Evidence for dopamine as a transmitter in dorsal hippocampus

Ito, Koichi; Ott, Tilmann; McGaugh, James L.

doi:10.1016/0006-8993(82)90630-8

Cited by 91 publications

(23 citation statements)

References 14 publications

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“…The dorsal hippocampus, which like the striatum is also highly vulnerable to ischemia, also contains DA nerve terminals (Scatton et al, 1980;Ishikawa et al, 1982) which might release significant DA during ischemia. These DA nerve terminals are from a projection originating in DA nerve cell bodies in area A 10 (ventral tegmentum) and area A9 (pars lateralis of the substantia nigra) (Scattonet al, 1980;Lindvall and Bjorklund, 1983).…”

Section: Discussionmentioning

confidence: 99%

“…We and others have postulated that this DA may play a role in the evolution of regional ischemic damage in the striatum (Weinberger et al, 1983(Weinberger et al, , 1985Globus et al, , 1988. As the dorsal hippocampus contains DA nerve terminals (Ishikawa et al, 1982) and receives DA projections from the ventral tegmentum and area A9 of the substantia nigra (Scatton et al, 1980;Swanson, 1982), we felt it reasonable to test whether DA is also released into the extracellular space of this brain region during ischemia. If DA release can be demonstrated in the hippocampus, it would strengthen the hypothesis that catecholamines play a role in neuronal damage during ischemia.…”

Section: Introductionmentioning

confidence: 99%

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Ischemia in the dorsal hippocampus is associated with acute extracellular release of dopamine and norepinephrine

Bhardwaj

Brannan

Martinez-Tica

et al. 1990

J. Neural Transmission

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The cerebral dialysis technique was employed to monitor extracellular concentrations of dopamine (DA), norepinephrine (NE), dihydroxyphenylacetic acid (DOPAC), and homovanillic acid (HVA) in the dorsal hippocampus of gerbils before and after cerebral ischemia induced by carotid artery occlusion. Extracellular concentrations of DA and NE in the dorsal hippocampus increased from baseline levels of less than 35 fmol/collection interval to 180 and 200 fmol/collection, respectively, within 36 minutes following carotid artery ligation (n = 8 animals). Extracellular concentrations of the DA metabolites, DOPAC and HVA, did not change significantly following carotid artery ligation. These data demonstrate that ischemia in the dorsal hippocampus is associated with a mared release of DA and NE. This release may contribute to the selective vulnerability of the dorsal hippocampus to neuronal damage during ischemia.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Ischemia in the dorsal hippocampus is associated with acute extracellular release of dopamine and norepinephrine

Bhardwaj

Brannan

Martinez-Tica

et al. 1990

J. Neural Transmission

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“…As the largest aggregate of NE‐containing neurons in the brain ( Grazanna et al ., 1977 ), the locus coeruleus provides almost exclusively the noradrenergic innervations to the hippocampal formation ( Ungerstedt, 1971 ; Segal & Landis 1974 ; Loy & Moore, 1979 ; Wyss et al ., 1979 , Loy et al ., 1980 , Foote et al ., 1983 ). In addition, noradrenergic terminals are distributed uniformly within the entire hippocampal formation ( Ishikawa et al ., 1982 ). Binding sites identified in the hippocampal formation are primarily α 1 ‐ or α 2 ‐adrenoceptors ( Biegon et al ., 1982 ; Dooley & Bittinger, 1982 ).…”

Section: Discussionmentioning

confidence: 99%

Hippocampal noradrenergic neurotransmission in concurrent EEG desynchronization and inhibition of penile erection induced by cocaine in the rat

Chang

Chan

2000

British J Pharmacology

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1 We previously reported that cocaine may induce activation of cortical (cEEG) and hippocampal (hEEG) electroencephalographic signals, concurrent with inhibition of penile erection, via an action on the hippocampal formation. The present study further evaluates the role of noradrenergic neurotransmission at the hippocampal formation in this process, using adult, male Sprague-Dawley rats anaesthetized and maintained by chloral hydrate. 2 Unilateral microinjection of cocaine (100 nmoles) into the hippocampal CA1 or CA3 sub®eld or dentate gyrus elicited signi®cant activation of both cEEG and hEEG activity. At the same time, the intracavernous pressure (ICP), our experimental index for penile erection, underwent a discernible reduction. 3 Co-administration of equimolar doses (250 pmoles) of prazosin, naftopidil, yohimbine or rauwolscine signi®cantly reversed those e ects elicited by cocaine on cEEG, hEEG and ICP. 4 Microinjection unilaterally of equimolar doses (5 nmoles) of norepinephrine, phenylephrine or BHT 933 into the hippocampal formation, similar to cocaine, also induced appreciable cEEG and hEEG excitation, with a simultaneous decrease in ICP. 5 We conclude that cocaine may activate cEEG and hEEG and decrease ICP via noradrenergic neurotransmission, possibly engaging at least a 1A/D -, a 2B -and a 2C -adrenoceptors at the hippocampal formation.

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“…The evidence for these projections is largely anatomical, derived from anterograde (Simon, Le Moal & Calas, 1979) and retrograde tracing experiments (Carter & Fibiger, 1977;Schwab, (Spencer, Wheal & Mitchell, 1985). Interest in these projections was prompted by reports that dopamine may act as a neurotransmitter is the hippocampus (Swanson & Hartman, 1975; Bischoff, Scatton & Korf, 1979;Karoum, Commissiong, Neff & Wyatt, 1980;Ishikawa, Ott & McGaugh, 1982). Since lesions of either the SN or the VTA are reported to cause a decrease in the dopamine content of the hippocampus (Scatton, Simon, Le Moal & Bischoff, 1980), these nuclei may correspond to a dopaminergic mesohippocampal pathway.…”

Section: Introductionmentioning

confidence: 99%

Synaptic inhibition in the rat hippocampus in vivo following stimulation of the substantia nigra and ventral tegmentum.

Spencer

Wheal

1990

The Journal of Physiology

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SUMMARY1. The effects of stimulating the substantia nigra (SN) or the ventral tegmental area (VTA) on the excitability of cells in the rat hippocampal formation have been investigated in vivo.2. A train of conditioning stimuli to either of the midbrain nuclei produced inhibition of evoked population spikes recorded in the CAI pyramidal cell layer of the hippocampus.3. These trains of pulses had no effect on the evoked synaptic field potential recorded in the stratum radiatum although they were effective in suppressing glutamate-induced firing of cells in the hippocampus. These observations suggest that the inhibition is mediated through a postsynaptic mechanism.4. The inhibition of the test population spike was observed at a latency of 50 ms after the conditioning train to either the SN or the VTA but did not reach a maximum until 300-500 ms and 500-750 ms post-conditioning, respectively. The total duration of the inhibition in each case was about 5 s.5. Following stimulation of the VTA, comparable levels of inhibition were recorded in the ventral and dorsal hippocampus. However, after stimulation of the SN, significantly less inhibition was observed in the ventral hippocampus.6. Unlike the effects on the commissural-evoked population spike in CAL, stimulation of SN or VTA had no effect on perforant path-induced granule cell excitability in the dentate gyrus.7. These results suggest that activity in the substantia nigra or ventral tegmental areas could have a powerful regulatory or feedback role in suppressing hippocampal excitability.

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Evidence for dopamine as a transmitter in dorsal hippocampus

Cited by 91 publications

References 14 publications

Ischemia in the dorsal hippocampus is associated with acute extracellular release of dopamine and norepinephrine

Ischemia in the dorsal hippocampus is associated with acute extracellular release of dopamine and norepinephrine

Hippocampal noradrenergic neurotransmission in concurrent EEG desynchronization and inhibition of penile erection induced by cocaine in the rat

Synaptic inhibition in the rat hippocampus in vivo following stimulation of the substantia nigra and ventral tegmentum.

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