Acetylcholine receptors containing the beta-2 subunit are involved in the reinforcing properties of nicotine

Article Abstract:

Nicotine stimulates dopamine release in the ventral striatum of wild-type mice. However, this effect is not observed in the ventral striatum of beta-2 mutant mice. Mesencephalic dopaminergic neurons from mice lacking the beta-2 subunit do not respond to nicotine any more. In these mutant mice, self-administration of nicotine is reduced. A rise in dopamine release mediated through beta-2-containing nicotine acetylcholine receptors is one of the main substrates for the addictive characteristics of nicotine.

Nicotine, Dopaminergic mechanisms

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Spatio-temporal dynamics of cyclic AMP signals in an intact neural circuit

Article Abstract:

The stomatogastric ganglion cells in the lobster receive fast cyclic AMP signals due to synaptic release of endogenous neuromodulators in an intact neural circuit. This produces rapid changes in the configuration of the neural circuitry. The prolonged stimulation of the cyclic AMP leads to its diffusion throughout the cell body. This provides the neuromodulatory signals a mechanism for the coordination of various functions within the different regions of the neuron.

Cyclic adenylic acid, Cyclic adenosine monophosphate, Neurotransmitters, Neural circuitry, Ganglia, Autonomic, Autonomic ganglia

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Abnormal avoidance learning in mice lacking functional high-affinity nicotine receptor in the brain

Article Abstract:

Experimental studies of the beta-2-subunit of neuronal nicotinic acetylcholine receptors (nAChR) suggest that mutations in this subunit cause absence of nicotine binding sites, leading to unusual nicotine-independent avoidance. The mutant mice exhibit better passive avoidance than normal mice. Nicotine administration does not elicit any response from thalamic neurons, as revealed by electrophysiological studies.

Mutation (Biology), Mutation, Binding sites (Biochemistry), Active sites (Biochemistry), Acetylcholine, Acetylcholine receptors, Conditioned response, Conditioned responses

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