Studies on the Role of Central 5-HT Neurons in Avoidance Learning: A Behavioral and Biochemical Analysis

Ögren, Sven Ove; Fuxé, Kjell; Archer, Trevor; Hall, Håkan; Holm, A. C.; Køhler, Christer

doi:10.1007/978-1-4684-3860-4_37

Cited by 40 publications

(11 citation statements)

References 28 publications

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“…Some suggest that, by itself, serotonin has only a secondary role in such behav iors [36][37][38][39][40][41][42]. Depletion of serotonin, however, may re duce the ability of other neurotransm itter systems to modulate dentate granule cells responsiveness.…”

Section: Discussionmentioning

confidence: 99%

Raphe Grafts in the Hippocampus, But Not in the Entorhinal Cortex, Reverse Hippocampal Hyperexcitability of Serotonin-Depleted Rats and Restore Their Responsiveness to Fenfluramine

Richter‐Levin

Segal²

1992

Dev Neurosci

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We compared the effects of embryonic raphe grafted into either the hippocampus or the entorhinal cortex, on the responsiveness of dentate granule cells to stimulation of the perforant path. Raphe grafts in the hippocampus reversed the hyperexcitability of granule cells, resulting from depletion of the serotonergic innervation. Such grafts also restored the responsiveness of the granule cells to application of a serotonin releasing drug, fenfluramine (FFA). In contrast, hyperexcitability was not reversed when the graft was placed in the entorhinal cortex. Furthermore, although some increase in population spike size was observed in these rats after application of FFA, this increase had a response profile which was different from that of control and of lesioned rats that were grafted in the hippocampus. These results suggest that the serotonergic innervation, within the hippocampus and not in the entorhinal cortex, modulates granule cells excitability.

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Section: Discussionmentioning

confidence: 99%

Raphe Grafts in the Hippocampus, But Not in the Entorhinal Cortex, Reverse Hippocampal Hyperexcitability of Serotonin-Depleted Rats and Restore Their Responsiveness to Fenfluramine

Richter‐Levin

Segal²

1992

Dev Neurosci

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“…However, unlike other neurotransmitters such as acetylcholine (Deutsch 1973), norepinephrine (Dismukes and Rake 1972;Quartermain 1982), or dopamine (Quartermain and Altman 1982;Altman and Quartermain 1983), stimulation of the serotonergic nervous system impairs (Essman 1973a;Wetzel et al 1980;Ogren et al 1981;Ogren 1982b), while interference often enhances (Brody 1970;Lorens 1973;Vorhees et al 1975;Wetzel et al 1980) learning and memory. However, the latter conclusion should be regarded with caution as disruption of serotonergic neurotransmission has produced equivocal effects Lorens 1978 ;()gren et al 1981).…”

mentioning

confidence: 99%

Enhancement of the memory of a previously learned aversive habit following pre-test administration of a variety of serotonergic antagonists in mice

Altman

Normile

1986

Psychopharmacology

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The present study examined the effects of pre-test administration of a number of serotonergic receptor antagonists on the retrieval of a previously learned aversive habit in the mouse. All of the receptor antagonists (pirenperone, ketanserin, mianserin, methysergide and metergoline) produced a dose-dependent increase in the latency to complete 5 s of drinking 48 h after training. This suppression of drinking could not be attributed to nonspecific effects of the drugs on behavior (e.g., illness, reduced thirst, or activity), as non-contingently trained mice failed to exhibit similar elevations in their test scores. These results are, therefore, further support for an important role for serotonin in the processes underlying learning and memory.

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“…It is well documented that systemic administration of PCA causes an acute increase in serotonergic activity in the central nervous system through a mechanism involving release of endogenous 5-HT (Sanders-Bush & Steranka 1978) as well as inhibition of re-uptake (Ross 1976). The effect of PCA on other monoaminergic transmitters is weak (Messing et al 1976, Ogren et al 1981.…”

Section: Discussionmentioning

confidence: 99%

Test‐dependent antinociceptive effect of spinal serotonin release induced by intrathecal p‐chloroamphetamine in mice

Berge

Fasmer

Jørgensen

et al. 1985

Acta Physiologica Scandinavica

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The effect of direct intrathecal injection of p-chloroamphetamine (PCA) into the lumbar subarachnoid space was investigated in mice. PCA (0.6 - 20 micrograms) induced a dose-related prolongation of response latencies in the tail-flick test, but failed to affect the hind-paw lick response in a hot-plate test employing slowly rising temperature. PCA (5 micrograms) given intracerebroventricularly did, however, significantly elevate the response temperature in the hot-plate test. The antinociceptive effect of PCA in the tail-flick test was prevented by spinalization, by pretreatment with the selective serotonergic re-uptake blocker zimelidine (20 mg X kg-1 i.p.) and by the serotonin synthesis inhibitor p-chlorophenylalanine (300 + 300 + 150 mg X kg-1 i.p. 72, 48 and 24 h before test). It is concluded that PCA given intrathecally releases serotonin from spinal terminals, which may under certain conditions induce antinociception.

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Studies on the Role of Central 5-HT Neurons in Avoidance Learning: A Behavioral and Biochemical Analysis

Cited by 40 publications

References 28 publications

Raphe Grafts in the Hippocampus, But Not in the Entorhinal Cortex, Reverse Hippocampal Hyperexcitability of Serotonin-Depleted Rats and Restore Their Responsiveness to Fenfluramine

Raphe Grafts in the Hippocampus, But Not in the Entorhinal Cortex, Reverse Hippocampal Hyperexcitability of Serotonin-Depleted Rats and Restore Their Responsiveness to Fenfluramine

Enhancement of the memory of a previously learned aversive habit following pre-test administration of a variety of serotonergic antagonists in mice

Test‐dependent antinociceptive effect of spinal serotonin release induced by intrathecal p‐chloroamphetamine in mice

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