigm, (3) kindled rats with a few additional limbic seizures (528 +/- 66 seizures), (4) kindled rats with many limbic seizures (1,523 +/- 130 seizures), and (5) rats experiencing limbic status epilepticus (SE) induced by "continuous" hippocampal stimulation. The RRHS and SE protocols induced significant neuronal loss in the CA1 region, but no evidence was found for additional cell loss with increasing numbers of intermittent seizures. These intermittent seizures were, however, associated with a significant thickening of the basal and apical dendritic fields of the CA1 region. These findings indicate that intermittent seizures produce no significant hippocampal neuronal loss and may result in a hypertrophy of CA1 dendritic fields.