Ionic mechanisms involved in dopamine induced slow depolarization

S142

24 Neurotransmitters III Receptor biophysics INHIBITION OF SYNAPTIC TRANSMISSION BY 5-HYDROXYTRYPTAMINE IN ,THE RABBIT CILIARY GANGLION

HITOSHI

TATSUMI*,

Physiology,

YOSHIFUMI

Medical

KATAYAMA,

and

Research Institute,

KIICHIRO

MORITA*,

Department

of

Tokyo Medical and Dental University,

Autonomic

2-3-10

Kanda

Surugadai, Chiyedaku, Tokyo 101, Japan

Intracellular rabbit

recordings were made from neurons in the ciliary ganglion isolated from the

previously

killed by air embolism.

superfusion.

5-hydroxytryptamine

applied

to

the

of

the

by

cholinergic

fast excitatory postsynaptic potential (e.p.s.p.)

depression of the e.p.s.p,

5-HT

(I ~M - I mM) reversibly depressed the amplitude

preparation

in every neuron.

was dependent on the concentration of 5-HT.

the depression of the e.p.s.p, control.

The degree of

The relative value of

amplitude in 5-HT (300~M) was 0.46 ±0.03 (mean +_s.e. mean) of

The effect of 5-HT lasted throughout the application of the drug and was

observed with repeated applications.

5-HT

at

a

depolarization. postsynaptic miniature

high

This

concentration

means

sensitivity

e.p.s.p.s.

to

constantly

5-HT at concentrations of less than 3 0 0 ~ M did not change

the amplitude of the depolarizations produced by acetylcholine while

(5-HT) was

(I mM) slightly

(ACh) applied iontophoretically,

reduced

the

amplitude

that 5-HT (< 300~M)

inhibits the e.p.s.p,

ACh.

5-HT (100~M)

Futhermore,

the

ACh

without changing

the

decreased

of

the

frequency

of

These results suggest that 5-HT acts on presynaptic nerve terminals and

depresses ACh release.

IONIC

MECHANISMS

INVOLVED

KAZUHIKO,,SASAKI TAKASHIMA , and Iwate 020 Dopamine

with

current

occurrence

of

by the

mechanism

i) The

response was

not

in the

effect The

on

increase of

the

seemed the

was

this

The

resistance of

when

type

when

the

activity,

augmented

when

to the

3)Changes

often

This of the

the

increase

in e i t h e r

net

a the

is membrane.

follows:

decreased.

in the

The

affinity

extracellular in D A - r e c e p t o r

[K+] ° or

with

reveals

resting as

[Na +] was but

of A p l y s i a

response

investigated

extracellular

cells

measured

however,

response.

was

ganglion

Morioka

of

[Ca ++ ] was activity

[CI-] ° c a u s e d

but

little

of r e s p o n s e .

membrane.

that

DA-induced

[cAMP], The

to be v o l t a g e - d e p e n d e n t , media.

response

due

affinity.

method,

this

in the

was

was

in the

or by d e p o l a r i z a t i o n

this

response

augmentation

in i n t r a c e l l u l a r

perfusing

DEPOLARIZATION

resistance

clamp

during

IBMX

depressed

suggested

receptor

SLOW

observed

in m e m b r a n e

voltage

to the d e c r e a s e

receptor

result

increase

underlying

2)The The

depolarization

presence

due

DA-receptors. decreased.

an

negative

augmented

depresson

slow

pulse.

The

ionic

INDUCED

, MITSUHIKO MATSUMOTO , MASANORI SHOZUSHIMA , KOICHIRO, M A K O T O SATO., Dept. P h y s i o l . , Sch. Med., Iwate Med. Univ.,

induced

is a s s o c i a t e d constant

IN D O P A M I N E

which

receptor

activation

produced

an

Na+-channels and

once

inhibited

increase

opened

by the

of

this

type

an

in N a + - p e r m e a b i l i t y

by D A - r e c e p t o r

presence

caused

of

normal

activation [Ca++] ° in