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Lesion of NPY Receptor-expressing Neurons in Perifornical Lateral Hypothalamus Attenuates Glucoprivic Feeding
Removing specific hunger-related neurons in the side hypothalamus reduces feeding caused by low sugar
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Abstract
Selective destruction of NPY-sensitive neurons in the perifornical lateral hypothalamus significantly reduces glucoprivic feeding in male and female rats.
- Glucoprivic feeding is linked to the activation of certain neurons in the perifornical lateral hypothalamus during glucose deficits.
- Lesioning NPY receptor-expressing neurons in the PeFLH using NPY-saporin resulted in decreased feeding in response to 2-deoxy-D-glucose (2DG).
- The lesions did not affect other physiological responses, including locomotor activity, hyperglycemia, or corticosterone release, during glucoprivation.
- Male rats with PeFLH lesions exhibited reduced body weights and less feeding during the dark cycle, effects not observed in female rats.
- These findings suggest that the NPY pathway to the PeFLH is essential for glucoprivic feeding but not for other counterregulatory responses.
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