Abstract
Leptin is an adipose-derived hormone that regulates energy balance. Leptin receptors are expressed in extrahypothalamic sites and several reports showed that leptin can influence feeding and locomotor behavior via direct actions on dopaminergic neurons. The leptin deficient mouse (ob/ob) has been used as an animal model of blunted leptin action, and presents with obesity and mild type 2 diabetes. We used ob/ob mice to study the effect of repeated 7-day methamphetamine (METH) administration analyzing locomotion, behavioral sensitization, and somatosensory thalamic mRNA expression of voltage-gated calcium channels and glutamatergic receptors using RT-PCR. We observed reduced METH-mediated responses in ob/ob mice associated with enhanced in mRNA expression of key voltage-gated and glutamate receptors in the somatosensory thalamus. Results described here are important for understanding the control of locomotion and thalamocortical excitability by leptin.
Highlights
Leptin is an adipose-derived hormone [1] known to control appetite and energy expenditure [2]
Leptin receptors are predominantly expressed in the hypothalamus, they have been described to be expressed in extrahypothalamic areas like somatosensory thalamic nuclei and the mesolimibic dopamine system [4,5,6]
At day 7, basal locomotor activity showed interactive effects between genotype and treatment, and we found differences betwee wild type (WT)-vehicle and ob mice (OB), but no changes in locomotion after after METH between genotypes (Figure 1C, left)
Summary
Leptin is an adipose-derived hormone [1] known to control appetite and energy expenditure [2]. Our group has described multiple METH-mediated alterations in mouse cortical and sub-cortical areas [13,14,15,16], including changes in mRNA levels of membrane receptors and voltage-gated ion channels in medial prefrontal neurons [17]. A psychostimulant that can increase DA neurotransmission, enhanced low threshold T-type calcium channel protein levels in mouse somatosensory thalamus neurons [18]. Selective targeting of T-type calcium channels using specific blockers reduced cocaine-mediated hyperlocomotion concomitantly with a reduction in GABAergic neurotransmission onto thalamic ventrobasal nucleus [19], suggesting the involvement of somatosensory ventrobasal thalamic nucleus in locomotor alterations
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