TY - JOUR
T1 - Behavior-related changes in the activity of substantia nigra pars reticulata neurons in freely moving rats
AU - Gulley, Joshua M.
AU - Kuwajima, Masaaki
AU - Mayhill, Emily
AU - Rebec, George V.
N1 - Funding Information:
Supported by the National Institute of Drug Abuse (DA 02451). J.M.G. is the recipient of a predoctoral N.R.S.A. fellowship (DA 05921). We also greatly appreciate Paul Langley for technical assistance and Faye Caylor for help in preparing the manuscript.
PY - 1999/10/16
Y1 - 1999/10/16
N2 - As one of the primary targets of the striatum, the substantia nigra pars reticulata (SNr) has been hypothesized to play a role in normal motor behavior. Specifically, inhibition of usually high, tonic SNr output is predicted to correlate with motor activation. While support for this has come primarily from electrophysiological studies in primates performing goal-directed movements, we tested this hypothesis in rats behaving in an open-field arena. SNr single-unit activity was recorded during spontaneous bouts of open-field behavior (e.g., head and body movements, locomotion) and after rats were given D-amphetamine (1.0 mg/kg, s.c.), which reliably increases motor activity and elevates the firing of motor-related striatal neurons. Prior to drug administration, SNr neurons had either regular, slightly irregular or irregular firing patterns when animals rested quietly. During movement, some inhibitions were observed, but the majority (~79%) of analyzed units increased firing by as much as 38%. Regardless of the predrug behavioral response of the cell, amphetamine strongly inhibited firing rate (~90% below nonmovement baseline) and changed firing pattern such that all cells fired irregularly. Subsequent injection with the dopamine antagonist haloperidol (1.0 mg/kg, s.c.) reversed amphetamine-induced inhibitions in all tested cells, which supports a role for dopamine in this effect. These results suggest that the pattern of striatal activity established by amphetamine, which may be critical for determining the drug-induced behavioral pattern, is represented in the SNr regardless of the predrug behavioral response of the cell. Copyright (C) 1999 Elsevier Science B.V.
AB - As one of the primary targets of the striatum, the substantia nigra pars reticulata (SNr) has been hypothesized to play a role in normal motor behavior. Specifically, inhibition of usually high, tonic SNr output is predicted to correlate with motor activation. While support for this has come primarily from electrophysiological studies in primates performing goal-directed movements, we tested this hypothesis in rats behaving in an open-field arena. SNr single-unit activity was recorded during spontaneous bouts of open-field behavior (e.g., head and body movements, locomotion) and after rats were given D-amphetamine (1.0 mg/kg, s.c.), which reliably increases motor activity and elevates the firing of motor-related striatal neurons. Prior to drug administration, SNr neurons had either regular, slightly irregular or irregular firing patterns when animals rested quietly. During movement, some inhibitions were observed, but the majority (~79%) of analyzed units increased firing by as much as 38%. Regardless of the predrug behavioral response of the cell, amphetamine strongly inhibited firing rate (~90% below nonmovement baseline) and changed firing pattern such that all cells fired irregularly. Subsequent injection with the dopamine antagonist haloperidol (1.0 mg/kg, s.c.) reversed amphetamine-induced inhibitions in all tested cells, which supports a role for dopamine in this effect. These results suggest that the pattern of striatal activity established by amphetamine, which may be critical for determining the drug-induced behavioral pattern, is represented in the SNr regardless of the predrug behavioral response of the cell. Copyright (C) 1999 Elsevier Science B.V.
KW - Amphetamine
KW - Motor behavior
KW - Movement-related cell
KW - Substantia nigra pars reticulata
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U2 - 10.1016/S0006-8993(99)01932-0
DO - 10.1016/S0006-8993(99)01932-0
M3 - Article
C2 - 10529445
AN - SCOPUS:0032849496
SN - 0006-8993
VL - 845
SP - 68
EP - 76
JO - Brain Research
JF - Brain Research
IS - 1
ER -