Neuroscience 2003 Abstract
| Presentation Number: | 247.6 |
|---|---|
| Abstract Title: | Modulation of natural reward circuitry. |
| Authors: |
Jo, Y.*1
; Wiedl, D.1
; Role, L. W.1
1Dept. Anat. & Cell. Biol. Ctr. Neruobiol, Columbia Univ. Col. Physicians & Surgeons, New York, NY |
| Primary Theme and Topics |
Synaptic Transmission and Excitability - Neurotransmitters -- Acetylcholine |
| Secondary Theme and Topics | Autonomic, Neuroendocrine and Other Homeostatic Systems<br />- Regulation of Food Intake and Body Weight<br />-- Neuropeptide regulators |
| Session: |
247. ACh: CNS ACh Projections & Effects II Poster |
| Presentation Time: | Sunday, November 9, 2003 2:00 PM-3:00 PM |
| Location: | Morial Convention Center - Hall F-I, Board # B31 |
| Keywords: | ACETYLCHOLINESTERASE, CANNABINOIDS, FEEDING, HYPOCRETIN |
Feeding behavior is one of most important motivated behaviors and the most potent drive for feeding is its reward nature in human and mammal. The lateral hypothalamus is critical for regulation of feeding behavior and is considered an important structure for the brain reward circuitry. Synaptic interactions within the hypothalamus per se as well as the activity of the feeding-related projection neurons in the lateral hypothalamus are subject to extensive modulation.
Despite the well-known physiological effects of nicotine and delta9(-)-tetrahydrocannabinol (THC) administered exogenously, relatively little is known of the hypothalamic actions of their endogenous counterparts. Our present study provided a neurophysiological analysis of the modulation of the excitability of melanin-concentrating hormone (MCH) synthesizing neurons in the lateral hypothalamus (LH) implicated in natural reward behavior. We first identified MCH neurons based on the electrophysiological profile. MCH neurons showed a strong accommodation in response to a direct injection of depolarizing current. Both endogenous acetylcholine (ACh) and cannabinoid signaling modulated GABA release, the former increased, and the latter decreased GABA release. An ACh-esterase inhibitor, ambenonium (500nM), augmented GABA release in a TTX-independent manner. Such effect was completely blocked by nicotinic ACh receptor antagonists, alpha-bungarotoxin (50nM) and mecamylamine (1microM). Brief depolarization (5s) of postsynaptic neuron induced a decrease in the amplitude of evoked GABAergic inhibitory postsynaptic currents. This effect was completely abolished by cannabinoid receptor type 1 antagonist. Injection of anandamide into the postsynaptic neurons via the patch pipette decreased GABA release. Our study provides a comprehensive understating of how the activity of MCH neurons are tuned by endogenous modulatory controls.
Despite the well-known physiological effects of nicotine and delta9(-)-tetrahydrocannabinol (THC) administered exogenously, relatively little is known of the hypothalamic actions of their endogenous counterparts. Our present study provided a neurophysiological analysis of the modulation of the excitability of melanin-concentrating hormone (MCH) synthesizing neurons in the lateral hypothalamus (LH) implicated in natural reward behavior. We first identified MCH neurons based on the electrophysiological profile. MCH neurons showed a strong accommodation in response to a direct injection of depolarizing current. Both endogenous acetylcholine (ACh) and cannabinoid signaling modulated GABA release, the former increased, and the latter decreased GABA release. An ACh-esterase inhibitor, ambenonium (500nM), augmented GABA release in a TTX-independent manner. Such effect was completely blocked by nicotinic ACh receptor antagonists, alpha-bungarotoxin (50nM) and mecamylamine (1microM). Brief depolarization (5s) of postsynaptic neuron induced a decrease in the amplitude of evoked GABAergic inhibitory postsynaptic currents. This effect was completely abolished by cannabinoid receptor type 1 antagonist. Injection of anandamide into the postsynaptic neurons via the patch pipette decreased GABA release. Our study provides a comprehensive understating of how the activity of MCH neurons are tuned by endogenous modulatory controls.
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2003 Neuroscience Meeting Planner. New Orleans, LA: Society for Neuroscience, 2003. Online.
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