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INNERVATION OF PVN.PROJECTING NEURONS IN TIlE VLM BY NEURONS FROM TIIE NTS: A COMBINED RETROGRADE AND ANTERI)GRADE TRACT-TRACING STUDY IN TIlE RAT. IlIT_OSIII__KAWANO AND SADAIIIKO MASUKO, l/epartment _Jff__Anatnmy,Saga ._Medical~chttol, 5-1-1 /Saheshima, Saga 849, Japan
Thc vcntrolatcral medulla ohlongata (VLM). a rcgion for rcgulating a cartho~,ascular function, is clcctrophysiologically suggcstcd to bc situated in a ncural pathway from the nuclcus tmclus solitarius (NTS) to the paravcr~ricular hypothalamic nuclcus (PVN). To dcmonstratc synaptic contacts of VLM-projccting NTS neurons to PVNprojccting VLM ncurons, an electron microscopic study was dCmc using the rats, which, under ahcsthcsia, rcccivcd a rclrogradc tracc~, WGA-ItRP-colloidal gold, in the PVN and an antcrogradc traccr, Phaseohts vtdgari~-letwoagghttinin (PtlAI.). in the NTS Rctrogradcly labeled neurons wcrc found in the VI.M al the Icvcls bclwccn 28~11 ,t.tm caudal to and 2400/_tin rostral to the obcx with a peak numbcr (256.5 -+ 61.0, mean _+S ILM.) at the lcvcls bctwccn 480-960/2m rostral to the obcx A total of 1330.5 +_ 320.4 rctrogradcly labclcd neurons was tbund in the ipsilatcral VIA1. PttAI.immunorcactivc nerve terminals synapscd mainly to dcndrilcs and scarccly to soma. PttAl.-immunorcactivc nerve terminals which synapscd to the dendrites or soma of rctrogradcly labeled neurons wcrc "also t'~und These findings show a morphological evidence thai VLM-ncurons which projcct to the PVN arc innervated by ncuronal affcrcnts originated from the NTS
225
PROPERTIES OF SYNAPTIC TRANSMISSION IN THE HIPPOCAMPUS OF 'REELER' MUTANT MOUSE AKIHIRO ISHIDA, KUNIKO SHIMAZAKI AND NOBUFUMI KAWAI, Department of Physiology, Jichi
Medical School, Minamikawaclfi-machi, Tochigi-ken 329-04, Japan The laminar organization of the hippocampus of the homozygous reeler mutant mouse is extremely disrupted. Frequently, CA1 pyramidal layers are divided by two layers. Using slice preparations of the hippocampus of reeler mouse we have studied morphological organization and functional properties of the disrupted pyramidal cell layers. Laminar analysis of the field excitatory postsynaptic potentials (fEPSPs) by stimulating Schaffer collateral/commissural fibers revealed double peaks, indicating that the input fibers make synaptic contacts with the dendrites of the pyramidal neurons in two distinct layers. The threshold stimulus intensity for evoking fEPSPs in reeler mouse did not greatly differ from that in normal mouse but the slope for input-out relationship was considerably lower in reeler mouse. We made simultaneous recordings from two distinct pyramidal layers and compared fEPSPs evoked by a stimulus input. In most of the slices from reeler mouse, tetanic stimulation produced LTP in one layer but failed to evoke LTP in the other layer.
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EFFECTS OF ATP-SENSITIVE K ÷ CHANNEL MODULATORS ON GABAergic TRANSMISSION IN RAT CULTURED HIPPOCAMPAL NEURONS. OHNO-SHOSAKU, T., SAWADA, S. AND YAMAMOTO, C. Department of Physiology, Faculty of Medicine, Kanazawa University, Kanazawa 920 Effects of ATP-sensitive K ÷ (KA'rP) channel activators (diazoxide and cromakalim) and an inhibitor (tolbutamide) on the GABAergic transmission were explored by applying the patch-clamp technique to both presynaptic and postsynaptic hippocampal neurons prepared from neonatal rats. Application of 0.5 mM diazoxide and 0.5 mM cromakalim reduced GAl3Aergic synaptic currents to 57 % and 8 1 % of control, respectively. The currents induced by exogenously applied GABA (10 p_M) was not affected by cromakalim, or was reduced by diazoxide less intensively than the synaptic currents, indicating that these drugs suppressed the GABA release by activating KA'rP channels present in the presynaptic terminals. Application of baclofen (GABAb agonist) reduced GABAergic synaptic currents to 48% (I laM) and 14% (10 I.tM). These effects of baclofen were partially inhibited by 1 mM Ba 2÷, but never inhibited by 0.5 mM tolbutamide. These results indicate that KATP channels present in synaptic terminals are not involved in the GABAb-mediated. presynaptic inhibition of GABAergic transmission in the hippocampus.