Differential Effects of the Histamine H3Receptor Agonist Methimepip on Dentate Granule Cell Excitability, Paired-Pulse Plasticity and Long-Term Potentiation in Prenatal Alcohol-Exposed Rats

AbstractLong-term potentiation (LTP) and long-term depression (LTD) of synaptic efficacies are involved in establishment of long-term memories. In this process, neurons need to adjust the overall efficacy of their synapses by using mechanisms of homeostatic plasticity to balance their activity and control their firing rate. For instance, in the dentate granule cell in vivo, induction of homosynaptic LTP in the tetanized medial perforant path is accompanied by heterosynaptic LTD in the non-tetanized lateral perforant path. We used the compartmental model of this cell to test the following hypotheses: 1. Using plasticity and metaplasticity rules both based on postsynaptic voltage we can reproduce homosynaptic LTP and concurrent heterosynaptic LTD, provided there is an ongoing noisy spontaneous activity; 2. Frequency of an ongoing noisy spontaneous activity along the lateral path determines the magnitude of heterosynaptic LTD. In experiments where procaine was used to block the lateral spontaneous activity, no heterosynaptic LTD occurred. However, when the procaine was washed out and a second tetanization was applied to the medial path, no heterosynaptic LTD could have been induced neither. Our simulations predict that the reduced frequency of spontaneous activity in the lateral perforant path can account for this lasting absence of heterosynaptic LTD.

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Plasticity in the projection from the anterior thalamic nuclei to the anterior cingulate cortex in the rat in vivo: paired-pulse facilitation, long-term potentiation and short-term depression

Neuroscience ◽

10.1016/s0306-4522(01)00554-1 ◽

2002 ◽

Vol 109 (3) ◽

pp. 401-406 ◽

Cited By ~ 19

Author(s):

C. Gemmell ◽

S.M. O’Mara

Keyword(s):

Anterior Cingulate Cortex ◽

Long Term Potentiation ◽

Anterior Cingulate ◽

Thalamic Nuclei ◽

Short Term ◽

Paired Pulse ◽

Term Potentiation ◽

Anterior Thalamic Nuclei

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Pre- and Postnatal Propylthiouracil-Induced Hypothyroidism Impairs Synaptic Transmission and Plasticity in Area CA1 of the Neonatal Rat Hippocampus

Endocrinology ◽

10.1210/en.2003-0395 ◽

2003 ◽

Vol 144 (9) ◽

pp. 4195-4203 ◽

Cited By ~ 87

Author(s):

Li Sui ◽

M. E. Gilbert

Keyword(s):

Thyroid Hormone ◽

Synaptic Transmission ◽

Long Term Potentiation ◽

Synaptic Function ◽

Learning Deficits ◽

Paired Pulse ◽

Area Ca1 ◽

Term Potentiation ◽

Paired Pulse Depression

Abstract Thyroid hormones are essential for neonatal brain development. It is well established that insufficiency of thyroid hormone during critical periods of development can impair cognitive functions. The mechanisms that underlie learning deficits in hypothyroid animals, however, are not well understood. As impairments in synaptic function are likely to contribute to cognitive deficits, the current study tested whether thyroid hormone insufficiency during development would alter quantitative characteristics of synaptic function in the hippocampus. Developing rats were exposed in utero and postnatally to 0, 3, or 10 ppm propylthiouracil (PTU), a thyroid hormone synthesis inhibitor, administered in the drinking water of dams from gestation d 6 until postnatal day (PN) 30. Excitatory postsynaptic potentials and population spikes were recorded from the stratum radiatum and the pyramidal cell layer, respectively, in area CA1 of hippocampal slices from offspring between PN21 and PN30. Baseline synaptic transmission was evaluated by comparing input-output relationships between groups. Paired-pulse facilitation, paired-pulse depression, long-term potentiation, and long-term depression were recorded to examine short- and long-term synaptic plasticity. PTU reduced thyroid hormones, reduced body weight gain, and delayed eye-opening in a dose-dependent manner. Excitatory synaptic transmission was increased by developmental exposure to PTU. Thyroid hormone insufficiency was also dose-dependently associated with a reduction paired-pulse facilitation and long-term potentiation of the excitatory postsynaptic potential and elimination of paired-pulse depression of the population spike. The results indicate that thyroid hormone insufficiency compromises the functional integrity of synaptic communication in area CA1 of developing rat hippocampus and suggest that these changes may contribute to learning deficits associated with developmental hypothyroidism.

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