Activation of the hypothalamic feeding centre upon visual prey detection

The visual system plays a major role in food/prey recognition in diurnal animals, and food intake is regulated by the hypothalamus. However, whether and how visual information about prey is conveyed to the hypothalamic feeding centre is largely unknown. Here we perform real-time imaging of neuronal activity in freely behaving or constrained zebrafish larvae and demonstrate that prey or prey-like visual stimuli activate the hypothalamic feeding centre. Furthermore, we identify prey detector neurons in the pretectal area that project to the hypothalamic feeding centre. Ablation of the pretectum completely abolishes prey capture behaviour and neurotoxin expression in the hypothalamic area also reduces feeding. Taken together, these results suggest that the pretecto-hypothalamic pathway plays a crucial role in conveying visual information to the feeding centre. Thus, this pathway possibly converts visual food detection into feeding motivation in zebrafish.

Responses to Moving Visual Stimuli in Pretectal Neurons of the Small-Spotted Dogfish (Scyliorhinus canicula)

Single-unit recordings were performed from a retinorecipient pretectal area (corpus geniculatum laterale) in Scyliorhinus canicula. The function and homology of this nucleus has not been clarified so far. During visual stimulation with a random dot pattern, 45 (35%) neurons were found to be direction selective, 10 (8%) were axis selective (best neuronal responses to rotations in both directions around one particular stimulus axis), and 75 (58%) were movement sensitive. Direction-selective responses were found to the following stimulus directions (in retinal coordinates): temporonasal and nasotemporal horizontal movements, up- and downward vertical movements, and oblique movements. All directions of motion were represented equally by our sample of pretectal neurons. Additionally we tested the responses of 58 of the 130 neurons to random dot patterns rotating around the semicircular canal or body axes to investigate whether direction-selective visual information is mapped into vestibular coordinates in pretectal neurons of this chondrichthyan species. Again all rotational directions were represented equally, which argues against a direct transformation from a retinal to a vestibular reference frame. If a complete transformation had occurred, responses to rotational axes corresponding to the axes of the semicircular canals should have been overrepresented. In conclusion, the recorded direction-selective neurons in the Cgl are plausible detectors for retinal slip created by body rotations in all directions.

VERTICAL GAZE PALSY AFTER THALAMIC STIMULATION FOR TOURETTE SYNDROME

OBJECTIVE We describe a patient who developed a vertical gaze paralysis after deep brain stimulation performed for intractable Tourette syndrome due to a small deep bleeding in the upper mesencephalon. CLINICAL PRESENTATION A 39-year-old man underwent thalamic deep brain stimulation for intractable Tourette syndrome. Immediately postoperatively, he had diplopia and dizziness. The neurological examination revealed vertical gaze palsy with preserved vertical oculocephalic movements. A postoperative computed tomography scan revealed a discrete high-density lesion across the midline at the distal end of the left electrode. This area corresponds with the pretectal area, including the rostral interstitial nucleus of the medial longitudinal fasciculus, with sparing of the oculomotor and rubral nuclei. INTERVENTION Six months postoperatively, maximal upward and downward smooth pursuit eye movements were achieved. Upward saccadic velocities were still reduced by 20 to 25 degrees. CONCLUSION This case report describes a complication that might demand special attention during the planning of thalamic deep brain stimulation for the treatment of Tourette syndrome. Examination of both horizontal and vertical eye movements during deep brain stimulation surgery is recommended.

Involuntary Vocalisations and a Complex Hyperkinetic Movement Disorder Following Left Side Thalamic Haemorrhage

A variety of involuntary speech phenomena as for example palilalia have been described as consequences of neurological disorders. Palilalia is the involuntary repetition of syllabels, words and phrases in ongoing speech. We describe a 73 year old woman who suffered from a hypertensive thalamic haemorrhage. MRI revealed that the lesion was predominantly located within the pulvinar, extending to the lateroposterior thalamic nuclei and to the pretectal area with possible involvement of the medial geniculate body. Few months after the event she developed involuntary vocalisations with whole words and meaningless syllables being rapidly reiterated. In contrast to typical palilalia these vocalisations were not meaningfully related to the ongoing speech of the patient. In addition, the patient developed a complex hyperkinetic movement disorder with right-sided painful hemidystonia and bilateral clonic jerks and a right-sided postural tremor.

Zebrafish aussicht mutant embryos exhibit widespread overexpression of ace (fgf8) and coincident defects in CNS development

During the development of the zebrafish nervous system both noi, a zebrafish pax2 homolog, and ace, a zebrafish fgf8 homolog, are required for development of the midbrain and cerebellum. Here we describe a dominant mutation, aussicht (aus), in which the expression of noi and ace is upregulated. In aus mutant embryos, ace is upregulated at many sites in the embryo, while noi expression is only upregulated in regions of the forebrain and midbrain which also express ace. Subsequent to the alterations in noi and ace expression, aus mutants exhibit defects in the differentiation of the forebrain, midbrain and eyes. Within the forebrain, the formation of the anterior and postoptic commissures is delayed and the expression of markers within the pretectal area is reduced. Within the midbrain, En and wnt1 expression is expanded. In heterozygous aus embryos, there is ectopic outgrowth of neural retina in the temporal half of the eyes, whereas in putative homozygous aus embryos, the ventral retina is reduced and the pigmented retinal epithelium is expanded towards the midline. The observation that aus mutant embryos exhibit widespread upregulation of ace raised the possibility that aus might represent an allele of the ace gene itself. However, by crossing carriers for both aus and ace, we were able to generate homozygous ace mutant embryos that also exhibited the aus phenotype. This indicated that aus is not tightly linked to ace and is unlikely to be a mutation directly affecting the ace locus. However, increased Ace activity may underly many aspects of the aus phenotype and we show that the upregulation of noi in the forebrain of aus mutants is partially dependent upon functional Ace activity. Conversely, increased ace expression in the forebrain of aus mutants is not dependent upon functional Noi activity. We conclude that aus represents a mutation involving a locus normally required for the regulation of ace expression during embryogenesis.

Projections of single retinal ganglion cells to the visual centers: An intracellular staining study in a plethodontid salamander

The projection specificity of retinal ganglion cells and the morphology of their terminals were studied in the plethodontid salamander Plethodon jordani. In an in vitro approach, ganglion cells were stained with biocytin and reconstructed by means of light microscopy. Single retinal ganglion cells often have multiple terminal structures in the thalamus, pretectum, and tectum. The projection pattern in the diencephalic neuropils is related to the depth of the terminal arbor within the tectal fiber layer. Terminal arbors in the tectum differ in location, size, and branching pattern. The following types could be distinguished: The most superficial of the optic terminals in layer 1 are relatively small with a diameter of about 100 μm. With the exception of a few varicosities (beads) in the pretectal neuropils, their stem axons have no further collaterals or terminal arbors in the diencephalic neuropils. Intermediate terminals in layer 2 fan out to form a dense plexus with a medio-lateral extent of 180 μm on average. Some terminals in this layer show obvious antenna-like fibers reaching toward the surface of the tectum. The axons of layer 2 projecting neurons have additional collaterals and terminal arbors in the thalamus and pretectum. The deep layer 3 terminals spread out over a diameter of 400 μm on average and their degree of branching is moderate. The axons of layer 3 projecting ganglion cells have dense additional terminal arbors in the thalamus and pretectum. The deepest retinal terminals in the tectum are found within the predominantly efferent fiber layers. This type consists of an unbranched, but beaded axon which runs rostro-caudally with several bends and loops. The stem axon has an additional very dense terminal arborization in the neuropil of the nucleus Bellonci pars medialis and additional sparse collaterals in the pretectal area.

Genetic control of brain morphogenesis through Otx gene dosage requirement

Understanding the genetic mechanisms that control patterning of the vertebrate brain represents a major challenge for developmental neurobiology. Previous data suggest that Otx1 and Otx2, two murine homologs of the Drosophila orthodenticle (otd) gene, might both contribute to brain morphogenesis. To gain insight into this possibility, the level of OTX proteins was modified by altering in vivo the Otx gene dosage. Here we report that Otx genes may cooperate in brain morphogenesis and that a minimal level of OTX proteins, corresponding either to one copy each of Otx1 and Otx2, or to only two copies of Otx2, is required for proper regionalization and subsequent patterning of the developing brain. Thus, as revealed by anatomical and molecular analyses, only Otx1−/−; Otx2+/− embryos lacked mesencephalon, pretectal area, dorsal thalamus and showed an heavy reduction of the Ammon's horn, while the metencephalon was dramatically enlarged occupying the mesencencephalic area. In 8.5 days post coitum (d.p.c.) Otx1−/−; Otx2+/− embryos, the expression patterns of mesencephalic-metencephalic (mes-met) markers such as En-1 and Wnt-1 confirmed the early presence of the area fated to give rise to mesencephalon and metencephalon while Fgf-8 transcripts were improperly localized in a broader domain. Thus, in Otx1−/−; Otx2+/− embryos, Fgf-8 misexpression is likely to be the consequence of a reduced level of specification between mes-met primitive neuroepithelia that triggers the following repatterning involving the transformation of mesencephalon into metencephalon, the establishment of an isthmic-like structure in the caudal diencephalon and, by 12.5 d.p.c., the telencephalic expression of Wnt-1 and En-2. Taken together these findings support the existence of a molecular mechanism depending on a precise threshold of OTX proteins that is required to specify early regional diversity between adjacent mes-met territories and, in turn, to allow the correct positioning of the isthmic organizer.