Apparent sprouting of striatal serotonergic terminals after dopamine-depleting brain lesions in neonatal rats

Stachowiak, Michal K.; Bruno, John P.; Snyder, Abigail M.; Stricker, Edward M.; Zigmond, Michael J.

doi:10.1016/0006-8993(84)90665-6

Cited by 227 publications

(86 citation statements)

References 15 publications

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“…For example, a serotonergic hyperinnervation of the striatum was found (Descarries et al 1992;Frohna et al 1997;Kostrzewa et al 1998;Luthman et al 1990;Stachowiak et al 1984;Towle et al 1989;Zhang et al 2002a). By contrast, no such changes were observed in the noradrenergic system (Luthman et al 1990;Ordway 1995).…”

Section: Alpha-synuclein Lacking Micementioning

confidence: 99%

Animal models of attention deficit/hyperactivity disorder (ADHD): a critical review

Sontag

Tucha

Walitza

et al. 2010

ADHD Atten Def Hyp Disord

102

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Attention deficit/hyperactivity disorder (ADHD) involves clinically heterogeneous problems including attention deficits, behavioural hyperactivity and impulsivity. Several animal models of ADHD have been proposed, ranging from models with neurotoxic lesions to genetically manipulated animals. An ADHD model is supposed to show phenomenological similarities with the disorder, i.e. it should mimic the three core symptoms (face validity). A model should also conform to an established or hypothesized pathophysiological basis of the disorder (construct validity).Finally, an animal model should be able to predict previously unknown aspects of the neurobiology of ADHD or to provide potential new treatments (predictive validity). The currently proposed models are heterogeneous with regard to their pathophysiological alterations and their ability to mimic behavioural symptoms and to predict response to medication. This might reflect the heterogeneous nature of ADHD. Since the knowledge about the biology of ADHD from human studies is limited, one cannot at present decide which model best represents ADHD or certain ADHD subtypes. Animal models with good face and predictive validity may be useful for investigations of the underlying biological substrates of ADHD. At present, the models in use should be described as animal models of ADHD-like symptoms rather than models of ADHD.

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Section: Alpha-synuclein Lacking Micementioning

confidence: 99%

Animal models of attention deficit/hyperactivity disorder (ADHD): a critical review

Sontag

Tucha

Walitza

et al. 2010

ADHD Atten Def Hyp Disord

102

View full text Add to dashboard Cite

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“…First, 5-HT 1A and 5-HT 2 receptors modulate DA release and cocaine-induced locomotion in rats (De Deurwaerdère and Spampinato, 1999;Carey et al, 2001;Broderick et al, 2004). Second, serotonergic hyperinnervation of the striatum occurs after DA neuron lesions, and these receptors contribute to the hyperlocomotion observed in monoamine-depleted animals (Stachowiak et al, 1984;Mignon and Wolf, 2002;Zhang et al, 2002;Bishop et al, 2003). Third, the residual locomotor response to psychostimulants in a 1B knockout mice is mediated by compensatory 5-HT 2A signaling (Auclair et al, 2004).…”

Section: Da Receptor Supersensitivity In Dbhà/à Micementioning

confidence: 99%

Dopamine β-Hydroxylase Knockout Mice have Alterations in Dopamine Signaling and are Hypersensitive to Cocaine

Schank

Ventura

Puglisi-Allegra

et al. 2005

Neuropsychopharmacol

119

117

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Multiple lines of evidence demonstrate that the noradrenergic system provides both direct and indirect excitatory drive onto midbrain dopamine (DA) neurons. We used DA b-hydroxylase (DBH) knockout (DbhÀ/À) mice that lack norepinephrine (NE) to determine the consequences of chronic NE deficiency on midbrain DA neuron function in vivo. Basal extracellular DA levels were significantly attenuated in the nucleus accumbens (NAc) and caudate putamen (CP), but not prefrontal cortex (PFC), of DbhÀ/À mice, while amphetamine-induced DA release was absent in the NAc and attenuated in the CP and PFC. The decrease in dopaminergic tone was associated with a profound increase in the density of high-affinity state D 1 and D 2 DA receptors in the NAc and CP, while DA receptors in the PFC were relatively unaffected. As a behavioral consequence of these neurochemical changes, DbhÀ/À mice were hypersensitive to the psychomotor, rewarding, and aversive effects of cocaine, as measured by locomotor activity and conditioned place preference. Antagonists of DA, but not 5-HT, receptors attenuated the locomotor hypersensitivity to cocaine in DbhÀ/À mice. As DBH activity in humans is genetically controlled and the DBH inhibitor disulfiram has shown promise as a pharmacotherapy for cocaine dependence, these results have implications for the influence of genetic and pharmacological DBH inhibition on DA system function and drug addiction.

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“…Both neonatal and adult lesions actually lead to a 5-HT axonal hyperinnervation within the dorsal striatum (Stachowiak et al, 1984;Breese et al, 1985;Zhou et al, 1991;Molina-Holgado et al, 1994;Mrini et al, 1995;Balcioglu et al, 2003;Maeda et al, 2003). Consistently, striatal 5-HT levels and 5-HTT binding have been reported to be increased in this animal model of PD (Commins et al, 1989;Zhou et al, 1991;Guerra et al, 1997;Mendlin et al, 1999;Balcioglu et al, 2003).…”

Section: -Ht Receptors' Expression In Pd Animal Models and In Patientsmentioning

confidence: 67%

Serotonin modulation of the basal ganglia circuitry: therapeutic implication for Parkinson's disease and other motor disorders

Matteo

Pierucci

Esposito

et al. 2008

Progress in Brain Research

133

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Several recent studies have emphasized a crucial role for the interactions between serotonergic and dopaminergic systems in movement control and the pathophysiology of basal ganglia. These observations are supported by anatomical evidence demonstrating large serotonergic innervation of all the basal ganglia nuclei. In fact, serotonergic terminals have been reported to make synaptic contacts with both substantia nigra dopamine-containing neurons and their terminal areas such as the striatum, the globus pallidus and the subthalamus. These brain areas contain a high concentration of serotonin (5-HT), with the substantia nigra pars reticulata receiving the greatest input. In this chapter, the distribution of different 5-HT receptor subtypes in the basal ganglia nuclei will be described. Furthermore, evidence demonstrating the serotonergic control of basal ganglia activity will be reviewed and the contribution of the different 5-HT receptor subtypes examined. The new avenues that the increasing knowledge of 5-HT in motor control has opened for exploring the pathophysiology and pharmacology of Parkinson's disease and other movement disorders will be discussed. It is clear that these avenues will be fruitful, despite the disappointing results so far obtained by clinical studies with selective 5-HT ligands. Nevertheless, these studies have led to a great increase in the attention given to the neurotransmitters of the basal ganglia and their connections.

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Apparent sprouting of striatal serotonergic terminals after dopamine-depleting brain lesions in neonatal rats

Cited by 227 publications

References 15 publications

Animal models of attention deficit/hyperactivity disorder (ADHD): a critical review

Animal models of attention deficit/hyperactivity disorder (ADHD): a critical review

Dopamine β-Hydroxylase Knockout Mice have Alterations in Dopamine Signaling and are Hypersensitive to Cocaine

Serotonin modulation of the basal ganglia circuitry: therapeutic implication for Parkinson's disease and other motor disorders

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