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GABA release from proopiomelanocortin neurons
Shane T Hentges1, Mitsuru Nishiyama, Linda S Overstreet
1Vollum Institute, Oregon Health and Science University, Portland, Oregon 97239, USA. hentgess@ohsu.edu
Summary
Proopiomelanocortin (POMC) neurons release GABA, inhibiting themselves and influencing food intake. This rapid inhibition, distinct from peptide signaling, may affect distant brain areas.
Area of Science:
- Neuroscience
- Neuroendocrinology
- Cellular Neuroscience
Background:
- Proopiomelanocortin (POMC) neurons regulate food intake and energy balance.
- POMC neurons release alpha-melanocyte-stimulating hormone to reduce feeding.
- Neuropeptide Y (NPY) neurons stimulate feeding and release GABA to inhibit POMC neurons.
Purpose of the Study:
- To investigate reciprocal inhibition in POMC neurons.
- To determine if POMC neurons release rapid neurotransmitters.
- To explore the role of GABA in POMC neuron function.
Main Methods:
- Primary cultures of fluorescently labeled POMC neurons with autapses.
- Evoked action potentials and recorded synaptic currents.
- GABA(A) receptor antagonists and opioid inhibition assays.
- In situ RNA hybridization for POMC and glutamic acid decarboxylase (GAD).
Main Results:
- POMC neurons with autapses exhibited short-latency synaptic currents upon action potential.
- Autaptic currents were blocked by GABA(A) antagonists and reduced by opioids.
- Approximately one-third of POMC neurons co-expressed POMC and GAD mRNAs in vivo.
- Vesicular GABA transporter immunoreactivity was found in extrahypothalamic POMC terminals.
Conclusions:
- POMC neurons can rapidly inhibit themselves via GABA release.
- This GABAergic inhibition complements sustained peptide signaling.
- Rapid inhibition likely impacts distant POMC projections rather than local circuits.