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. Author manuscript; available in PMC: 2022 Apr 28.
Published in final edited form as: Brain Res. 1996 Sep 9;733(1):83–100. doi: 10.1016/0006-8993(96)00541-0

Table 2.

Modulation of cataplexy by local perfusion with monoaminergic drugs

Perfused drug (bilateral) VTA (n = 4) PRF (n = 4) GP/putamen (n = 4) BF (n = 6) Amygdala (n = 4)

Dopaminergic:
 Agonists: (10−4 – 10−2 M)
  Quinpirole + + 0 + 0 0
  SKF38393 0 0 0 0 0
  7-OH-DPAT + + 0 + 0 0
  Amphetamine 0 0 0 0 0
 Antagonists: (10−3 – 10−2 M)
  Raclopride - 0 - 0 0
  SCH 23390 0 0 0 0 0
Adrenergic:
 agonists: (10−4 – 10−2 M)
  BHT-920 + + 0 + 0 0
 Antagonists: (10−3 M)
  Yohimbine 0 0 0 0 0
  Prazosin 0 0 0 0 0

Effects of several monoaminergic compounds perfused locally in various brain regions on cataplexy in narcoleptic canines. All drugs are classified according to primary neurotransmitter receptor activity, although BHT-920 is also a strong agonist at D2 dopamine receptors. Cataplexy in narcoleptic canines was measured using the repeated Food-Elicited Cataplexy Tests (FECT) during the middle (20–30 min) and end (50–60 min) of a 60-min perfusion with each drug. 0 indicates no significant effect on cataplexy versus four baselines FECT’s, – indicates a significant reduction (P < 0.05) (but not a complete inhibition) in cataplexy versus four baseline FECT’s, + indicates a significant increase (P < 0.05) in cataplexy versus four baseline FECT’s and + + indicates a significant increase (P < 0.0l) in cataplexy versus four baseline FECT’s followed by the development of status cataplecticus in at least 50% of the animals. Significance was determined using a one-factor repeated ANOVA. The number of animals tested for each brain region studied, and each drug studied in that brain region, is shown in parenthesis under the each brain region heading.