Immunocytochemical localization of dopamine in the prefrontal cortex of the rat at the light and electron microscopical level

Eden, C.G. van; Hoorneman, E.M.D.; Buijs, R.M.; Matthijssen, M.A.H.; Geffard, M.; Uylings, H.B.M.

doi:10.1016/0306-4522(87)92964-2

Cited by 256 publications

(156 citation statements)

References 33 publications

Supporting

Mentioning

133

Contrasting

Unclassified

Order By: Relevance

“…In the rodent PFC, afferents from the VTA region (A10) provide dense dopamine input to the deep layers V-VI. The significantly sparser, but extensively collateralized, dopamine innervation to the superficial layer I-III of the rodent PFC originates in the A9 medial substantial nigra and the lateral A10 regions (Descarries et al 1987;van Eden et al 1987;Berger et al 1991). On the other hand, the primate and human PFC receive dense bilaminar dopamine inputs: one to the deep layers V-VI, and the other to the superficial layers I-II, with the middle layer III receiving comparatively sparse dopamine innervation (Gaspar et al 1989;Berger et al 1991;Lewis et al 1992;Smiley et al 1992;Williams and Goldman-Rakic 1993;Krimer et al 1997).…”

Section: Mammallian Pfc and The Mesocortical Dopamine Inputsmentioning

confidence: 99%

“…The most common synaptic target of the dopamine terminals in the PFC of rodent, primate, or human seems to be the dendritic spines and shafts of putative pyramidal neurons (Van Eden et al 1987;GoldmanRakic et al 1989;Verney et al 1990;Smiley et al 1992;Smiley and Goldman-Rakic 1993;Carr and Sesack 1996). Both tyrosine hydroxylase-or dopamine-immunoreactive axonal terminals have been found to form symmetric synapses on the spines and shafts of small diameter distal dendrites derived from pyramidal neurons.…”

Section: Mammallian Pfc and The Mesocortical Dopamine Inputsmentioning

confidence: 99%

“…Mesocortical dopamine projections terminate on dendrites, soma, and from terminals of GABAergic nonpyramidal interneurons that synaptically contact pyramidal neurons in the PFC. Most of the dopamine terminals form no synaptic specialization on these cellular elements of GABAergic interneurons (van Eden et al 1987;Séguéla et al 1988;Goldman-Rakic et al 1989;Verney et al 1990;Benes et al 1993;Smiley and Goldman-Rakic 1993;Sesack et al 1995). Both D1 and D4 receptor immunoreactivity have recently been found in parvalbumin-containing GABAergic interneurons in monkey PFC (Mrzijak et al 1996;Muly et al 1997).…”

mentioning

confidence: 99%

“…On the other hand, the primate and human PFC receive dense bilaminar dopamine inputs: one to the deep layers V-VI, and the other to the superficial layers I-II, with the middle layer III receiving comparatively sparse dopamine innervation (Gaspar et al 1989; Berger et al 1991; Lewis et al 1992;Smiley et al 1992;Williams and Goldman-Rakic 1993; Krimer et al 1997). Thus, in all species, the deep layers V-VI receive dense dopamine innervation, but the density of dopamine innervation in the superficial layers I-III varies across species.The most common synaptic target of the dopamine terminals in the PFC of rodent, primate, or human seems to be the dendritic spines and shafts of putative pyramidal neurons (Van Eden et al 1987; GoldmanRakic et al 1989;Verney et al 1990;Smiley et al 1992;Smiley and Goldman-Rakic 1993; Carr and Sesack 1996). Both tyrosine hydroxylase-or dopamine-immunoreactive axonal terminals have been found to form symmetric synapses on the spines and shafts of small diameter distal dendrites derived from pyramidal neurons.…”

mentioning

confidence: 99%

See 3 more Smart Citations

Developing a Neuronal Model for the Pathophysiology of Schizophrenia Based on the Nature of Electrophysiological Actions of Dopamine in the Prefrontal Cortex

Yang

Seamans

Gorelova

1999

Neuropsychopharmacology

164

View full text Add to dashboard Cite

This review covers some recent findings of the electrophysiological mechanisms through which mesocortical dopamine modulates prefrontal cortical neurons. Dopamine has been shown to modulate several ionic conductances located along the soma-dendritic axis of prefrontal cortical pyramidal neurons. These ionic currents include high-voltage-activated calcium currents and slowly inactivating NaReceived May 12, 1998; revised May 27, 1998; accepted May 29, 1998. 162 C.R. Yang et al. N EUROPSYCHOPHARMACOLOGY 1999 -VOL . 21 , NO Schizophrenia strikes one in one hundred people worldwide, regardless of cultural or racial origins. As the illness progresses and if it remains unattended, patients are frequently trapped in psychological, social, and economic devastation (Gottesman 1991;Jablensky 1995). Currently, our incomplete understanding of the neurobiological bases of schizophrenia suggests that defects in the genetic controls of brain development in such limbic regions (including temporal lobe structures such as hippocampus and the amygdala) as well as the prefrontal cortex (PFC) lead to cell loss or deformation, cytoarchitectural disorganization, and abnormal innervation in these brain regions (Roberts and Bruton 1990;Stevens 1992; Bogerts 1993;Shapiro 1993; Akbarian et al. 1993 Akbarian et al. , 1996Ross and Pearlson 1996;Weinberger 1996; Karayiorgou and Gogos 1997; Lewis 1997;Selemon et al. 1995Selemon et al. , 1998.Some results from recent imaging studies of brains from living schizophrenics have suggested that there are defective functional communications between the interconnected cortical (PFC and cingulate cortex) and limbic subcortical structures (thalamus, striatum, and temporal lobe limbic structures)(see reviews of Liddle 1996; Pfefferbaum and Marsh 1995; Andreasen 1997; Heckers et al. 1998). Findings from these studies suggest that in schizophrenics, abnormal recruitment of several interconnected cortical and subcortical structures may underlie such symptom clusters as psychomotor poverty, thought disorganization, and reality distortion (Liddle et al. 1992; Liddle 1996; Fletcher 1998; Heckers et al. 1998).As noted in Figure 1, the PFC receives converging limbic, association cortical, and mesocortical dopamine inputs. These inputs interact in the PFC and are involved functionally in high-level cognitive processes (Fuster 1995). Among the many brain regions that PFC output innervates, two important subcortical regions are emphasized in this review. These are the nucleus accumbens (where mesoaccumbens dopamine neurons terminate) and the ventral tegmental area (VTA, where the midbrain dopamine neurons reside) Groenewegen et al. 1990; Berendse et al. 1992a Berendse et al. , 1992bSesack and Pickel 1992;Gorelova and Yang 1997b). Several of the interconnected limbic, cortical, and subcortical structures known to be affected in schizophrenia are targets of the ascending midbrain dopamine systems that normally provide functional modulation of neurotransmission (Björklund and Lindvall 1984;Mogenson et ...

show abstract

Section: Mammallian Pfc and The Mesocortical Dopamine Inputsmentioning

confidence: 99%

Section: Mammallian Pfc and The Mesocortical Dopamine Inputsmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

Developing a Neuronal Model for the Pathophysiology of Schizophrenia Based on the Nature of Electrophysiological Actions of Dopamine in the Prefrontal Cortex

Yang

Seamans

Gorelova

1999

Neuropsychopharmacology

164

View full text Add to dashboard Cite

show abstract

“…The targets of the prefrontal cortical dopamine (DA) innervation include both GABAergic interneurons and glutamatergic pyramidal cells (Sesack et al, 1995a;Verney et al, 1990;Seguela et al, 1988;van Eden et al, 1987). Because local circuit GABA interneurons also synapse with pyramidal cells (DeFelipe and Farinas, 1992), the cortical DA innervation can both directly and indirectly alter pyramidal cell activity and hence overall cortical output.…”

Section: Introductionmentioning

confidence: 99%

The Neurotensin Agonist PD149163 Increases Fos Expression in the Prefrontal Cortex of the Rat

Petrie

Bubser

Casey

et al. 2004

Neuropsychopharmacol

View full text Add to dashboard Cite

Dopaminergic axons innervating the prefrontal cortex (PFC) target both pyramidal cells and GABAergic interneurons. Many of these dopamine (DA) axons in the rat coexpress the peptide neurotransmitter neurotensin. Previous electrophysiological data have suggested that neurotensin activates GABAergic interneurons in the PFC. Activation of D2-like DA receptors increases extracellular GABA levels in the PFC, as opposed to the striatum, where D2 receptor activation inhibits GABAergic neurons. Because activation of presynaptic D 2 release-modulating autoreceptors in the PFC suppresses DA release but increases release of the cotransmitter neurotensin, D2 agonists may enhance the activity of GABAergic interneurons via release of neurotensin. In order to determine if neurotensin can activate GABAergic interneurons, we treated rats with the peptide neurotensin agonist, PD149163, and examined Fos expression in PFC neurons. Systemic administration of PD149163 increased overall Fos expression in the PFC, but not in the dorsal striatum. PD149163 induced Fos in PFC interneurons, as defined by the presence of calcium-binding proteins, and in pyramidal cells. Pretreatment with the high-affinity neurotensin antagonist, SR48692, blocked neurotensin agonist-induced Fos expression. These data suggest that neurotensin activates interneurons in the PFC of the rat.

show abstract

Hippocampal afferents to the rat prefrontal cortex: Synaptic targets and relation to dopamine terminals

1996

View full text Add to dashboard Cite

Afferents to the prefrontal cortex (PFC) from the hippocampal formation and from midbrain dopamine (DA) neurons have been implicated in the cognitive and adaptive functions of this cortical region. In the present study, we investigated the ultrastructure and synaptic targets of hippocampal terminals, as well as their relation to DA terminals within the PFC of adult rats. Hippocampal afferents were labeled either by anterograde transport of wheat germ agglutinin-horseradish peroxidase (WGA-HRP) from the ventral hippocampal formation or by anterograde degeneration following fimbria lesion. Hippocampal terminals in the PFC, identified by either method, formed primarily asymmetric axospinous synapses, with a small percentage forming asymmetric axodendritic synapses. Dopamine terminals in the PFC were identified by peroxidase immunocytochemistry for either tyrosine hydroxylase or DA and formed primarily symmetric synapses onto dendritic spines and small caliber dendritic shafts. Spines that received symmetric synaptic contact from DA terminals invariably also received an asymmetric synapse from an unlabeled terminal, forming a triadic complex. Hippocampal and DA terminals in the PFC were not often observed in the same area of the neuropil, and no examples of convergence of hippocampal and DA terminals onto common postsynaptic targets were observed. Further analysis revealed that spines receiving synaptic contact from hippocampal terminals did not receive additional synaptic contact from any other source. However, when localized to the same area of the neuropil, hippocampal and DA terminals were often in direct apposition to one another, without forming axo-axonic synapses. These results suggest that 1) hippocampal terminals primarily form excitatory synapses onto spiny pyramidal neurons, 2) hippocampal afferents are unlikely to be synaptically modulated by DA or non-DA terminals at the level of the dendritic spine, and 3) appositions between hippocampal and DA terminals may facilitate presynaptic interactions between these afferents to the PFC.

show abstract

Immunocytochemical localization of dopamine in the prefrontal cortex of the rat at the light and electron microscopical level

Cited by 256 publications

References 33 publications

Developing a Neuronal Model for the Pathophysiology of Schizophrenia Based on the Nature of Electrophysiological Actions of Dopamine in the Prefrontal Cortex

Developing a Neuronal Model for the Pathophysiology of Schizophrenia Based on the Nature of Electrophysiological Actions of Dopamine in the Prefrontal Cortex

The Neurotensin Agonist PD149163 Increases Fos Expression in the Prefrontal Cortex of the Rat

Hippocampal afferents to the rat prefrontal cortex: Synaptic targets and relation to dopamine terminals

Contact Info

Product

Resources

About