PubMed · 8658106
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T Beardsley. 1996. Waking up.. https://doi.org/10.1038/scientificamerican0796-14
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In the present study the neuronal expression of Fos, the protein product of c-fos, was used to study changes in neuronal activity in nerve terminal regions of the ascending dopaminergic system during nicotine withdrawal. Rats were infused for 14 days with nicotine (9 mg/kg/day nicotine hydrogen tartrate) via minipumps, whereas control animals carried empty pumps. Withdrawal was induced by the nicotinic receptor (nAChR) antagonist mecamylamine (1 mg/kg, s.c.). The behavior of each animal was observed after mecamylamine injection and subsequently its brain was processed for Fos-like immunoreactivity. Following mecamylamine, the score of abstinence signs increased in the nicotine-treated rats as compared to controls. The number of Fos-positive nuclei was substantially increased in the central nucleus of amygdala (CNA) in animals undergoing mecamylamine-precipitated withdrawal, whereas no significant changes in c-fos expression were observed in the basolateral amygdaloid nucleus, the core and the shell of the nucleus accumbens, the dorsolateral striatum, or the medial prefrontal cortex. Since there are indications of involvement of amygdaloid dopaminergic neurotransmission in anxiety-a core symptom of withdrawal from dependence-producing drugs-in a second experiment utilizing microdialysis we examined whether nicotine withdrawal affects dopaminergic neurotransmission in the CNA. Following mecamylamine injection, dopamine (DA) significantly decreased in nicotine-treated animals compared with controls. These results indicate that the mecamylamine-precipitated nicotine withdrawal reaction is accompanied by a selective induction of c-fos and a concurrent decrease in DA release in the CNA, which may have a bearing on symptoms such as anxiety and distress, which frequently are associated with the nicotine abstinence reaction in humans.
This study examines the organisation of the pathways from the amygdala to the thalamus. Amygdaloid nuclei (medial, central, basolateral and olfactory groups) of Sprague-Dawley rats were injected with biotinylated dextran using stereotaxic coordinates and their brains were then aldehyde-fixed and processed using standard methods. We have three major findings. First, the amygdala has a distinct set of projections to particular nuclei of the thalamus. The thalamic nuclei with the heaviest amygdaloid terminations include the zona incerta, the mediodorsal and the midline nuclei. Second, nuclei of different amygdaloid groups project to the thalamus in slightly different patterns. For example, some groups of nuclei project to the thalamic reticular nucleus (e.g. medial, olfactory) whilst others do not (e.g. central, basolateral). Thus, there is a certain amount of heterogeneity within the amygdaloid projections to the thalamus. Third, when we compare our results on the amygdalo-thalamic pathways to the many previous descriptions of the thalamo-amygdaloid pathways, we note that they are largely out of register. In other words, some of the thalamic nuclei that project to a given group of amygdaloid nuclei do not necessarily receive a projection back from that same amygdaloid nucleus. Hence, there is no substrate for a strong feed-back relationship between the thalamus and the amygdala, as there has been shown for other centres of the brain (e.g. between the thalamus and neocortex).
Repeated administration of an opioid in the presence of specific environmental cues can induce tolerance specific to that setting (associative tolerance). Prolonged or repeated administration of an opioid without consistent contextual pairing yields non-associative tolerance. Here we demonstrate that cholecystokinin acting at the cholecystokinin-B receptor is required for associative but not non-associative morphine tolerance. Morphine given in the morphine-associated context increased Fos-like immunoreactivity in the lateral amygdala and hippocampal area CA1. Microinjection of the cholecystokinin B antagonist L-365,260 into the amygdala blocked associative tolerance. These results indicate that cholecystokinin acting in the amygdala is necessary for associative tolerance to morphine's analgesic effect.