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Time schedule of apomorphine administration determines the degree of globus pallidus excitation
Abstract:
Intravenous administration of a single 320 microgram/kg bolus dose of apomorphine significantly increased in unit activity of rat globus pallidus neurons. Significantly attenuated responses to apomorphine were observed when 320 microgram/kg apomorphine was administered i.v. in divided doses (5, 35, 280 microgram/kg) 3-5 min apart or when 320 microgram/kg apomorphine was given i.v. 8 min after a nonexcitatory 'priming' dose (20 microgram/kg i.v.) of apomorphine. These results suggest that the expression and magnitude of apomorphine-induced excitation of pallidal neurons is influenced by the time schedule of drug administration.
Insights
A single dose of apomorphine excites rat globus pallidus neurons. However, divided or primed doses of apomorphine significantly reduce this excitation, indicating administration timing impacts neural responses.
Area of Science:
- Neuroscience
- Pharmacology
Background:
- Apomorphine is a dopamine receptor agonist.
- The globus pallidus plays a crucial role in motor control and reward pathways.
Purpose of the Study:
- To investigate the effect of apomorphine administration timing on globus pallidus neuronal activity in rats.
Main Methods:
- Intravenous administration of apomorphine in rats.
- Electrophysiological recording of globus pallidus neuronal unit activity.
- Varying single, divided, and primed dosing schedules of apomorphine.
Main Results:
- A single bolus dose of apomorphine (320 microgram/kg) significantly increased globus pallidus neuronal activity.
- Divided doses or a priming dose of apomorphine attenuated the excitatory response in globus pallidus neurons.
- The timing of apomorphine administration influenced the magnitude of neuronal excitation.
Conclusions:
- The temporal pattern of apomorphine administration critically affects its impact on globus pallidus neuronal activity.
- This suggests complex dose-response and time-dependent mechanisms underlying apomorphine's effects on basal ganglia circuitry.