S32 TRANSPLANTATION OF ACTIVATED MACROPHAGES INDUCES CNS AXONAL REGROWTH FOLLOWING INJURY O. Lazarov-Spiegler, A.S. Solomon and M. Schwartz Dept. of Neurobiology, Weizmann Institute of Science, Rehovot, Israel We have recently suggested that the failure of adult mammalian central nervous system (CNS) axons to regenerate is associated with a deficient inflammatory reaction, that could be circumvented in tran- sected optic nerve by local transplantation of blood monocytes, preacti- vated by regenerative sciatic nerve. Here we show that the resulting axonal regrowth extended at least as far as the optic chiasma. This was demonstrated by retrograde labeling following injection of fluorescent dye into the optic chiasma 10 weeks after optic nerve transection. Re- growth of optic nerve axons was confirmed by a double labeling: im- mediately after nerve transection 4-Di-10-Asp was injected into the injury site, and 10 weeks later Fast blue was applied distally to it. No retinal ganglion cells (RGC) were labeled with the second dye only. Of the RGC that were labeled with the first dye, 47% were also labeled with the second dye, indicating regrowth of almost half of the injured axons following transplantation with sciatic nerve-preactivated macro- phages. Less than 5% were double-labeled following transplantation of optic nerve-preincubated macrophages. No double-labeled RGC were detected in control (nontransplanted) optic nerves. We further show that the axonal regrowth is associated with rapid and efficient myelin clear- ance from the site of injury in optic nerves transplanted with sciatic nerve-preactivated macrophages. This study thus suggests that the evolution of the mammalian CNS as an immune privileged site is di- rectly correlated with its failure to regenerate after injury. DOES PHYSIOLOGY REGULATE OUR AVIDITY FOR SALT? M. Leshem Dept. of Psychology, Haifa University, Haifa, Israel ‘Salt appetite’ is known in many mammals. It is the behavior that contends with sodium requirements in accordance with past experience, present challenges and future needs, and it is regulated physiologically by the mechanisms of sodium homeostasis. Past experience of sodium deficit leaves its imprint on fetus, infant and adult as a permanently increased avidity for salt to prevent recurrence of the deficit. The likely mechanism is that the hormones of salt necessity, angiotensin and al- dosterone, have signaled the brain that the animal is born into a salt- sparse ecology, and changed brain and behavior accordingly. A present sodium deficit arouses ‘sodium hunger’ to motivate the urgent search for salt. And to meet future sodium needs, the spontaneous hedonic avidity for sodium both staves off mineral deficit and motivates learn- ing about sodium resources to meet future eventualities. Since these behaviors occur in our dietary relatives (omnivores) and our evolution- ary relatives (primates), they must occur in humans. I show that all three of these sodium appetites have now been demonstrated in hu- mans. In humans, permanent or transient modification of the avidity for salt is given to common events that influence salt homeostasis in the long- and short-term: morning sickness, childhood vomiting, childhood diarrhea, exercise-induced perspiration. If these conclusions are rein- forced by further research, the implications for salt intake and its atten- dant health risks are clearly significant. QUANTITATIVE ANALYSIS OF THALAMOCORTICAL SYNAPSES IN DEVELOPING MOUSE BARRELS D.L. Lev 1 , E. Barkai 2 , Y. Grossman 2 , E. Weinfeld 1 and E.L. White 1 Zlowtowski Center for Neuroscience, Depts. of Morphology 1 and Physiology 2 , Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer Sheva, Israel This study focuses on the development of synapses made by tha- lamocortical afferents to mouse barrel cortex. Goals are to determine the timing of thalamocortical (TC) synaptogenesis, whether TC syn- apses are subject to overproduction and elimination, and at various developmental stages, the numbers of boutons per axon length and the number of synapses per bouton, the identities of postsynaptic elements and whether changes occur during development in specific synaptic patterns. One approach to labeling TC axon terminals involves the anterograde transport of the fluorescent dye, DiI, followed by photo- conversion prior to electron microscopy. Results to date indicate that some TC synapses are formed as early as P7. All TC synapses are asymmetrical. A persistent problem with the DiI method is the inability in most instances to differentiate unequivocally between TC and local axon collaterals of retrogradely labeled corticothalamic cells. Une- quivocal identification of TC afferents will be made using the antero- grade transport of intracellularly injected horseradish peroxidase. Supported by Israel Science Foundation 335/96 to E.L.W.; Israeli National Institute of Psychobiology and Ministry of Science to E.B. and Y.G. HUMAN D 3 DOPAMINE RECEPTOR IN THE MEDULOBLASTOMA TE671 CELL LINE: CROSS-TALK BETWEEN D 1 AND D 3 RECEPTORS B. Levavi-Sivan, C.S. Fishburn and B.H. Park Dept. of Immunology, Weizmann Institute of Science, Rehovot, Israel The D 3 dopamine receptor is thought to have an important func- tional role in mediating the effects of dopamine in behavioral and cog- nitive functions. In order to study the functional properties of the D 3 receptor, we have searched for a cell line in which this subtype is ex- pressed endogenously. We found that the neuron-derived human me- dulloblastoma cell line TE671, expresses the D 3 receptor in the absence of the other two inhibitory dopamine receptors, D 2 and D 4 . D 1 dopa- mine receptor is also expressed in this cell line. TE671 D 3 receptor was cloned and sequenced and found to be identical to the D 3 receptor previously cloned from human brain. Short exposure (20–30 min) of TE671 cells to dopamine resulted in the appearance of a short-lived D 3 - like receptor mRNA. The dopamine induced effect was abolished by butaclamol. We have then tested whether there might be an interrela- tionship or cross talk between D 3 and D 1 pathways in TE671 cells, resulting in receptor upregulation. We have employed D 3 or D 1 specific agonists and antagonists and followed the activation of each receptor subtype, selectively, following RT-PCR and specific hybridizations. Exposure of TE671 cells to the D 3 agonist 7-OH-DPAT (DPAT) in- creased specifically the expression of the D 3 receptor mRNA. Likewise, exposure of cells to the D 1 agonist to SKF38393 (SKF) increased the expression of D 1 receptor mRNA. In addition we have observed that whereas DPAT did not affect the expression of the D1 receptor, SKF caused an increase in the expression of D 3 receptor. This increase was inhibited by the D 1 antagonist SCH23390 (SCH). The increase in D 3 expression, following activation of the D 1 receptor may suggest a cross-talk between these receptors or activation of some step in the cascade of their signal transduction. IS THE TEMPORAL PATTERN IMPORTANT IN THE COCKROACH’S WIND DETECTION SYSTEM? R. Levi and J. M. Camhi Dept. of Cell and Animal Biology, Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem, Israel The ultimate way to understand a neural code is to be able to alter the behavior it produces by controlled changes to the code. We took this approach in studying the neural code responsible for the escape behavior of the cockroach. The cockroach senses a predator by the wind produced by its approach and correspondingly turns away and runs. This turning can be reproduced with the animal fixed to a slippery surface free to move only its legs, and using wind as a stimulus. Under these conditions when the wind is presented from different directions the leg movement varies accordingly. Simultaneously it is possible to inject spikes into a single interneuron in a group of giant interneurons (GI) controlling the escape behavior. This altered activity results in a