Effects of serotonergic activity in nucleus accumbens septi on drug-induced circling

Jackson, E.A.; Kelly, Peter H.; Schultz, Linda

doi:10.1016/0028-3908(85)90005-x

Cited by 19 publications

(5 citation statements)

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“…One of these regions, the nucleus accumbens (Acb) in the ventral striatum is a major site where both 5-HT and dopamine modulate a variety of behaviors (Pijnenburg et al, 1976;Carter and @cock, 1977;Berger et al, 1985;Jackson et al, 1985;Nakahara et al, 1989;Geyer et al, 1990) including motivationrelated processes (Mogenson et al, 1980;Mogenson and Yang, 1991), motor function (Alheid and Heimer, 1988) and reward mechanisms (Nakahara et al, 1989). However, we previously found little morphological evidence for direct interactions between axons containing 5-HT and dopamine within the Acb (Van Bockstaele and Pickel, 1993).…”

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confidence: 96%

“…Our previous study (Van Bockstaele and Pickel, 1993) indicated that 5-HT-labeled axon terminals were more numerous in the shell and more frequently formed synaptic contacts specifically of the symmetric variety than the 5-HT-labeled axon terminals identified in the core subregion. Both 5-HT and GABA have been implicated in similar activities in the Acb including modulation of locomotor activity (Pijnenburg et al, 1976;Carter and Pycock, 1977;Soubrie et al, 1984;Jackson et al, 1985;Geyer et al, 1990;Layer et al, 19921, reward mechanisms (Nakahara et al, 1989) and analgesia processes (Han and Xuan, 1986).…”

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confidence: 98%

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Pre- and postsynaptic sites for serotonin modulation of GABA-containing neurons in the shell region of the rat nucleus accumbens

1996

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The shell of the nucleus accumbens received a dense serotonergic innervation and contains abundant gamma-aminobutyric acid (GABA)-immunoreactive neurons. Moreover, serotonin (5-hydroxytryptamine: 5-HT) and GABA have been implicated in a variety of common motivational and motor-related functions partially ascribed in this brain area. We used immunoelectron microscopy of antisera directed against 5-HT and GABA in the same section of tissue to examine whether there were cellular substrates that might indicate more specific sites for functional interactions involving these transmitters in the shell region of the rat nucleus accumbens. Immunogold-silver labeling for GABA was localized to perikarya, dendrites, axons and axon terminals, whereas immunoperoxidase labeling for 5-HT was restricted to axons and axon terminals. Approximately half (187/366) of the 5-HT-immunoreactive axon terminals apposed or formed synaptic junctions with postsynaptic neurons. These junctions were mainly of the symmetric-type (83/187) characteristic of inhibitory transmitters, and were equally prevalent on dendrites with and without detectable gold-silver labeling for GABA. Of the 187 5-HT-labeled axon terminals with recognized synaptic contacts, 36% also showed convergence on a common dendrite with a GABA-labeled axon terminal. In addition, 5-HT- and GABA-immunoreactive axon terminals were commonly (83/366) identified in direct apposition to one another. Within a single plane of section, 41% of the apposed GABA-immunoreactive axon terminals formed symmetric-type junctions with dendrites or somata, whereas, the apposed 5-HT-labeled axon terminals rarely showed postsynaptic contacts. These results indicate that 5-HT-containing axon terminals may postsynaptically inhibit GABAergic neurons and their targets within the shell of the rat nucleus accumbens. Additionally, our results strongly suggest that, in this brain region, appositions between 5-HT and GABA axons and axon terminals may facilitate presynaptic interactions between these transmitter systems.

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confidence: 96%

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confidence: 98%

Pre- and postsynaptic sites for serotonin modulation of GABA-containing neurons in the shell region of the rat nucleus accumbens

1996

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“…Some of these fibres contain 5-hydroxytryptamine (5-HT), arising from the raphe nuclei of the midbrain, and the nucleus accumbens receives a moderately dense innervation (Saavedra, Brownstein & Palkovits, 1974;Bobillier, Seguin, Petitjean, Salvert, Touret & Jouvet, 1976;Azmitia, 1978;Miller, Richardson, Fibiger & McLennan, 1978;Parent, Descarries & Beaudet, 1981;Steinbusch, 1981). Application of 5-HT directly into the nucleus decreases locomotor activity (Pijenburg, Honig, Van der Heyden & Van Rossum, 1976), and reduces or blocks the circling behaviour of rats with unilateral lesions of the nigrostriatal pathway (Pycock, 1980;Jackson, Kelly & Schultz, 1985). Catalepsy in rats induced by neuroleptics can be reduced by electrolytic or neurochemical lesions of ascending 5-HT neurones (Costall, Fortune, Naylor, Marsden & Pycock, 1975;Carter & Pycock, 1978).…”

Section: Introductionmentioning

confidence: 99%

5‐Hydroxytryptamine acts at 5‐HT2 receptors to decrease potassium conductance in rat nucleus accumbens neurones.

North

Uchimura

1989

The Journal of Physiology

135

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SUMMARY1. Intracellular recordings were made from neurones in the nucleus accumbens in slices from the rat brain maintained in vitro.2. 5-Hydroxytryptamine (5-HT, 1-100 ,tM) depolarized 170 of 203 (84 %) neurones and caused them to discharge action potentials. The depolarization was associated with an increase in the input resistance, and was reversed in polarity by conditioning hyperpolarization; this reversal potential was linearly related to the logarithm of the extracellular potassium concentration.3. Application of 5-HT to neurones voltage-clamped near their resting potential (typically about -80 mV) caused an inward current and a decrease in the slope conductance. The current caused by 5-HT reversed polarity at the potassium equilibrium potential. Analysis with an equivalent circuit model of the neurone at steady state indicated that 5-HT selectively reduced the inward rectifier potassium conductance.4. The depolarization caused by 5-HT persisted in tetrodotoxin (1 ,1M). It was reduced but not abolished by a solution that contained lower levels of calcium (0'24 instead of 2-4 mM), higher levels of magnesium (5 instead of 1-2 mM), and cobalt (2 mM).5. The depolarization caused by 5-HT was competitively antagonized by the 5-HT2 antagonists ketanserin and mianserin with dissociation equilibrium constants of 3 and 45 nm respectively: spiperone (300 nM) also blocked the action of 5-HT. The depolarization was not mimicked or blocked by a number of other agonists and antagonists selective for the 5-HT1 and 5-HT3 receptor types.

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“…Local injection of phencyclidine into the NAcc excludes complex neurotransmitter interactions occurring at different brain levels after its systemic administration (Garey and Heath,1976; Hiramatsu et al,1989; Johnson and Jones,1990; Snell et al,1988). Micro‐injection of serotonergic drugs, such as 8‐OH‐DPAT and DOI, into this nucleus affected locomotor activity (Jackson et al,1985; Plaznik et al,1994). However, our present results do not support a local interaction in the NAcc of projections from the DRN with the locomotor hyperactivity action of phencyclidine.…”

Section: Discussionmentioning

confidence: 99%

Differential role of serotonin projections from the dorsal and median raphe nuclei in phencyclidine‐induced hyperlocomotion and fos‐like immunoreactivity in rats

Kusljic¹,

Buuse²

2012

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Altered brain serotonin activity is implicated in schizophrenia. We have previously shown differential involvement of serotonergic projections from the dorsal or median raphe nucleus in phencyclidine-induced hyperlocomotion in rats, a behavioral model of aspects of schizophrenia. Here we further investigated the effects of serotonergic lesions of the raphe nuclei on phencyclidine-induced hyperlocomotion by parallel assessment of Fos-like immunoreactivity (FLI), a marker of neuronal activation in the brain. Male Sprague-Dawley rats were anesthetized with pentobarbitone and stereotaxically microinjected with 5 μg of the serotonergic neurotoxin, 5,7-dihydroxytryptamine (5,7-DHT), into either the dorsal raphe (DRN) or median raphe nucleus (MRN). Two weeks after the surgery, rats with lesions of the MRN, but not those with lesions of the DRN, showed significant enhancement of the hyperlocomotion induced by injection of 2.5 mg/kg of phencyclidine. Rats with MRN lesions also showed significantly higher levels of FLI in the polymorphic layer of the dentate gyrus in the dorsal hippocampus (PoDG) when compared with sham-operated controls. Rats with lesions of the DRN showed significantly higher levels of FLI in the nucleus accumbens (NAcc). These results indicate that FLI in the PoDG, but not the NAcc, correlates with enhanced phencyclidine-induced locomotor hyperactivity in MRN-lesioned rats. These results support our previous studies suggesting a role of serotonergic projections from the MRN to the dorsal hippocampus in some of the symptoms of schizophrenia.

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Effects of serotonergic activity in nucleus accumbens septi on drug-induced circling

Cited by 19 publications

References 37 publications

Pre- and postsynaptic sites for serotonin modulation of GABA-containing neurons in the shell region of the rat nucleus accumbens

Pre- and postsynaptic sites for serotonin modulation of GABA-containing neurons in the shell region of the rat nucleus accumbens

5‐Hydroxytryptamine acts at 5‐HT2 receptors to decrease potassium conductance in rat nucleus accumbens neurones.

Differential role of serotonin projections from the dorsal and median raphe nuclei in phencyclidine‐induced hyperlocomotion and fos‐like immunoreactivity in rats

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