Obstructive sleep apnea (OSA), which is the most common sleep-related breathing disorder, is characterized as frequent upper airway collapse and obstruction. It is a treatable disorder but if left untreated is associated with complications in several organ systems. The health risk to OSA patients shows a strong association with acute cardiovascular events, and with chronic conditions. To the central nervous system, OSA causes behavioral and neuropsychologic deficits including daytime sleepiness, depression, impaired memory, mood disorders, cognition deficiencies, language comprehension and expression deficiencies, all of which are compatible with impaired hippocampal function. Furthermore, there exists a significant correlation between disease severity and cognitive deficits in OSA. Children with severe OSA have significantly lower intelligence quotient (IQ) and executive control functions compared to normal children matched for age, gender and ethnicity. This corroborates the findings of several pediatric studies of cognition in childhood OSA, where deficits are reported in general intelligence and some measures of executive function. In studies of OSA, it is difficult to differentiate the effects of its two main pathologic traits, intermittent hypoxia (IH) and sleep fragmentation. Many OSA studies, utilize IH as the only exposure factor in OSA studies. These approaches simplify research process and attain most of the academic goals. IH, continuous hypoxia and intermittent continuous hypoxia can all result in decreases in arterial O2. There are striking differences to them in the response of physiological systems. There are multiple studies showing that IH treatment in a rodent model of OSA can impair performance of standard water maze tests associated with deficits in spatial learning and memory which most likely are hippocampal-dependent. Cellular damage to the hippocampal cornuammonis 1 (CA1) region likely contributes to neuropsychological impairment among OSA patients, since neural circuits in the hippocampus are important in learning and memory. In this article, studies of hippocampal impairments from IH are reviewed for elucidating the mechanisms and relationships between hippocampal impairments and IH of OSA.
Hippocampus ; physiopathology ; Humans ; Hypoxia ; etiology ; physiopathology ; Sleep Apnea, Obstructive ; etiology ; physiopathology

Animals ; Hippocampus ; pathology ; physiopathology ; Male ; Motor Activity ; Rats ; Rats, Wistar

AIMTo investigate the regulatory network of hippocampal-systemic arterial blood pressure during epileptic network reestablishment.

METHODS7.2 microg picrotoxin (PTX) was microinjected into the right HPC (RHPC) to induce rat epilepsy. Contralateral hippocampal EEG, single unit discharges, femoral artery blood pressure and ECG were recorded simultaneously.

RESULTSPTX might induce: (1) A resemblance interspike intervals (ISI) spot distribution of long duration neuronal burst and unit after discharges in contralateral HPC. (2) Delayed the initiation time of hippocampal neuronal bursts coupled with arterial blood pressure depression. (3) Hippocampal neuronal burst or unit after discharges coupled complexly with arterial blood pressure depression. (4) Resemblance hippocampal EEG interpeak intervals (IPI) and neuronal firing ISI spot distribution coupled with arterial blood pressure depression.

CONCLUSIONDuring contralateral hippocampal epileptic network reestablishment after microinjection of PTX to the RHPC, the function of the hippocampal-arterial blood pressure regulatory network could be modulated by characteristic network and neuronal temporal code patterning.

Animals ; Blood Pressure ; physiology ; Electrocardiography ; Electroencephalography ; Epilepsy ; physiopathology ; Hippocampus ; physiology ; physiopathology ; Male ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo investigate whether the waveform of electrical stimulus affects the antiepileptic effect of focal low-frequency stimulation (LFS).

METHODSThe antiepileptic effects of the LFS in sine, monophase square and biphase square waves were investigated in hippocampal kindled mice, respectively.

RESULTSCompared to the control group, sine wave focal LFS (30 s) inhibited seizure stages (2.85 ± 0.27 vs 4.75 ± 0.12, P<0.05), lowered incidence of generalized seizures (53.6% vs 96.5%, P<0.01) and reduced afterdischarge durations [(16.2 2 ± 1.69)s vs (30.29 ± 1.12)s, P<0.01] in hippocampal kindled mice, while monophase or biphase square wave LFS (30 s) showed no antiepileptic effect. Monophase square LFS (15 min) inhibited seizure stages (3.58 ± 0.16, P<0.05) and incidence of generalized seizures (66.7%,P<0.01), but had weaker inhibitory effect on hippocampal afterdischarge durations than sine wave LFS. In addition, pre-treatment and 3 s but not 10 s post-treatment with sine wave LFS resulted in suppression of evoked seizures (P<0.05 or P<0.01).

CONCLUSIONThe antiepileptic effect of LFS is dependent on its waveform. Sine wave may be optimal for closed-loop LFS treatment of epilepsy.

Animals ; Anticonvulsants ; Electric Stimulation ; Epilepsy ; Hippocampus ; physiopathology ; Kindling, Neurologic ; Mice ; Seizures ; physiopathology

In vitro electrical neurophysiological and behavioural studies have shown that diabetes mellitus negatively affects hippocampal function. In this study, by using in vivo extracellular recording, the spontaneous neural activity was obtained from hippocampus of anaesthetized rats in both streptozotocin-induced diabetes group and normal control group. Temporal relationship between neuronal firing and slow oscillation (1-4 Hz) of local field potentials (LFPs) in hippocampus was analyzed using coherence and phase locking measurement. Lower coherence value (0.617+/-0.028) was observed in diabetic rats than that in control rats (0.730+/-0.024) (P=0.005). Furthermore, phase-locking measurement using von Mises fitting parameterized by a concentration parameter kappa showed a lower degree (kappa= 0.347+/-0.113) of temporal coordination between neuronal spiking and slow oscillation of LFPs in the hippocampus of diabetic rats than that of normal ones (kappa= 1.174+/-0.134) (P<0.001). Both approaches demonstrated that diabetes can indeed impair the temporal coordination between neuronal spiking and slow oscillation of population activity in hippocampus. This observed neural coordination impairment may serve as a network level mechanism for diabetes-induced memory deterioration.
Action Potentials ; Animals ; Diabetes Mellitus, Experimental ; physiopathology ; Hippocampus ; physiopathology ; Memory ; Oscillometry ; Rats

AIM AND METHODSTo investigate the role of the duration of ischemic preconditioning and the interval between the ischemic preconditioning and the following injured ischemia in induction of ischemic tolerance of the hippocampus, using 4 vessel occlusion (4VO) global ischemic model of rats.

RESULTSIschemia for 6 min resulted in a apparent delayed neuron death (DND) in the hippocampus, while ischemia for 3 min did not cause DND in the hippocampus. Ischemic preconditioning for 3 min could apparently decrease DND caused by ischemia for 6 min followed the preconditioning at intervals of reperfusion 1 or 3 d (P < 0.01), indicating the protective effect of the ischemic preconditioning against the following severe ischemia. However, ischemic preconditioning for 1 min did not produce any apparent protective effect. The DND could not be decreased not only, but increased in a condition of ischemic preconditioning for 5 min followed by 6 min injured ischemia at a interval of 1 d or ischemic preconditioning for 3 min followed by ischemia for 6 min at a interval of 1 h.

CONCLUSIONGlobal ischemic preconditioning could induce tolerance of the hippocampus to ischemic injury. The proper duration of ischemic preconditioning and the interval between the preconditioning and the following injured ischemia might be 3 min and 1 to 3 days, respectively, in the 4VO rat model.

Animals ; Hippocampus ; physiopathology ; Ischemic Attack, Transient ; physiopathology ; Ischemic Preconditioning ; Rats ; Rats, Sprague-Dawley

BACKGROUNDTraumatic brain injury (TBI) often causes cognitive deficits and remote symptomatic epilepsy. Hippocampal regional excitability is associated with the cognitive function. However, little is known about injury-induced neuronal loss and subsequent alterations of hippocampal regional excitability. The present study was designed to determine whether TBI may impair the cellular circuit in the hippocampus.

METHODSForty male Wistar rats were randomized into control (n = 20) and TBI groups (n = 20). Long-term potentiation, extracellular input/output curves, and hippocampal parvalbumin-immunoreactive and cholecystokinin-immunoreactive interneurons were compared between the two groups.

RESULTSTBI resulted in a significantly increased excitability in the dentate gyrus (DG), but a significantly decreased excitability in the cornu ammonis 1 (CA1) area. Using design-based stereological injury procedures, we induced interneuronal loss in the DG and CA3 subregions in the hippocampus, but not in the CA1 area.

CONCLUSIONSTBI leads to the impairment of hippocampus synaptic plasticity due to the changing of interneuronal interaction. The injury-induced disruption of synaptic efficacy within the hippocampal circuit may underlie the observed cognitive deficits and symptomatic epilepsy.

Animals ; Brain Injuries ; physiopathology ; Hippocampus ; physiopathology ; Long-Term Potentiation ; Male ; Neuronal Plasticity ; physiology ; Rats ; Rats, Wistar

This review summarizes the present advance of effects of stress on hippocampal structure and function and the role of hippocampus in feedback regulation of thalamic-pituitary-adrenocortical (HPA) axis during stress. It shows that stress can affect hippocampal structure and function, on the other hand, the hippocampus can also suppress the stress reaction through the feedback regulation of HPA axis, but chronic stress can attenuate this regulation, then significantly impair its structure and function.
Animals ; Hippocampus/physiopathology* ; Humans ; Hypothalamo-Hypophyseal System/physiology* ; Pituitary-Adrenal System/physiology* ; Stress, Physiological/physiopathology*

In this paper, one method was introduced, which was a combination of the cue-related morphine addiction model and a technique for obtaining chronic extracellular recordings of single unit in freely moving rats. With the combination and improvement of this technique, we have successfully applied this new method to study the neuronal activity of the hippocampus CA1 region in morphine withdrawal rats. In all, we found some more accurate and objective cellular characteristics of hippocampal neurons, and considered these characteristics as one of electrophysiological indexes of morphine addiction rats.
Action Potentials ; physiology ; Animals ; Electrophysiology ; instrumentation ; Hippocampus ; physiopathology ; Morphine Dependence ; physiopathology ; psychology ; Neurons ; physiology ; Rats ; Substance Withdrawal Syndrome ; physiopathology ; psychology

In order to extract more information from extracellular action potential (EAP) of neurons recorded deep in the brain tissue, we established simulation models of various pyramidal neurons in the hippocampal CA1 region and investigated the effects of dendrite currents, cell morphology and ion mechanisms on the formation of EAP waveforms. The results show that dendrite currents have significant effects on the EAP at the locations far from cell body, but not on those near cell body. The differences of shape of various pyramidal neurons result in large changes in the EAP amplitudes. However, the shapes of these different EAP are very similar. Ion mechanisms, such as calcium channels, have little effect on EAP waveforms. These results provide important information for experimental EAP recordings, EAP data analysis, and developing new methods to extract more neuronal data from EAP.
Action Potentials ; physiology ; Animals ; Computer Simulation ; Hippocampus ; cytology ; physiopathology ; Models, Biological ; Neurons ; physiology ; Pyramidal Cells ; physiopathology ; Rats