Biomedical subjects

A N Sieve

Publications and source records attributed to A N Sieve.

5 recordsLinked to original sources

PubMed2006

Restraint stress decreases virus-induced pro-inflammatory cytokine mRNA expression during acute Theiler's virus infection.

Stressful life events have been associated with the onset and/or exacerbation of multiple sclerosis (MS). Our previous studies have indicated that restraint stress (RS) reduces inflammation and virus-induced chemokine expression in the Theiler's virus-induced demyelination (TVID) model of MS. Here we report that RS significantly reduced the virus-induced interferon-gamma mRNA levels in the brain. Additionally, mRNA levels of lymphotoxin-beta, tumor necrosis factor-alpha, and interferon-gamma in the brain were negatively correlated with viral titers in the brain. These results indicated an immunosuppressive effect of stress during early TVID causing impaired viral clearance, which may be a potential exacerbating factor for later demyelination.

Animals↗

PubMed2004

Alterations in chemokine expression following Theiler's virus infection and restraint stress.

Restraint stress (RS) applied to mice during acute infection with Theiler's virus causes corticosterone-induced immunosuppression. This effect was further investigated by measuring chemokine changes in the spleen and central nervous system (CNS) using an RNase Protection Assay. mRNAs for lymphotactin (Ltn), interferon-induced protein-10 (IP-10), MIP-1 beta, monocyte chemoattractant protein-1 (MCP-1) and TCA-3 were detected in the spleen at day 2 pi, but not in the brain of CBA mice infected with Theiler's virus. Ltn, IP-10 and RANTES were elevated in both the spleen and the brain at day 7 pi, and were significantly decreased by RS in the brain. RS also resulted in decreased inflammation within the CNS.

Animals↗

PubMed2001

Pain and negative affect: evidence the inverse benzodiazepine agonist DMCM inhibits pain and learning in rats.

RATIONALE: The anxiogenic DMCM, an inverse benzodiazepine agonist, was used to explore the relationship between negative affective states and pain. Past work suggests that the outcome obtained may depend on both the intensity of the affective state and the way in which pain is inferred. OBJECTIVES: The present study was designed to test the impact of relatively low doses of DMCM on multiple measures of pain reactivity and learning. METHODS: In experiment 1, systemic injections of 0.00, 0.015, 0.06, and 0.25 mg/kg DMCM were administered before vocalization and tail movements were assessed in response to a gradually incremented shock and radiant heat stimulus. Experiment 2 tested the effects of DMCM on Pavlovian conditioning. DMCM-treated subjects experienced a context paired with an aversive unconditioned stimulus (US) and conditioned freezing was assessed the next day. RESULTS: Experiment 1 showed that DMCM inhibits both a spinal nociceptive reflex (tail-flick to heat) and a supraspinal measure of pain (vocalization to shock). Because these inhibitory effects could reflect a disruption in motor function, experiment 2 employed a remote test based on Pavlovian conditioning. A moderate dose of DMCM undermined learning, implying that the drug decreased the affective impact of the aversive US. CONCLUSIONS: DMCM induces hypoalgesia on a wide range of assays. Furthermore, pharmacologically inducing a negative affective state blocks Pavlovian fear conditioning. It is suggested that DMCM induces a state of panic and that this state inhibits pain.

Affect↗

PubMed2001

Shock-induced hyperalgesia: IV. Generality.

Brief-moderate shock (3, 0.75 s, 1.0 mA) has opposite effects on different measures of pain, inducing antinociception on the tail-flick test while lowering vocalization thresholds to shock and heat (hyperalgesia) and enhancing fear conditioned by a gridshock unconditioned stimulus (US). This study examined the generality of shock-induced hyperalgesia under a range of conditions and explored parallels to sensitized startle. Reduced vocalization thresholds to shock and antinociception emerged at a similar shock intensity. Severe shocks (3, 25 s, 1.0 mA or 3, 2 s, 3.0 mA) lowered vocalization threshold to shock but increased vocalization and motor thresholds to heat and undermined fear conditioned by a gridshock or a startling tone US. All shock schedules facilitated startle, but only brief-moderate shock inflated fear conditioning. The findings suggest that brief-moderate shock enhances the affective impact of aversive stimuli, whereas severe shocks attenuate pain.

Affect↗

PubMed1999

Shock-induced hyperalgesia: evidence forebrain systems play an essential role.

Exposure to a few moderately intense (1-mA) tailshocks has opposite effects on two measures of pain reactivity in rats. Tail-withdrawal to radiant heat is inhibited (antinociception) while vocalization thresholds are lowered (hyperalgesia) to both heat and shock (King et al., 1996). Prior work indicates that this hyperalgesia represents an unconditioned response and that it enhances the acquisition of both conditioned freezing and an avoidance response to thermal pain. The present experiments begin to explore the neural mechanisms that underlie hyperalgesia. Experiments 1 and 2 demonstrated that hyperalgesia is eliminated by both decerebration and pentobarbital anesthesia. Lesions limited to the frontal pole had a similar effect (Experiment 3). Experiment 4 showed that lesioning the frontal pole also disrupted the acquisition of conditioned fear.

Animals↗