Anterograde and retrograde tracing of projections from the ventral tegmental area to the hippocampal formation in the rat

Gasbarri, Antonella; Packard, Mark G.; Campana, Elena; Pacitti, C

doi:10.1016/0361-9230(94)90288-7

Cited by 242 publications

(161 citation statements)

References 49 publications

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“…The rapid acquisition of bicuculline selfadministration in MORÀ/À mice demonstrate that these mutants have no learning deficit in our task, providing that they are efficiently reinforced with a non m-dependent pharmacological agent. Despite early reports that the hippocampus does not receive a significant DA innervation (Loy et al, 1980), projections from the VTA have been described in the stratum moleculare of the CA1 (Gasbarri et al, 1994(Gasbarri et al, , 1997Goldsmith and Joyce, 1994). Novel stimuli increase c-fos in the hippocampus (Jenkins et al, 2004).…”

Section: Discussionmentioning

confidence: 91%

Brain Regional Fos Expression Elicited by the Activation of μ- but not δ-Opioid Receptors of the Ventral Tegmental Area: Evidence for an Implication of the Ventral Thalamus in Opiate Reward

David

Matifas

Gavello-Baudy

et al. 2007

Neuropsychopharmacol

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Both m-opioid receptors (MORs) and d-opioid receptors (DORs) are expressed in the ventral tegmental area (VTA) and are thought to be involved in the addictive properties of opiates. However, their respective contributions to opiate reward remain unclear. We used intracranial self-administration (ICSA) to study the rewarding effects of morphine microinjections into the VTA of male and female MORÀ/À and DORÀ/À mice. In brains of mice tested for intra-VTA morphine self-administration, we analyzed regional Fos protein expression to investigate the neural circuitry underlying this behavior. Male and female WT and DORÀ/À mice exhibited similar selfadministration performances, whereas knockout of the MOR gene abolished intra-VTA morphine self-administration at all doses tested. Naloxone (4 mg/kg) disrupted this behavior in WT and DOR mutants, without triggering physical signs of withdrawal. Morphine ICSA was associated with an increase in Fos within the nucleus accumbens, striatum, limbic cortices, amygdala, hippocampus, the lateral mammillary nucleus (LM), and the ventral posteromedial thalamus (VPM). This latter structure was found to express high levels of Fos exclusively in self-administering WT and DORÀ/À mice. Abolition of morphine reward in MORÀ/À mice was associated with a decrease in Fos-positive neurons in the mesocorticolimbic dopamine system, amygdala, hippocampus (CA1), LM, and a complete absence within the VPM. We conclude that (i) VTA MORs, but not DORs, are critical for morphine reward and (ii) the role of VTA-thalamic projections in opiate reward deserves to be further explored.

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Section: Discussionmentioning

confidence: 91%

Brain Regional Fos Expression Elicited by the Activation of μ- but not δ-Opioid Receptors of the Ventral Tegmental Area: Evidence for an Implication of the Ventral Thalamus in Opiate Reward

David

Matifas

Gavello-Baudy

et al. 2007

Neuropsychopharmacol

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“…During exploratory behaviors, when gamma-frequency activity occurs in the DG and DGCs fire at high rates (1,3,(37)(38)(39), the reward salience of an external stimulus is signaled by release of dopamine from VTA projections to the molecular layer of the DG (40). Consistent with these observations, in mice where NMDA receptors have been genetically ablated in mesolimbic dopamine neurons, the CPP response to rewards of cocaine or food is impaired (5, 6), suggesting a loss of reward-primed spatial memory .…”

Section: Discussionmentioning

confidence: 99%

Dopamine modulates synaptic plasticity in dendrites of rat and human dentate granule cells

Hamilton

Wheatley

Sinclair

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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The mechanisms underlying memory formation in the hippocampal network remain a major unanswered aspect of neuroscience. Although high-frequency activity appears essential for plasticity, salience for memory formation is also provided by activity in ventral tegmental area (VTA) dopamine projections. Here, we report that activation of dopamine D1 receptors in dentate granule cells (DGCs) can preferentially increase dendritic excitability to both highfrequency afferent activity and high-frequency trains of backpropagating action potentials. Using whole-cell patch clamp recordings, calcium imaging, and neuropeptide Y to inhibit postsynaptic calcium influx, we found that activation of dendritic voltagedependent calcium channels (VDCCs) is essential for dopamineinduced long-term potentiation (LTP), both in rat and human dentate gyrus (DG). Moreover, we demonstrate previously unreported spike-timing-dependent plasticity in the human hippocampus. These results suggest that when dopamine is released in the dentate gyrus with concurrent high-frequency activity there is an increased probability that synapses will be strengthened and reward-associated spatial memories will be formed.A s an animal explores a specific location, place cells in the dentate gyrus (DG) of the hippocampus fire bursts of action potentials (APs) (1) that can result in the formation of a new, long-term contextual memory (2). This is part of the "pattern separation" mechanism, whereby only a small population of dentate granule cells (DGCs) become very active and pass on the incoming cortical input to be later represented or "completed," in the downstream CA3 network (3). Memory formation related to a specific place can be enhanced by an associated salience, such as reward (4). Recent work suggests that disruption of mesocorticolimbic dopamine responses blocks conditioned place preference (CPP), a reward-driven form of spatial memory (5, 6). Furthermore, nicotine-induced CPP requires dopamine D1 receptor (D1R) activation in the DG (7). The medial perforant pathway (MPP) carries spatial information to the middle third of the molecular layer (8). In DGCs, D1Rs are concentrated throughout the dendritic tree (9). This suggests that bursting activity in DGCs, coincident with local dopamine release, may enhance formation of salient memories, but a mechanism remains unknown.One potential mechanism mediating plasticity is the coincidence of backpropagating dendritic APs with appropriately timed synaptic input (10); this mechanism requires postsynaptic Ca 2+ influx (11). Ca 2+ channels have been implicated in nonlinear, frequency-dependent responses in dendrites (12) and D1Rs can potentiate dendritic excitability in hippocampal area CA1 (13). Because the molecular layer of the DG is innervated by dopaminergic terminals from the ventral tegmental area (VTA) (14) we examined the possibility that interactions at the level of DGC dendrites between firing frequency, dendritic Ca 2+ responses, and D1Rs, may mediate plasticity in medial perforant path synaptic inputs....

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“…It is well established that dopaminergic reward circuitry in the brain, that is, dopaminergic projections from the midbrain ventral tegmental area (VTA) to the nucleus accumbens (NAc) and frontal cortex, plays an important role in drug addiction by enhancing dopamine efflux in the NAc, either directly or indirectly (Koob et al 1992;Spanagel and Weiss 1999). The hippocampus, on the other hand, is positioned to influence brain reward pathways by receiving inputs from both the NAc and VTA and establishing a feedback loop through efferent projections to the NAc (Gasbarri et al 1991(Gasbarri et al , 1994Floresco et al 2001;Bannerman et al 2004). These neuroanatomical observations suggesting that the hippocampus interacts with reward circuitry were further substantiated by functional studies showing that manipulations of hippocampal subfields alter the firing of VTA dopaminergic cells and dopaminergic responses in NAc (Mitchell et al 2000;Floresco et al 2001;Charara and Grace 2003;Won et al 2003;Zornoza et al 2005a,b).…”

Section: Drug Abuse and Addictionmentioning

confidence: 99%

Adult Neurogenesis and Psychiatric Disorders

Kang

Wen

Song

et al. 2016

Cold Spring Harb Perspect Biol

164

118

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Psychiatric disorders continue to be among the most challenging disorders to diagnose and treat because there is no single genetic or anatomical locus that is causative for the disease. Current treatments are often blunt tools used to ameliorate the most severe symptoms, at the risk of disrupting functional neural systems. There is a critical need to develop new therapeutic strategies that can target circumscribed functional or anatomical domains of pathology. Adult hippocampal neurogenesis may be one such domain. Here, we review the evidence suggesting that adult hippocampal neurogenesis plays a role in emotional regulation and forms of learning and memory that include temporal and spatial memory encoding and context discrimination, and that its dysregulation is associated with psychiatric disorders, such as affective disorders, schizophrenia, and drug addiction. Further, adult neurogenesis has proven to be an effective model to investigate basic processes of neuronal development and converging evidence suggests that aberrant neural development may be an etiological factor, even in late-onset diseases. Constitutive neurogenesis in the hippocampus of the mature brain reflects large-scale plasticity unique to this region and could be a potential hub for modulation of a subset of cognitive and affective behaviors that are affected by multiple psychiatric disorders.

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Anterograde and retrograde tracing of projections from the ventral tegmental area to the hippocampal formation in the rat

Cited by 242 publications

References 49 publications

Brain Regional Fos Expression Elicited by the Activation of μ- but not δ-Opioid Receptors of the Ventral Tegmental Area: Evidence for an Implication of the Ventral Thalamus in Opiate Reward

Brain Regional Fos Expression Elicited by the Activation of μ- but not δ-Opioid Receptors of the Ventral Tegmental Area: Evidence for an Implication of the Ventral Thalamus in Opiate Reward

Dopamine modulates synaptic plasticity in dendrites of rat and human dentate granule cells

Adult Neurogenesis and Psychiatric Disorders

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