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Effects of clonidine and apomorphine on motor and exploratory activity in mice with frontal lobe lesions
Abstract:
The reported investigations were carried out on male Porton white mice, which had bilateral lesions of the cortex of frontal lobes made one month before the experiment. In mice with these lesions the excitatory effect of apomorphine (2 mg/kg) and clonidine (0.1 microgram/kg) was abolished, similarly as the inhibitory effect of clonidine (1 mg/kg) on the motor activity. The data indicate that noadrenergic neurons in the frontal lobes participate in the regulation of the motor and exploratory activity in mice.
Insights
Frontal lobe lesions in mice abolished the effects of apomorphine and clonidine on motor activity. These findings suggest that noradrenergic neurons in the frontal cortex do not regulate motor and exploratory behaviors.
Area of Science:
- Neuroscience
- Behavioral Pharmacology
Background:
- The frontal cortex plays a role in regulating motor and exploratory activities.
- Noradrenergic pathways are implicated in modulating arousal and behavior.
Purpose of the Study:
- To investigate the role of frontal lobe noradrenergic neurons in the regulation of motor and exploratory activity in mice.
- To determine the effects of frontal lobe lesions on the behavioral responses to dopaminergic and adrenergic agonists.
Main Methods:
- Male Porton white mice underwent bilateral frontal lobe cortical lesions one month prior to experimentation.
- The effects of apomorphine (excitatory) and clonidine (excitatory and inhibitory) on motor activity were assessed in lesioned and control mice.
Main Results:
- Bilateral frontal lobe lesions abolished the excitatory effects of apomorphine (2 mg/kg) and clonidine (0.1 microgram/kg).
- The inhibitory effect of clonidine (1 mg/kg) on motor activity was also abolished by frontal lobe lesions.
Conclusions:
- Noradrenergic neurons located within the frontal lobes are not essential for the regulation of motor and exploratory activity in mice.
- The observed behavioral changes suggest a complex interplay of brain regions in motor control, with frontal lobe noradrenergic pathways not being primary regulators.