Senktide

Cell experiment:

Experiments are performed on brain slices (300 μM thick) from 150 g male Wistar rats and extracellular recordings are made by conventional techniques. Drugs (including Senktide) are applied by bath perfusion and removal is achieved simply by returning to the control drug-free solution. Extracellular electrodes are filled with aCSF and have resistances of 5 to 14 MΩ. For intracellular recordings, electrodes are filled with 1 M potassium acetate and have d.c. resistances of 70 to 110 MΩ. Neurons are considered to be dopaminergic if they have a characteristic waveform, slow firing rate (~5 Hz) and inhibitory response to dopamine[2].

Animal experiment:

For the Senktide dose-response curve, gerbils are first allowed to habituate to the test area for 30 min. Animals (n=10 to 12 per drug treatment group) are anesthetized with isoflurane, a small incision is made in the skin over bregma, and an injection of Senktide at 0.01, 0.03, 0.06, 0.1, 0.3 or 0.6 nmol in 5 μL of vehicle is placed i.c.v. using a syringe with a 4.5 mm long needle. Wounds are clipped shut, and animals allowed to awaken from anesthesia, then placed directly into the locomotor activity boxes and recording commenced. For testing of the NK1 receptor antagonist aprepitant (1, 3 or 10 mg/kg p.o.), gerbils are first treated with aprepitant or vehicle (0.9% NaCl with 0.3% Tween80) and returned to the home cage for 90 min. Animals are then placed in the open field for 30 min of habituation. During the last 5 min of habituation, 0.03 nmol Senktide is injected i.c.v[1].

References:

[1]. Nordquist RE, et al. The tachykinin NK3 receptor agonist senktide induces locomotor activity in male Mongolian gerbils. Eur J Pharmacol. 2008 Dec 14;600(1-3):87-92.
[2]. Keegan KD, et al. The selective NK3 receptor agonist senktide excites a subpopulation of dopamine-sensitiveneurones in the rat substantia nigra pars compacta in vitro. Br J Pharmacol. 1992 Jan;105(1):3-5.