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.