Differential effects of long and short train theta burst stimulation on LTP induction in rat anterior cingulate cortex slices: Multi-electrode array recordings

Objective

There is substantial evidence supporting the notion that the anterior cingulate cortex (ACC) is an important limbic structure involved in multiple brain functions such as sensory perception, motor conflict monitoring, memory, emotion and cognition. It has been shown that long term potentiation (LTP) is an important synaptic model of neural plasticity in the ACC, however, little is known about the spatiotemporal properties of ACC at network level. The present study was designed to see the LTP induction effects across different layers of the ACC by using different conditioning stimuli (CS) protocols.

Methods

A unique multi-electrode array recording technique was used in the acutely-dissociated ACC slices of rats. Long and short train theta burst stimulation (TBS) paradigms were applied in layer V–VI as the CS and the LTP induction effects were compared across different layers of the ACC. Briefly, both long and short train TBS are composed of bursts (4 pulses at 100 Hz) with a 200 ms interval, however, the former (TBS1) was with 10 trains and the latter (TBS2) was with 5 trains. After test stimulation at layer V–VI in the ACC, network field potentials (FPs) could be simultaneously recorded across all layers of the ACC.

Results

The waveforms of FPs were different across different layers. Namely, positive-going waveforms were recorded in layer I and negative-going waveforms were recorded in layers V–VI, in contrast, complex waveforms were localized mainly in layers II–III. Following application of two CS protocols, the induction rate of LTP was significantly different between TBS1 and TBS2 regardless of the spatial properties. TBS1 had more than 60% success, while TBS2 was less than 25% in induction of LTP. Moreover, both the 2 CS protocols could induce LTP in layers II–III and layers V–VI without layer-related difference. However, no LTP was inducible in layer I.

Conclusion

The present findings indicate that stimulation protocols may, at least in part, account for a large portion of variations among previous LTP studies, and hence highlight the importance of selecting the best LTP induction protocol when designing such experiments. Moreover, the present results demonstrate the prominent superiority of multi-electrode array recording in revealing the network properties of synaptic activities in the ACC, especially in comparing the spatiotemporal characteristics between different layers of this structure.     

N-Methyl-

In hippocampal area CA1, long-term potentiation (LTP) is induced by tetanic stimulation protocols that activate N-methyl-D-aspartate (NMDA) receptors. In addition, some stimulation protocols can induce LTP during NMDA receptor blockade. An initial signal in both NMDA receptor-dependent and independent LTPs is increased intracellular Ca²⁺ concentration in postsynaptic neurons. It therefore seems possible that subsequent steps leading to expression and maintenance of potentiation are shared whether or not LTP is induced through NMDA receptor activation. We tested this hypothesis by applying a broad spectrum protein kinase, inhibitor, previously shown to inhibit NMDA receptor-dependent LTP. In agreement with earlier reports, we found that H-7 inhibited NMDA receptor-dependent LTP when applied either during tetanic stimulation, or beginning 30 min following tetanic stimulation. In contrast, NMDA receptorindependent LTP was not inhibited by H-7 applied during or following tetanic stimulation. We also tested for mutual occlusion between NMDA receptor-dependent and independent LTPs. Although induction of NMDA receptor-independent LTP did not occlude later induction of NMDA receptor-dependent LTP, induction of NMDA receptordependent LTP did occlude NMDA receptor-independent LTP. While the kinase inhibitor experiment showed a clear difference between NMDA receptor-dependent and independent LTPs, the occlusion experiments suggest an interaction between the signalling pathways for the two LTPs. © 1995 Wiley-Liss, Inc.     

Different mechanisms may be required for maintenance,of NMDA receptor-dependent and independent forms of long-term potentiation

In hippocampal area CA1, long-term potentiation (LTP) is induced by tetanic stimulation protocols that activate N-methyl-D-aspartate (NMDA) receptors. In addition, some stimulation protocols can induce LTP during NMDA receptor blockade. An initial signal in both NMDA receptor-dependent and independent LTPs is increased intracellular Ca²⁺ concentration in postsynaptic neurons. It therefore seems possible that subsequent steps leading to expression and maintenance of potentiation are shared whether or not LTP is induced through NMDA receptor activation. We tested this hypothesis by applying a broad spectrum protein kinase, inhibitor, previously shown to inhibit NMDA receptor-dependent LTP. In agreement with earlier reports, we found that H-7 inhibited NMDA receptor-dependent LTP when applied either during tetanic stimulation, or beginning 30 min following tetanic stimulation. In contrast, NMDA receptorindependent LTP was not inhibited by H-7 applied during or following tetanic stimulation. We also tested for mutual occlusion between NMDA receptor-dependent and independent LTPs. Although induction of NMDA receptor-independent LTP did not occlude later induction of NMDA receptor-dependent LTP, induction of NMDA receptordependent LTP did occlude NMDA receptor-independent LTP. While the kinase inhibitor experiment showed a clear difference between NMDA receptor-dependent and independent LTPs, the occlusion experiments suggest an interaction between the signalling pathways for the two LTPs. © 1995 Wiley-Liss, Inc.     

NMDA receptor, protein kinase C and calmodulin system participate in the long-term potentiation in guinea pig superior colliculus slices

To investigate the involvement ofN-methyl-d-aspartate (NMDA) receptor, protein kinase C (PKC) and calmodulin on long-term potentiation (LTP) formation in the superior colliculus (SC), the effects of an NMDA receptor antagonist (d-APV), PKC inhibitors (H-7, K-252a, K-252b, polymyxin B), a protein kinase A (PKA) inhibitor (H-8) and a calcium/calmodulin-dependent kinase inhibitor (calmidazolium) on LTP formation were studied in guinea pig SC slices. APV (100 μM) masked the expression of LTP by tetanic stimulation, but the LTP once formed was not influenced by application of APV. LTP was blocked by application of H-7 (100 μM), but LTP reappeared 20 min after removal of H-7 from the perfusion medium without further tetanic stimulation. On the other hand, established LTP was also inhibited by application of H-7 even 90 min after the tetanic stimulation. Application of K-252a (500 nM) inhibited LTP formation, but K-252b (500 nM) had no inhibitory effect on LTP formation since K-252b, unlike K-252a, cannot permeate the cell membrane. Tetanic stimulation was applied 20 min after application of polymyxin B (1 μM) to the medium but it could not induce LTP, while established LTP was not influenced by the drug. Application of calmidazolium (50 μM) inhibited LTP formation, but had no inhibitory effect on LTP once formed. These results suggest that both the NMDA receptor and calmodulin system are involved in the induction of LTP after tetanic stimulation. This leads to PKC activation which maintains the LTP.     

Effects of a nitric oxide synthase inhibitor on NMDA receptor function in organotypic hippocampal cultures

Nitric oxide (NO) has been proposed to trigger long-term potentiation (LTP) at CA3 to CA1 synapses. We previously reported that NO synthesis inhibitors and blockers reduce an electrophysiological index of NMDA receptor activation in acute hippocampal slices. We now show that the NOS inhibitor, N^G-methyl-

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-arginine (MLA), also reversibly prevents LTP induction in organotypic hippocampal slices and significantly reduces a biochemical index of NMDA receptor function. These results further indicate that MLA inhibits LTP induction by interfering with NMDA receptor functions.     

Effects of synaptic plasticity regulated by 17β-estradiol on learning and memory in rats with Alzheimer’s disease

Objective

To investigate whether estrogen modulates learning and memory and long-term potentiation (LTP) in the hippocampus of rats with Alzheimer’s disease (AD).

Methods

The rats were divided into ovariectomy (OVX) and estrogen replacement therapy (ERT) groups. Rats in the ERT group received OVX, followed by ERT, while rats in the OVX group received only OVX. The rat model of AD was established by injection of 1 μL (10 μg/μL) amyloid-beta peptide 1–40(Aβ_1–40) into the hippocampus. The learning and memory ability and LTP were determined by Morris water maze and electrophysiological method, respectively.

Results

The escape latency in Morris water maze significantly decreased in ERT group compared with that in OVX group (P < 0.05). Besides, rats in ERT group exhibited a significant enhancement of the magnitude of LTP at 30 min after high-frequency stimulation (HFS), compared with that in OVX group (P < 0.01).

Conclusion

ERT can attenuate the cognitive deficits in the rat model of AD, and estrogen can regulate LTP and synaptic remodeling in AD rats.     

The effects of Zn on long-term potentiation of C fiber-evoked potentials in the rat spinal dorsal horn

Tetanic stimuli of peripheral C fibers produces long-term potentiation (LTP) in the spinal cord, which may contribute to sensitization of spinal pain-sensitive neurons. Zn²⁺ is widely distributed in the central nervous system and has blocked (LTP) in the hippocampus. The present study examined the effects of Zn²⁺ on the induction and maintenance of C fiber-evoked LTP in the deep dorsal horn of spinalized rats in vivo. The sciatic nerve was stimulated by tetanic stimuli for inducing LTP. (1) Topical administration of Zinc chloride (15 μM) to the spinal cord 15 min before tetanic stimulation completely blocked the induction of LTP, but not the baseline C responses. When Zn²⁺ was given 2 h after induction of LTP, no significant effect occurred. (2) Chelation of Zn²⁺ by disodium calcium ethylene diaminetelraacetate (CaEDTA) (500 μM) resulted in no effect on LTP. (3) Coadministration of Zn²⁺ (15 μM) and N-methyl-D-aspartic acid (NMDA) (5 μM) significantly attenuated C fiber-evoked potentials, which was prevented by the NMDA receptor antagonist AP-5 (100 μM). The present results showed that Zn²⁺ may contribute to the modulation of the formation, but not the maintenance, of spinal LTP. NMDA receptors may be involved in Zn²⁺-induced modulation.     

Role of phosphorylation of ERK in induction and maintenance of LTP of the C-fiber evoked field potentials in spinal dorsal horn

Previous works have shown that activation of extracellular signal-regulated kinase (ERK)/cAMP response element binding protein (CREB) pathway is essential for long-term potentiation (LTP) in hippocampus. In the present study, the role of the ERK/CREB pathway in LTP of C-fiber evoked field potentials in spinal dorsal horn, which is relevant to pathologic pain, was investigated in adult rats. Western blotting analysis showed that the protein level of phosphorylated ERK (p-ERK) in ipsilateral spinal dorsal horn was transiently increased after LTP induction, starting at 15 min and returning to control at 60 min after tetanic stimulation and that the protein level of p-CREB increased at 30 min, persisting for at least 3 hr after LTP induction. Double immunofluorescence staining showed that p-ERK and p-CREB were only located in neurons but not in glial cells in the spinal dorsal horn after LTP induction. More importantly, we found that spinal application of PD 98059 (100 microM), a selective MEK inhibitor, at 30 min before tetanic stimulation blocked LTP induction and prevented the increase in p-ERK and p-CREB in spinal dorsal horn. When applied 15 min after LTP induction, PD98059 reversed established LTP. The drug, however, did not affect the spinal LTP, when applied at 30 min after LTP. Our results suggested that activation of ERK/CREB pathway in spinal dorsal neurons is necessary for induction and maintenance of long-term potentiation of the C-fiber evoked field potentials.     

The effects of Zn2+ on long-term potentiation of C fiber-evoked potentials in the rat spinal dorsal horn.

Tetanic stimuli of peripheral C fibers produces long-term potentiation (LTP) in the spinal cord, which may contribute to sensitization of spinal pain-sensitive neurons. Zn2+ is widely distributed in the central nervous system and has blocked (LTP) in the hippocampus. The present study examined the effects of Zn2+ on the induction and maintenance of C fiber-evoked LTP in the deep dorsal horn of spinalized rats in vivo. The sciatic nerve was stimulated by tetanic stimuli for inducing LTP. (1) Topical administration of Zinc chloride (15 microM) to the spinal cord 15 min before tetanic stimulation completely blocked the induction of LTP, but not the baseline C responses. When Zn2+ was given 2 h after induction of LTP, no significant effect occurred. (2) Chelation of Zn2+ by disodium calcium ethylene diaminetelraacetate (CaEDTA) (500 microM) resulted in no effect on LTP. (3) Coadministration of Zn2+ (15 microM) and N-methyl-D-aspartic acid (NMDA) (5 microM) significantly attenuated C fiber-evoked potentials, which was prevented by the NMDA receptor antagonist AP-5 (100 microM). The present results showed that Zn2+ may contribute to the modulation of the formation, but not the maintenance, of spinal LTP. NMDA receptors may be involved in Zn2+-induced modulation.     

Effects of pentobarbital anesthesia on nociceptive processing in the medial and lateral pain pathways in rats

Objective

To investigate the effects of pentobarbital anesthesia on nociceptive processing in the medial and lateral pain pathways.

Methods

Laser stimulation was employed to evoke nociceptive responses in rats under awake or anesthetic conditions. Pain-related neuronal activities were simultaneously recorded from the primary somatosensory cortex (SI), ventral posterolateral thalamus (VPL), anterior cingulate cortex (ACC), and medial dorsal thalamus (MD) with 4 eight-wire microelectrode arrays.

Results

Compared with the awake state, pentobarbital anesthesia significantly suppressed the neural activities induced by noxious laser stimulation. Meanwhile, the pain-evoked changes in the neuronal correlations between cortex and thalamus were suppressed in both medial and lateral pain pathways. In addition, the spontaneous firing rates in all the 4 areas were altered (including inhibition and excitation) under the condition of anesthesia.

Conclusion

The nociceptive processing in the brain can be dramatically changed by anesthesia, which indicates that there are considerable differences in the brain activities between awake and anesthetized states. It is better to employ awake animals for recording neural activity when investigating the sensory coding mechanisms, especially pain coding, in order to obtain data that precisely reflect the physiological state.     

Long-term Potentiation in the Striatum is Unmasked by Removing the Voltage-dependent Magnesium Block of NMDA Receptor Channels

We have studied the effects of tetanic stimulation of the corticostriatal pathway on the amplitude of striatal excitatory synaptic potentials. Recordings were obtained from a corticostriatal slice preparation by utilizing both extracellular and intracellular techniques. Under the control condition (1.2 mM external Mg2+), excitatory postsynaptic potentials (EPSPs) evoked by cortical stimulation were reversibly blocked by 10 microM 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), an antagonist of dl-alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) ionotropic glutamate receptors, while they were not affected by 30 - 50 microM 2-amino-5-phosphonovalerate (APV), an antagonist of N-methyl-d-aspartate (NMDA) glutamate receptors. In the presence of 1.2 mM external Mg2+, tetanic activation of cortical inputs produced long-term depression (LTD) of both extracellularly and intracellularly recorded synaptic potentials. When Mg2+ was removed from the external medium, EPSP amplitude and duration increased. In Mg2+-free medium, cortically evoked EPSPs revealed an APV-sensitive component; in this condition tetanic stimulation produced long-term potentiation (LTP) of synaptic transmission. Incubation of the slices in 30 - 50 microM APV blocked striatal LTP, while it did not affect LTD. In Mg2+-free medium, incubation of the slices in 10 microM CNQX did not block the expression of striatal LTP. Intrinsic membrane properties (membrane potential, input resistance and firing pattern) of striatal neurons were altered neither by tetanic stimuli inducing LTD and LTP, nor by removal of Mg2+ from the external medium. These findings show that repetitive activation of cortical inputs can induce long-term changes of synaptic transmission in the striatum. Under control conditions NMDA receptor channels are inactivated by the voltage-dependent Mg2+ block and repetitive cortical stimulation induces LTD which does not require activation of NMDA channels. Removal of external Mg2+ deinactivates these channels and reveals a component of the EPSP which is potentiated by repetitive activation. Since the striatum has been involved in memory and in the storage of motor skills, LTD and LTP of synaptic transmission in this structure may provide the cellular substrate for motor learning and underlie the physiopathology of some movement disorders.     

Involvement of microglia and interleukin-18 in the induction of long-term potentiation of spinal nociceptive responses induced by tetanic sciatic stimulation

Objective The present study aimed to investigate the potential roles of spinal microglia and downstream molecules in the induction of spinal long-term potentiation(LTP)and mechanical allodynia by tetanic stimulation of the sciatic nerve(TSS).Methods Spinal LTP was induced in adult male Sprague-Dawley rats by tetanic stimulation of the sciatic nerve(0.5 ms,100 Hz,40 V,10 trains of 2-s duration at 10-s intervals).Mechanical allodynia was determined using von Frey hairs.Immunohistochemical staining and Western blot were used to detect changes in glial expression of interleukin-18(IL-18)and IL-18 receptor(IL-18R).Results TSS induced LTP of C-fiber-evoked field potentials in the spinal cord.Intrathecal administration of the microglial inhibitor minocycline(200 μg/20 μL)1 h before TSS completely blocked the induction of spinal LTP.Furthermore,after intrathecal injection of minocycline(200 μg/20 μL)by lumbar puncture 1 h before TSS,administration of minocycline for 7 consecutive days(once per day)partly inhibited bilateral allodynia.Immunohistochemistry showed that minocycline inhibited the sequential activation of microglia and astrocytes,and IL-18 was predominantly colocalized with the microglial marker Iba-1 in the spinal superficial dorsal horn.Western blot re-vealed that repeated intrathecal injection of minocycline significantly inhibited the increased expression of IL-18 and IL-18Rs in microglia induced by TSS.Conclusion The IL-18 signaling pathway in microglia is involved in TSS-induced spinal LTP and mechanical allodynia.     

pH-Sensitive NMDA Inhibitors Improve Outcome in a Murine Model of SAH

Background

Despite intensive research, neurological morbidity from delayed cerebral ischemia remains common after aneurysmal subarachnoid hemorrhage (SAH). In the current study, we evaluate the neuroprotective effects of a pH-dependent GluN2B subunit-selective NMDA receptor antagonist in a murine model of SAH.

Methods

Following induction of SAH, 12 ± 2 week old male C57-BL/6 mice received NP10075, a pH-dependent NMDA receptor antagonist, or vehicle. In a separate series of experiments, NP10075 and the non-pH sensitive NMDA antagonist, NP10191, were administered to normoglycemic and hyperglycemic mice. Both histological (right middle cerebral artery diameter, NeuN, and Fluoro-Jade B staining) and functional endpoints (rotarod latency and neuroseverity score) were evaluated to assess the therapeutic benefit of NP10075.

Results

Administration of NP10075 was well tolerated and had minimal hemodynamic effects following SAH. Administration of the pH-sensitive NMDA antagonist NP10075, but not NP10191, was associated with a durable improvement in the functional performance of both normoglycemic and hyperglycemic animals. NP10075 was also associated with a reduction in vasospasm in the middle cerebral artery associated with hemorrhage. There was no significant difference between treatment with nimodipine + NP10075, as compared to NP10075 alone.

Conclusions

These data demonstrate that use of a pH-dependent NMDA antagonist has the potential to work selectively in areas of ischemia known to undergo acidic pH shifts, and thus may be associated with selective regional efficacy and fewer behavioral side effects than non-selective NMDA antagonists.     

Decreased postnatal neurogenesis in the hippocampus combined with stress experience during adolescence is accompanied by an enhanced incidence of behavioral pathologies in adult mice

Background

Although long-term potentiation (LTP) of synaptic strength is very persistent, current studies have provided evidence that various manipulations or pharmacological treatment when applied shortly after LTP induction can reverse it. This kind of reversal of synaptic strength is termed as depotentiation and may have a function to increase the flexibility and storage capacity of neuronal networks. Our previous studies have demonstrated that an increase in extracellular levels of adenosine and subsequent activation of adenosine A₁ receptors are important for the induction of depotentiation; however, the signaling downstream of adenosine A₁ receptors to mediate depotentiation induction remains elusive.

Results

We confirm that depotentiation induced by low-frequency stimulation (LFS) (2 Hz, 10 min, 1200 pulses) was dependent on adenosine A₁ receptor activation, because it was mimicked by bath-applied adenosine A₁ receptor agonist N ⁶-cyclopentyladenosine (CPA) and was inhibited by the selective adenosine A₁ receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX). Pretreatment of the hippocampal slices with the selective p38 mitogen-activated protein kinase (MAPK) inhibitors, 4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl]-5-(4-pyrudyl)-1H-imidazole (SB203580) or trans-1-(4-hydroxycyclohexyl)-4-(fluorophenyl)-5-(2-methoxypyrimidin-4-yl)imidazole (SB239063), prevented the induction of depotentiation by LFS and CPA. In agreement with electrophysiological observation, both LFS- and CPA-induced depotentiation are associated with an increase in p38 MAPK activation, which are blocked by DPCPX or SB203580 application.

Conclusion

These results suggest that activation of adenosine A₁ receptor and in turn triggering p38 MAPK signaling may contribute to the LFS-induced depotentiation at hippocampal CA1 synapses.     

Entorhinal cortex long-term potentiation evoked by theta-patterned stimulation of associative fibers in the isolated in vitro guinea pig brain

Long-term potentiation (LTP) induced in the lateral entorhinal cortex by theta-patterned tetanic stimulation of the piriform cortex was analyzed in the isolated guinea pig brain maintained in vitro. Monosynaptic excitatory postsynaptic potentials (EPSPs) evoked by stimulation of the piriform cortex are composed of an early and late component selectively blocked bynon-N-methyl-d-aspartate (non-NMDA) and NMDA receptor antagonists, respectively. LTP induction was dependent on NMDA receptor activation, being blocked by perfusing the preparation with 2-amino-5-phosphonovalerate (AP-5). LTP was expressed through synaptic enhancement of both early non-NMDA and late, possibly NMDA receptor-mediated responses.     

Emotional Dampening in Persons with Elevated Blood Pressure: Affect Dysregulation and Risk for Hypertension

Background

Persons with higher blood pressure have emotional dampening in some contexts. This may reflect interactive changes in central nervous system control of affect and autonomic function in the early stages of hypertension development.

Purpose

The purpose of this study is to determine the independence of cardiovascular emotional dampening from alexithymia to better understand the role of affect dysregulation in blood pressure elevations.

Methods

Ninety-six normotensives were assessed for resting systolic and diastolic (DBP) blood pressure, recognition of emotions in faces and sentences using the Perception of Affect Task (PAT), alexithymia, anxiety, and defensiveness.

Results

Resting DBP significantly predicted PAT emotion recognition accuracy in men after adjustment for age, self-reported affect, and alexithymia.

Conclusions

Cardiovascular emotional dampening is independent of alexithymia and affect in men. Dampened emotion recognition could potentially influence interpersonal communication and psychosocial distress, thereby further contributing to BP dysregulation and increased cardiovascular risk.     

Activation of NMDA receptors in hippocampal area CA1 by low and high frequency orthodromic stimulation and their contribution to induction of long-term potentiation

N-methyl-D-aspartate (NMDA) receptors are important in many instances of synaptic plasticity. In hippocampal area CA1, long-term potentiation (LTP) can be induced by both NMDA receptor-dependent and -independent mechanisms. Using intracellular recordings and single-electrode voltage clamp, we isolated and characterized NMDA receptor-mediated synaptic responses. NMDA receptor-mediated responses evoked by low frequency orthodromic stimulation were inhibited in a dose-dependent manner by the competitive antagonist D,L-2-amino-5-phosphonovaleric acid (APV). High frequency (tetanic) stimulation, which facilitates synaptic release of glutamate, failed to overcome the blockade of NMDA receptors by APV. Using extracellular recordings of field potentials, we studied the contribution of NMDA receptors to LTP induced by different patterns of tetanic stimulation. LTP was inhibited in a dose-dependent manner by APV, but was more sensitive to APV than were NMDA receptor-mediated synaptic responses. This most likely reflects a threshold for NMDA receptor activation in LTP induction. A component of LTP that resisted blockade by APV was induced by high (200 Hz), but not low (25 Hz), frequency tetanization. This NMDA receptor-independent component of LTP persisted for > 4 hours and accounted for approximately half the potentiation induced by 200 Hz tetanization. Procedures necessary to induce LTP at the Schaffer collateral/ commissural synapses in area CA1 by both NMDA receptor-dependent and -independent mechanisms are now well characterized. Using the same neuronal population, it will be possible to ask if processes involved in the maintenance of LTP are shared even when LTP is induced through two different mechanisms. © 1994 Wiley-Liss, Inc.     

Divergent Associations of Antecedent- and Response-Focused Emotion Regulation Strategies with Midlife Cardiovascular Disease Risk

Background

It is not known whether various forms of emotion regulation are differentially related to cardiovascular disease risk.

Purpose

The purpose of this study is to assess whether antecedent and response-focused emotion regulation would have divergent associations with likelihood of developing cardiovascular disease.

Methods

Two emotion regulation strategies were examined: reappraisal (antecedent-focused) and suppression (response-focused). Cardiovascular disease risk was assessed with a validated Framingham algorithm that estimates the likelihood of developing CVD in 10 years. Associations were assessed among 373 adults via multiple linear regression. Pathways and gender-specific associations were also considered.

Results

One standard deviation increases in reappraisal and suppression were associated with 5.9 % lower and 10.0 % higher 10-year cardiovascular disease risk, respectively, in adjusted analyses.

Conclusions

Divergent associations of antecedent and response-focused emotion regulation with cardiovascular disease risk were observed. Effective emotion regulation may promote cardiovascular health.     

A longitudinal examination of burden and psychological distress in carers of people with an eating disorder

Purpose

Eating disorders are chronic conditions that require ongoing, high level care. Despite the chronic nature of eating disorders, to date, previous research examining eating disorder carer burden and psychological distress has been cross-sectional only. Therefore, the current study aimed to conduct a preliminary longitudinal examination of the predictors of carer burden and psychological distress for carers of those with an eating disorder.

Methods

A self-report, quantitative questionnaire approach was utilised. Forty-two carers completed three self-report questionnaires over a period of 9 months (initial, 4½ and 9 months) assessing carer burden, psychological distress, carer needs, expressed emotion, coping strategies and social support.

Results

Maladaptive coping, expressed emotion and carer needs were significant longitudinal predictors of carer burden. Carer psychological distress could not be predicted longitudinally.

Conclusions

In order to reduce carer burden, interventions should test whether reducing maladaptive coping strategies, expressed emotion and addressing carer needs lead to lower carer burden and distress.