Initial expression of glutamate receptor channels in embryonic drosophila muscles

s31

206

INITIALEXPRESSION OF GLUTAMATE RECEPTORCHANNELSIN EMBRYONIC DROSOPHILA MUSCLES. KOH-ICHINISHIKAWA AND YOSHIAKIKIDOKORO

GunmaUniversity School of Yedicine,3-39-22

Showa-machi,Yaebashi,37l,Japan

We recorded unitary currents of glutamate receptor channels using the patch clamp technique in the cell-attached configuration. At 12.513 hr after fertilization motoneurons first conatct muscle cells. However, no single channel events were recorded at this time. Shortly after at 13.5 hr channel events were detected in the extra-junctional area. The single channel conductance was about 100~s and the kinetics were similar to channels in older embryos. Spontaneous synaptic currents were first recorded at around 14 hr after fertilization. The amplitude of synaptic currents increased abruptly between 19 and 22 hr. Meanwhile channel activities in the extrajunctional area remained at the similar level. Initial synaptic transmission and expression of functional glutamate receptor channels seem closely correlated.

207

ENDOGENOUS ATP MODULATES NICOTINIC TRANSMISSION THROUGH PRESYNAPTIC P, RECEPTORS IN RABBIT PARASYMPATHETIC GANGLIA. TOSHIHIKO NISHIMURA AND TAKASHI AKASU, Department of Physiology, Kurume University School of Medicine, 67 Asahi-machi, Kurume, 830, Japan. Membrane currents were recorded from neurons of rabbit vesical parasympathetic ganglia at 36 C, utilizing single electrode voltage clamp techniques in vitro. Nicotinic fast excitatory postsynaptic current (EPSC) was evoked by stimulation of the pelvic nerve. Suramin (lo-100 PM) or reactive blue 2 (I-30 PM), P,antagonists, increased amplitude of fast EPSC by 5-34 %. These agents did not increase the amplitude of inward current evoked by pressure application of acetylcholine (IACL), in presence of atropine (1 PM), suggesting that site for actions of P,-antagonists on the fast EPSC was presynaptic. Bath application of adenosine 5'-triphosphate (ATP) (0. l-l mM) depressed the amplitude of fast EPSC without affecting the I,,,. ATP-induced depression of the fast EPSC was antagonized by suramin but not by 8-cyclopentyltheophylline (10 uM; 8CPT). A, antagonist. Adenosine (0.1-l mM) also caused suppression of the fast EPSC that was antagonized by 8CPT but not by suramin. These data suggest that endogenous ATP, probably co-released with ACh, reduces amount of ACh-liberation through presynaptic P, receptors. We propose that presynaptic P, receptors compose a major step for negative feedback mechanism of cholinergic transmission.

208

EXCITATORY EFFECT OF ADENOSINE ON NEUROTRANSMISSION COLLICULUS

-IN VITRO AND IN VIVO STUDY.

IN THE SUPERIOR

YASUHIRO OKADA. HIROKAZU HIRAI,

Dept. of Phvsiol.. Kobe Univ. Sch. of Med.. Kobe, 650. Janan. In vitro study:

Slices of superior colliculus were prepared from guinea pig and postsynaptic

potentials were recorded in the superficial grey layer after stimulation of optic layer. and its derivatives showed only excitatory effect on neurotransmission. slice was enhanced by application of adenosine.

In vivo studv: Postsynaptic potentials were elicited in the (lOti)

EHNA (5 mg/kg, s.c.), a adenosine diaminase inhibitor. glutamate w;rs increased by application excitatory effect on neurotransmission

Adenosine (>lO%Q

The release of glutamate from the

superior colliculus aRer electrical stimulation to optic nerve in in vivo rat. potential was enhanced by direct application

field

of adenosine.

The amplitude of evoked

of adenosine and also by systemic application of Microdialysis study indicated that the release of These results indicates that adenosine shows

in the superior colliculus via increase of release of glutamate, an

excitatory neurotransmitter in retinotectal pathway.