Gaba(A) receptors in the pedunculopontine tegmental nucleus play a crucial role in rat shell-specific dopamine-mediated, but not shell-specific acetylcholine-mediated, turning behaviour.
The role of GABA(A) receptors in the pedunculopontine tegmental nucleus in turning behaviour of rats was studied. Unilateral injection of the GABA(A) receptor agonist, muscimol (25-100 ng), into the pedunculopontine tegmental nucleus dose-dependently produced contraversive pivoting, namely tight head-to-tail turning marked by abnormal hindlimb backward stepping. This effect was GABA(A) receptor specific, since it was prevented by the GABA(A) receptor antagonist, bicuculline (50 ng), which alone did not elicit turning behaviour. Unilateral injection of a mixture of dopamine D(1) ((+/-)-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine-7,8-diol [SKF 38393], 5 microg) and D(2) (quinpirole, 10 microg) receptor agonists into the nucleus accumbens shell has been found to elicit contraversive pivoting, whilst unilateral injection of the acetylcholine receptor agonist (carbachol, 5 microg) into the same site is known to elicit contraversive circling, namely turning marked by normal stepping. The pivoting induced by a mixture of SKF 38393 (5 microg) and quinpirole (10 microg) injected into the nucleus accumbens shell was significantly inhibited by bicuculline (50 ng) injected into the pedunculopontine tegmental nucleus, whereas muscimol (25 ng) had no effect. Neither muscimol (25 ng) nor bicuculline (50 ng) modulated the contraversive circling induced by carbachol (5 microg) injected into the nucleus accumbens shell. It is therefore concluded that unilateral stimulation of GABA(A) receptors in the pedunculopontine tegmental nucleus can elicit contraversive pivoting and that the pedunculopontine tegmental nucleus is one of the output stations of the accumbens region that mediates shell-specific, dopaminergic pivoting, but not of the accumbens region that mediates shell-specific, cholinergic circling.
Ikeda
H
H
Department of Pharmacology, Nihon University School of Dentistry, 1-8-13 Kanda-Surugadai, Chiyoda-ku, Tokyo 101-8310, Japan.
Akiyama
G
G
Matsuzaki
S
S
Sato
M
M
Koshikawa
N
N
Cools
A R
AR
D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D002799:Cholinergic Fibers / Q000187:drug effects / Q000378:metabolism; D004298:Dopamine / Q000378:metabolism*; D018491:Dopamine Agonists / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D007839:Functional Laterality / Q000502:physiology; D018755:GABA Agonists / Q000494:pharmacology; D018756:GABA Antagonists / Q000494:pharmacology; D008297:Male; D009043:Motor Activity / Q000187:drug effects / Q000502:physiology; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology; D009434:Neural Pathways / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D009714:Nucleus Accumbens / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D045042:Pedunculopontine Tegmental Nucleus / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D011930:Reaction Time / Q000187:drug effects / Q000502:physiology; D017447:Receptors, Dopamine D1 / Q000187:drug effects / Q000378:metabolism; D011963:Receptors, GABA-A / Q000187:drug effects / Q000378:metabolism*; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D018491:Dopamine Agonists; D018755:GABA Agonists; D018756:GABA Antagonists; D017447:Receptors, Dopamine D1; D011963:Receptors, GABA-A; D005680:gamma-Aminobutyric Acid; D000109:Acetylcholine; D004298:Dopamine