Morphological evidence for a dopaminergic terminal field in the hippocampal formation of young and adult rat

Verney, Catherine; Baulac, Michel; Berger, Brigitte; Alvarez, Chantal; Vigny, Annette; Helle, Karen B.

doi:10.1016/0306-4522(85)90275-1

Cited by 263 publications

(134 citation statements)

References 37 publications

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“…Hippocampal cholinergic nerve terminals originate from the medial septum and the vertical limb of the diagonal band of Broca and project to the hippocampal formation via the fimbria fornix (Mesulam et al, 1983;Woolf, 1991). The hippocampus also receives dopaminergic projections arising mainly from the ventral tegmental area with little contribution of the substantia nigra, pars compacta (Gasbarri et al, 1994;Verney et al, 1985).…”

Section: Introductionmentioning

confidence: 99%

Reduction in Acetylcholine Release in the Hippocampus of Dopamine D5 Receptor-Deficient Mice

Laplante

Sibley

Quirion

2004

Neuropsychopharmacol

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Activation of the dopamine D 1 -like receptor stimulates acetylcholine (ACh) release in the hippocampus, apparently through the molecularly defined d5 receptor. In the present study, we used a transgenic mouse completely deprived of functional d5 receptor (d5À/À) to confirm the role and elucidate the possible function of the d5 receptor subtype on hippocampal cholinergic neurotransmission. ACh release was measured using in vivo microdialysis in the mouse dorsal hippocampus of 4 months old homozygous (d5À/À), heterozygous (d5 þ /À), and the wild-type (d5 þ / þ ) littermates. Using the no net flux technique, a significant reduction in basal hippocampal ACh level was found in the d5À/À compared to d5 þ /À and d5 þ / þ mice. Moreover, the administration of SKF 38393, a D 1 -like receptor agonist, systemically (2.0 and 10.0 mg/kg ip), or locally through the dialysis probe (10 and 50 mM), produced a dose-dependent enhancement of ACh release in the d5 þ / þ , a moderate stimulation in the d5 þ /À but had no effect in the d5À/À mice. Quantitative receptor autoradiography revealed significant increases in M 1 -like but not in M 2 -like muscarinic receptor binding sites in the hippocampal formation. These results confirm and extend the role of the d5 receptor in the modulation of hippocampal ACh release and provide evidence for long-term alteration of hippocampal cholinergic neurotransmission resulting from the absence of the d5 receptors including chronically reduced ACh release and change in M 1 -like receptor levels.

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Section: Introductionmentioning

confidence: 99%

Reduction in Acetylcholine Release in the Hippocampus of Dopamine D5 Receptor-Deficient Mice

Laplante

Sibley

Quirion

2004

Neuropsychopharmacol

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“…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.…”

mentioning

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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“…Statistical comparison revealed that dopamine content was significantly higher in the dorsal hippocampus [F (1,23)05.84, p00.024]. This is opposite to the gradient commonly associated with rats (e.g., Verney et al 1985;PelegRaibstein et al 2006a;, although we have obtained a similar, yet non-significant, trend before in C57BL/6 mice (Bitanihirwe et al 2010). Hence, the possibility of a species difference might be likely, which may not be surprising given that a dorso-ventral gradient in hippocampal dopamine content is not consistent across rat strains (e.g., Rüedi-Bettschen et al 2006).…”

Section: Discussionmentioning

confidence: 87%

Baseline prepulse inhibition expression predicts the propensity of developing sensitization to the motor stimulant effects of amphetamine in C57BL/6 mice

et al. 2012

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Rationale The startle reflex to a sudden intense acoustic pulse stimulus is attenuated if the pulse is shortly preceded by a weak prepulse stimulus. This represents a form of sensory gating, known as prepulse inhibition (PPI), observable across species. PPI is modulated by dopamine and readily disrupted by acute amphetamine. Prior repeated exposures to amphetamine also disrupt PPI even when the drug is not present during test, suggesting that a sensitized mesolimbic dopamine system-inducible even by a single exposure to amphetamine-might be responsible. However, this causative link has been challenged by inconsistent efficacy between different amphetamine pre-treatment regimes, which all robustly sensitize the behavioral response to amphetamine. Methods Here, the presence of such a link in reverse was tested by comparing the propensity to develop amphetamine sensitization between high-and low-PPI expressing individuals identified within a homogeneous cohort of C57BL/6 mice. Comparison of dopamine content including its metabolites was performed separately in drug naïve mice by postmortem HPLC. Results Behavioral sensitization was substantially stronger in the low-PPI group compared with the high-PPI group, while the magnitude of their response to the first amphetamine challenge was similar. Dopamine content within the nucleus accumbens and medial prefrontal cortex was significantly higher in low-PPI relative to high-PPI mice. Conclusion Individuals with weak sensory gating characterized by low basal PPI expression may be more susceptible to the development of dopamine sensitization and therefore at greater risk of developing schizophrenia. Conversely, high baseline expression might predict a resistance to dopaminergic sensitization.

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Morphological evidence for a dopaminergic terminal field in the hippocampal formation of young and adult rat

Cited by 263 publications

References 37 publications

Reduction in Acetylcholine Release in the Hippocampus of Dopamine D5 Receptor-Deficient Mice

Reduction in Acetylcholine Release in the Hippocampus of Dopamine D5 Receptor-Deficient Mice

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

Baseline prepulse inhibition expression predicts the propensity of developing sensitization to the motor stimulant effects of amphetamine in C57BL/6 mice

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