Tetuhide H. Murakami

The effect of post-ischemic hypothermia and long-term administration of MK-801 on neuronal survival after 1-month in gerbils

1Dcpt. of Pharmacol, Yokohama City Univ Sch Mcd, Yokohama 236-0001. 7-Dept. for Ncurosci, Tokyo Mctrop Inst of Ncurosci, Tok~~o 183-8526 DOPA itself is a ncuromodulator in striata (hog A’eurohiol 19, 415451, 1996). Esogcr~ousl~~ applied DOPA stcrcosclccti\.cl!. c\,okcd ncuronal glutamate (Glu) with competitive inhibition by a DOPA antagonist in slices and caused delayed neuronal death via Glu rclcase in cultured fetal neurons, suggesting involvcmcnt of DOPA in an upstream process of mechanisms for Glu rcleasc and ncuronal death. WC tried to clarify whether DOPA is rclcascd. being a factor for Glu rclcasc and ncuronal death b! transient ischemia. Four vessels vxrc occluded for 10 min during striatal microdialysis of conscious rats. DOPA, DA and Glu wcrc mcasurcd by HPLC-ECD and spcctrophotomctcr. Ncuronal death H’as c\.aIuatcd 96 hr after ischcmia. lschcmia indeed cwkcd DOPA with DA and Glu. rcspcctivc peak being 5.6. __ 770and 8.3.fold of a basal Ic\,cl. Moderate striatal and SC! crc hippocampal ncuronal death occurred. Intrastriatal perfusion of NSD-1015 30 uM. a DOPA dccarbosylase inhibitor, markcdl!, incrcascd DOPA and Glu rclcasc by ischcmia with slight inhibition of DA rclcasc and csaggcratcd striatal ncuronal death. Furthcrmorc, DOPA cyclohcsyl cstcr (CHE) 10-100 nM, H no\ cl. poicnt and stable compctiti\ c DOPA antagonist, inhibit4 dose-dcpcndcntly incrcascs in Glu rclcasc without change of DA rclcasc. CHE 100 nM protcctcd striata from dclaycd ncuronal death. Hippocampal ncuronal death ~‘as ncithcr affected by KSD-1015 nor CHE. DOPA woked seems to bc a causal f’actor b!, itself \,ia its recognition site for incrcasc in Glu rclcasc and resultant dclayxl ncuronal death b\, tnrnsicnt ischcmia in rats.

1635 Ipsilateral motor control of forelimb affected by the hemisphectomy of the corpus callosum

Microiontophoretic application of carbachol onto sympathoexcitatory neurons in the rostra1 ventrolateral medulla (RVLM) of the rat increased the firing of RVLM sympathoexcitatory neurons and the increase of unit activity was blocked by the M2 receptor antagonist methoctramine but not by the Ml antagonist pirenxepine and the Mj antagonist 4-DAMP. Microiontophoretic application of physostigmine and pressure ejected application of 3,4-diaminopyridine also increased the neuronal firing rate. Intravenous administration of physostigmine increased the firing of these neurons. Microiontophoretic application of scopolamine onto the RVI.24 neurons reversed the excitatory response to intravenous physostigmine. These results suggest that in rats RVLIY sympathoexcitatory neurons have M2 muscarinic receptors and receive cholinergic innervation. Physostigmine injected systemically may exert its hypertesive effect through an activation of RVLM neurons.

1629 Alterations in number of apical dendritic spines of pyramidal neurons resulting from hemisphectomy- modified golgi method

1627 DIRECT PROJECTIONS FROM THE PRESUPPLEMENTARY MOTOR AREA (PRE-SMA) TO THE BASAL GANGLIA IN THE JAPANESE MONKEY. MASAHIKO TAKADA*. HIRONOBU TOKUNO*, MASAHIKO INASE **. ATSUSHI NAMBU***. TOSHIKAZU AKAZAWA***. *Dem. of Morohol. Brain Sci.. Fat. of Med.. Kvoto Univ.. Kvoto. 606-01. **Mol. & Cell. Neurosci. Sec.. Electrotech. Lab., Tsukuba, 305. ***Dept. of Neurobiol., Tokvo Metropol. Inst. for Neurosci,. Fuchu. Tokvo. 183, Japan.