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Role of the hippocampal CA1 region in incremental value learning.

ABSTRACT: It is generally believed that the hippocampus plays a crucial role in declarative memory-remembering facts and events-but not in gradual stimulus-response association or incremental value learning. Based on the finding that CA1 conveys strong value signals during dynamic foraging, we investigated the possibility that the hippocampus contributes to incremental value learning. Specifically, we examined effects of inactivating different subregions of the dorsal hippocampus on behavioral performance of mice performing a dynamic foraging task in a modified T-maze. A reinforcement learning model-based analysis indicated that inactivation of CA1, but not dentate gyrus, CA3, or CA2, impaired trial-by-trial updating of chosen value without affecting value-dependent action selection. As a result, it took longer for CA1-inactivated mice to bias their choices toward the higher-reward-probability target after changes in reward probability. Our results indicate, contrary to the traditional view, that the hippocampus, especially CA1, might contribute to incremental value learning under certain circumstances.

SUBMITTER: Jeong Y

PROVIDER: S-EPMC6026161 | biostudies-other | 2018 Jun

REPOSITORIES: biostudies-other

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Role of the hippocampal CA1 region in incremental value learning.

Jeong Yeongseok Y Huh Namjung N Lee Joonyeup J Yun Injae I Lee Jong Won JW Lee Inah I Jung Min Whan MW

Scientific reports 20180629 1

It is generally believed that the hippocampus plays a crucial role in declarative memory-remembering facts and events-but not in gradual stimulus-response association or incremental value learning. Based on the finding that CA1 conveys strong value signals during dynamic foraging, we investigated the possibility that the hippocampus contributes to incremental value learning. Specifically, we examined effects of inactivating different subregions of the dorsal hippocampus on behavioral performance ...[more]

PMID: 29959363

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Project description:G-protein-coupled receptor 158 (Gpr158) is highly expressed in striatum, hippocampus and prefrontal cortex. It gained attention as it was implicated in physiological responses to stress and depression. Recently, Gpr158 has been shown to act as a pathway-specific synaptic organizer in the hippocampus, required for proper mossy fiber-CA3 neurocircuitry establishment, structure, and function. Although rodent Gpr158 expression is highest in CA3, considerable expression occurs in CA1 especially after the first postnatal month. Here, we combined hippocampal-dependent behavioral paradigms with subsequent electrophysiological and morphological analyses from the same group of mice to assess the effects of Gpr158 deficiency on CA1 physiology and function. We demonstrate deficits in spatial memory acquisition and retrieval in the Morris water maze paradigm, along with deficits in the acquisition of extinction memory in the passive avoidance test in Gpr158 KO mice. Electrophysiological recordings from CA1 pyramidal neurons revealed normal basal excitatory and inhibitory synaptic transmission, however, Schaffer collateral stimulation yielded dramatically reduced post-synaptic currents. Interestingly, intrinsic excitability of CA1 pyramidals was found increased, potentially acting as a compensatory mechanism to the reductions in Schaffer collateral-mediated drive. Both ex vivo and in vitro, neurons deficient for or with lowered levels of Gpr158 exhibited robust reductions in dendritic architecture and complexity, i.e., reduced length, surface, bifurcations, and branching. This effect was localized in the apical but not basal dendrites of adult CA1 pyramidals, indicative of compartment-specific alterations. A significant positive correlation between spatial memory acquisition and extent of complexity of CA1 pyramidals was found. Taken together, we provide first evidence of significant disruptions in hippocampal CA1 neuronal dendritic architecture and physiology, driven by Gpr158 deficiency. Importantly, the hippocampal neuronal morphology deficits appear to support the impairments in spatial memory acquisition observed in Gpr158 KO mice.

Project description:The role of ATP and its stable analogue ATPgammaS [adenosine-5'-o-(3-thio)triphosphate] was studied in rat hippocampal neurotransmission under normoxic conditions and during oxygen and glucose deprivation (OGD). Field excitatory postsynaptic potentials (fEPSPs) from the dendritic layer or population spikes (PSs) from the soma were extracellularly recorded in the CA1 area of the rat hippocampus. Exogenous application of ATP or ATPgammaS reduced fEPSP and PS amplitudes. In both cases the inhibitory effect was blocked by the selective A(1) adenosine receptor antagonist DPCPX (8-cyclopentyl-1,3-dipropylxanthine) and was potentiated by different ecto-ATPase inhibitors: ARL 67156 (6-N,N-diethyl-D: -beta,gamma-dibromomethylene), BGO 136 (1-hydroxynaphthalene-3,6-disulfonate) and PV4 [hexapotassium dihydrogen monotitanoundecatungstocobaltate(II) tridecahydrate, K(6)H(2)[TiW(11)CoO(40)].13H(2)O]. ATPgammaS-mediated inhibition was reduced by the P2 antagonist suramin [8-(3-benzamido-4-methylbenzamido)naphthalene-1,3,5-trisulfonate] at the somatic level and by other P2 blockers, PPADS (pyridoxalphosphate-6-azophenyl-2',4'-disulfonate) and MRS 2179 (2'-deoxy-N (6)-methyladenosine 3',5'-bisphosphate), at the dendritic level. After removal of both P2 agonists, a persistent increase in evoked synaptic responses was recorded both at the dendritic and somatic levels. This effect was prevented in the presence of different P2 antagonists. A 7-min OGD induced tissue anoxic depolarization and was invariably followed by irreversible loss of fEPSP. PPADS, suramin, MRS2179 or BBG (brilliant blue G) significantly prevented the irreversible failure of neurotransmission induced by 7-min OGD. Furthermore, in the presence of these P2 antagonists, the development of anoxic depolarization was blocked or significantly delayed. Our results indicate that P2 receptors modulate CA1 synaptic transmission under normoxic conditions by eliciting both inhibitory and excitatory effects. In the same brain region, P2 receptor stimulation plays a deleterious role during a severe OGD insult.

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Role of the hippocampal CA1 region in incremental value learning.

Publications

Role of the hippocampal CA1 region in incremental value learning.

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