Table 2.
Model | Type of Treatment | Target | Effect | Reference |
---|---|---|---|---|
Tottering mice | 6-OHDA (s.c., dose 100 mg/kg) Acute effect on the first or second day after birth |
Noradrenergic terminals (hyperinnervation) + Noradrenergic terminals (destruction) |
Decrease in total duration of SWDs | Noebels, 1984 [72] |
GAERS rats | Salbutamol (i.p., 1.25–50, acute) Isoprenaline (i.p., 12.5–100, acute) |
Beta AR (activation) | No effect | Micheletti et al., 1987 [40] |
Propranolol (i.p., 1.25–80, acute) | Beta AR (inhibition) | No effect | ||
Prazosin (i.p., 0.25–4, acute) | Alpha1 AR (inhibition) | Increase in SWDs total duration | ||
ST 587 (i.p., 1–4, acute) Cirazoline (i.p., 0.1–4, acute) |
Alpha1 AR (activation) | Decrease in SWDs total duration | ||
Clonidine (i.p., 0.01–0.1, acute) | Alpha2 AR (activation) | Increase in SWDs total duration | ||
Yohimbine (i.p., 0.5–8, acute) | Alpha2 AR (inhibition) | <2 mg/kg: decrease in SWD total duration >4 mg/kg: very short decrease in SWDs total duration followed by the disappearance of the effect |
||
Desipramine (i.p., 5–40, acute) | NA reuptake (inhibition) 5HT reuptake (inhibition) |
No effect | ||
Mianserine (i.p., 1.25–40, acute) | NA release (activation) alpha1 AR (inhibition) alpha2 AR (inhibition) 5HT receptors (inhibition) |
No effect | ||
Fischer 344 rats | 6-OHDA (i.c., 200 μg, two injections with 48 h interval) | Noradrenergic terminals (destruction) | Increase in HVS incidence (4–7 days after administration) | Buzsáki et al., 1991 [41] |
6-OHDA (i.th., 50 μg, one injection) | Increase in HVS incidence (4–7 days after administration) | |||
DSP-4 (i.p., 50 mg/kg, acute) | No effect (4–7 days after administration) | |||
+ Xylazine (i.th., acute) |
Increase in HVS incidence after intracisternal or intrathalamic 6-OHDA | |||
Clonidine (i.p., 0.02 or 0.1 mg/kg) | Alpha2 AR (activation) | Increase in HVS incidence | ||
Xylazine (i.p., 0.5 or 2 mg/kg) | Alpha2 AR (activation) | Increase in HVS incidence | ||
Yohimbine (i.p., 1 or 5 mg/kg, acute) | Alpha2 AR (inhibition) | Decrease in HVS incidence 1 mg/kg: maximal effect |
||
Prazosin (i.p., 0.5 or 2 mg/kg) | Alpha1 AR (inhibition) | Increase in HVS incidence | ||
Desipramine (i.p., 1 or 10 mg/kg, acute) Amitriptyline (i.p., 1 or 10 mg/kg, acute) |
NA reuptake (inhibition) 5HT reuptake (inhibition) |
Decrease in HVS incidence | ||
Amitriptyline (i.p., 10 mg/kg, 21 days) | NA reuptake (inhibition) 5HT reuptake (inhibition) alpha2 AR (decreased density) |
Decrease in HVS incidence Decrease of the effect of intrathalamic xylazine Decrease of the effect of IP xylazine—not significant |
||
Clonidine (i.th., bilateral, 0.1 or 1 nmol, acute) | Alpha2 AR (activation) | Increase in HVS incidence (suppressed by 5 nmol of yohimbine) | ||
Clonidine (i.th., unilateral, 10 or 100 pmol, acute) | Alpha2 AR (activation) | Increase in HVS amplitude | ||
WAG/Rij rats | Clonidine (i.p., 0.00625 mg/kg, acute) | Alpha2 AR (activation) | Increase in SWDs incidence Decrease in total EEG power in the frontal cortex Increase in total EEG power in RTN Decrease in intracortical coherence |
Sitnikova and Luijtelaar 2005 [42] |
Dexmedetomidine (i.p., 1 mg/kg, IP, acute) | Alpha2 AR (activation) | Decrease in total SWDs number (very high dose) | Al-Gailani et al., 2022 [73] | |
GAERS rats | Atipamezole (i.c.v., 1–31 µg, acute) | Alpha2 AR (inhibition) | 12/31 µg: decrease in SWDs incidence and SWDs mean duration | Yavuz et al., 2020 [43] |
Atipamezole (i.c.v., 12 µg, 5 days) | Alpha2 AR (inhibition) | Decrease in total SWDs duration | ||
Dexmedetomidine (i.c.v., 0.1, 0.5, 2.5 µg, acute) | Alpha2 AR(activation) | Increased in total SWD, absence status epilepticus | Yavuz et al., 2022 [74] | |
Charles River rats | Clonidine (p.o., 0.0001–0.1 mg/kg, acute) | Alpha2 AR (activation) | Increase in the mean duration of SWDs | Kleinlogel, 1985 [75] |
Guanfacine (p.o., 0.0001–0.1 mg/kg, acute) | Alpha2 AR (activation) | Increase in the mean duration of SWDs | ||
Yohimbine (p.o., 0.1–10 mg/kg, acute) | Alpha2 AR (inhibition) | Decrease in the mean duration of SWDs (maximal effect with dose 1 mg/kg). 3.2 mg/kg: suppressed the effect of guanfacine (1 mg/kg) |
||
Prazosin (p.o., 0.32–10 mg/kg, acute) | Alpha1 AR (inhibition) | Increase in the mean duration of SWD | ||
Long-Evans rats | Yohimbine (i.p., 0.5–10 mg/kg, acute) | Alpha2 AR (inhibition) | 0.5–5 mg/kg: decrease in the mean duration of FEAD 10 mg/kg: no effect |
King and Burnham, 1982 [76] |
Wistar rats | Atipamezole (s.c., 0.1/1/10 mg/kg, acute) | Alpha2 AR (inhibition) | 0.1 mg/kg: no effect 1/10 mg/kg: suppression of HVS |
Riekkinen et al., 1990 [77] |
Guanfacine (i.p., 0.004/0.02/0.1 mg/kg, acute) | Alpha2 AR (activation) | Increase in HVS incidence and duration (0.004 mg/kg: no effect on duration) + Atipamezole (1 mg/kg): suppressed an increase in HVS duration Atipamezole (10 mg/kg): suppressed an increase in HVS duration and incidence |
||
+ unilateral RT lesion (VB also damaged) |
No HVS on the contralateral side; HVS still occurred on the ipsilateral side | |||
Atipamezole (s.c., minipump, 0.1 mg/kg/h, continuous) | Alpha2 AR (inhibition) | Decrease in HVS incidence during the 6-day administration No changes in sensitivity to Guanfacine (i.p., 0.001 mg/kg, acute) |
Jäkälä et al., 1992 [78] | |
Aged Wistar rats (10–12 months) | Atipamezole (i.p., 0.01–4 mg/kg, acute) | Alpha2 AR (inhibition) | Decrease in HVS incidence | Yavich et al., 1994 [79] |
Idazoxan (i.p., 0.1–4 mg/kg, acute) | Alpha2 AR (inhibition) | <0.5 mg/kg: decrease in HVS incidence >0.5 mg/g: disappearance of the effect |
||
Yohimbine (i.p., 0.1–4 mg/kg, acute) | Alpha2 AR (inhibition) | <0.5 mg/kg: decrease in HVS incidence >0.5 mg/g: disappearance of the effect |
||
Dexmedetomidine (i.p., 0.005 mg/kg, acute) | Alpha2 AR(activation) | Increase in HVS incidence | ||
Prazosin (i.p., 1 mg/kg, acute) | Alpha1 AR (inhibition) | Increase in HVS incidence |
Abbreviations: AR—adrenoreceptor, NA—noradrelaine, 5HT—serotonin. Type of EEG activity: FEAD—flash-evoked after discharge, HVS—high voltage spindles (the waveform similar to spike-wave discharges), SWDs—spike-wave discharges. Type of administration: i.p.,—intraperitoneal, i.c.—intracisternal; i.th.—intrathalamic; i.c.v.—intracerebroventricular, PO—perioral, SC—subcutaneous.