Neuroimmune and cortisol changes in selective serotonin reuptake inhibitor and placebo treatment of chronic posttraumatic stress disorder.

Background: To explore relations between neuroimmune and neuroendocrine systems relative to posttraumatic stress disorder (PTSD) treatment, cortisol and cytokine changes in response to selective serotonin reuptake inhibitor (SSRI) and placebo treatment of chronic PTSD were assessed prospectively.

Methods: Baseline measures of PTSD, depression, salivary 8 am and 4 pm cortisol, and serum interleukin-1beta (IL-1beta; pro-inflammatory) and soluble interleukin-2 receptors (IL-2R; cell-mediated immunity) were obtained for 58 PTSD and 21 control subjects. The PTSD subjects participated in a 10-week, double-blind treatment with citalopram (n = 19), sertraline (n = 18), or placebo (n = 7).

Using telerehabilitation to promote TBI recovery and transfer of knowledge.

Advances in the design and delivery of trauma care and acute medical management have increased the number of survivors of traumatic brain injury (TBI), producing societal consequences and medical challenges. Although access to health care for rural patients remains a critical challenge, teletherapy may represent a viable means for the delivery of therapeutic services to such patients. A case study is presented in which teletherapy was successfully utilized to improve the functional outcomes, both physical and cognitive, of a patient with a severe TBI.

Current directions in computer-assisted cognitive rehabilitation.

Technological advances over the past decade have given rise to the development of multiple computer-assisted cognitive rehabilitation programs. While results of investigations examining the efficacy of such techniques have been mixed, a positive trend for utilization of these procedures has been demonstrated. This review provides a discussion of the progression of research in this area, from anecdotal studies to controlled empirical investigations.

Clinical utility of the Trail Making Test practice time.

The Trail Making Test (TMT) is one of the most frequently used measures in clinical neuropsychology. Data obtained from the TMT practice times were analyzed to determine their utility in predicting success and failure on the full version of the test and to allow establishment of criteria by which to judge administration or discontinuation of the full test. Results indicated that TMT practice times were useful in predicting successful completion of Part A and B of the TMT.

Naloxone differentially alters fevers induced by cytokines.

Interferon-alpha (IFN-alpha), a cytokine acting as an endogenous pyrogen and a putative activator of the opioid system, binds to opiate receptors in vitro. The mu opioid receptor antagonist, naloxone hydrochloride (NLX), attenuates IFN-alpha-induced increases in the firing rate of cold-sensitive neurons within thermosensitive areas of the brain. The influence of NLX on fevers induced by central endogenous pyrogens was investigated in rats.

Chemokine-induced fever: intracerebroventricular actions of MIP-1 and MIP-1 alpha in rats.

The central pyrogenic actions in the rat of doublet macrophage inflammatory protein-1 (MIP-1) and MIP-1 alpha were determined by their intracerebroventricular infusion. Doses of 560 pg and 11.2 ng of MIP-1 or 10.

Prostaglandins and hypothalamic neurotransmitter receptors involved in hyperthermia: a critical evaluation.

The role of a prostaglandin of the E series (PGE) in the hypothalamic mechanisms underlying a fever continues to be controversial. This paper reviews the historical literature and current findings on the central action of the PGEs on body temperature (Tb). New experiments were undertaken to examine the local effect of muscarinic, nicotinic, serotonergic, alpha-adrenergic, or beta-adrenergic receptor antagonists at hypothalamic sites where PGE1 caused a rise in Tb of the primate.

Anatomical distribution of brainstem sites where PGE1 induces hyperthermia in macaque species.

The neuroanatomical distribution of sites in the diencephalon and mesencephalon within which a prostaglandin (PG) of the E series elicits hyperthermia was characterized in Macaca mulatta and Macaca nemestrina. In 420 experiments undertaken in 13 animals, 225 loci were examined for their reactivity to PGE1 microinjected in a dose of 30 or 100 ng given in a volume of 1.0-1.

Fever evoked by macrophage inflammatory protein-1 (MIP-1) injected into preoptic or ventral septal area of rats depends on intermediary protein synthesis.

Macrophage inflammatory protein-1 (MIP-1), a novel cytokine composed of alpha/beta subunits, is released from macrophages during infection. MIP-1 injected intravenously in the rabbit or into the anterior hypothalamic, preoptic area (AH/POA) of the rat causes an intense fever, which is not blocked by prostaglandin synthesis inhibitors, ibuprofin or indomethacin, respectively. The purpose of this study was to determine the role of de novo protein synthesis on the fever evoked by MIP-1 applied to thermosensitive cells of the AH/POA.

Electrical stimulation of the paraventricular nucleus attenuates pyrogen fever in the rabbit.

Arginine vasopressin (AVP) perfused within the ventral septal area (VSA) suppresses fever normally evoked by pyrogenic substances, including Salmonella abortus equi (SAE). Neurons containing AVP and located within the paraventricular nucleus (PVN) or the nearby bed nucleus of the stria terminalis (BnST) are believed to have projections to this septal region. A series of experiments was undertaken to determine whether electrical stimulation of these areas, which might be expected to cause the release of AVP within the VSA, would affect similarly the pathogenesis of fever.

Characteristics of pyrogen fevers are altered in the aged rabbit.

The febrile response to both intravenous and intracerebral administration of pyrogens was investigated in young and old male New Zealand White rabbits. Intravenous bacterial pyrogen evoked biphasic fevers in both groups of animals. However, the fevers in the group of older rabbits were significantly less than in younger animals.

Antipyretic action of centrally administered arginine vasopressin but not oxytocin in the cat.

The antipyretic action of central arginine vasopressin (AVP) was investigated in mongrel cats. Control push-pull perfusions in the ventral septal area (VSA), with the carrier vehicle alone, did not affect the febrile response to Salmonella typhosa administered intracerebroventricularly. When AVP was perfused similarly, the fever was suppressed in a dose-related manner.

Thermoregulatory actions of centrally-administered vasopressin in the rat.

Dependent upon the route and/or site of administration, arginine vasopressin (AVP) evoked a number of thermoregulatory actions in the conscious rat. Infused into a lateral cerebral ventricle, arginine vasopressin produced short-lasting hypothermia of rapid onset. Injected into the preoptic area, arginine vasopressin caused long-lasting hyperthermia of rapid onset that was antagonized by the prior administration of a V1 receptor antagonist, [d(CH2)5 Tyr(Me)AVP].

Alcohol dependence and withdrawal in the rat. An effective means of induction and assessment.

Numerous problems have been associated with previous attempts to develop a suitable method for the induction and assessment of alcohol dependence and withdrawal syndrome in the rat. Using our modification of a common inhalation method for the long-term administration of ethanol, these problems can be eliminated. Adult male rats (Long Evans and Brattleboro) were exposed to ethanol vapor concentrations of 7 to 35 mg/liter of air, which cause rapid development of tolerance and physical dependence.

Release of gamma-aminobutyric acid from the visual cortex of young kittens.

Barbiturate-anaesthetized kittens of less than one month of age were used for the quantitative determination of the in vivo release of endogenous gamma-aminobutyric acid (GABA) from visual cortex by two methods: push-pull perfusion and cortical cup superfusion. Analysis by high-performance liquid chromatography (HPLC) demonstrated that marked elevations of GABA were elicited during electrical stimulation of cortex (inside the cup or adjacent to the cannulae) and were released into the artificial extracellular fluid perfused within the collecting cup or through the cannulae. The results provide additional support for the view that GABA-mediated neuronal inhibition in early ontogenetic stages of visual cortex is widespread and robust.

Vasopressin-induced motor disturbances: localization of a sensitive forebrain site in the rat.

Arginine-vasopressin (AVP) microinjected into an area extending from the diagonal band of Broca to the anterior hypothalamus of the rat evokes severe motor disturbances, including barrel rotations and myoclonic/myotonic movements. These disturbances do not occur after administration of an artificial physiological solution or of oxytocin. Injection of this peptide into other areas of the brain does not cause these effects.

Determination of the endogenous and evoked release of catecholamines from the hypothalamus and caudate nucleus of the conscious and unrestrained rat.

The action of catecholamines within the CNS is important for the expression of numerous vegetative and behavioral functions. To understand the role these amines play, it is necessary to measure changes in the levels of these transmitter substances by utilizing new developments and methodology in the behaving animal. Utilizing new developments in methodology, it is possible to measure the release of amines into perfusates obtained from specific sites in the brain of the rat under basal and evoked conditions without prior purification or concentration.

The role of arginine vasopressin in alcohol dependence and withdrawal.

The development and maintenance of tolerance to the physiological and behavioral effects of repeated exposure to ethanol can be altered markedly by the presence of arginine vasopressin (AVP). In addition, AVP has been implicated in the etiology of convulsions, including those induced by exposure to high ambient temperatures. In light of these findings, experiments were conducted to determine the role, if any, that AVP might play in the pathogenesis of alcohol-withdrawal convulsions.

Perfusion of vasopressin within the ventral septum of the rabbit suppresses endotoxin fever.

The antipyretic action of arginine vasopressin (AVP), administered into a lateral cerebral ventricle or directly into the brain tissue via push-pull perfusion, was investigated in conscious New Zealand White rabbits. Administration of AVP into a lateral cerebral ventricle (ICV) was ineffective in reducing an endotoxin-induced fever and did not alter body temperature in the afebrile rabbit. Control push-pull perfusions with the carrier vehicle were without effect on endotoxin fevers or normal body temperature.

Perfusion of vasopressin within the rat brain suppresses prostaglandin E-hyperthermia.

These experiments were undertaken to determine whether arginine vasopressin (AVP) could suppress a prostaglandin hyperthermia and to localize sites of these actions in the rat. Prostaglandin E2 (PGE2) sensitive sites were localized in the ventral-septal area by microinjecting 200 ng/0.5 microliter of prostaglandin E2.

Aspartate and glutamate as synaptic transmitters of parallel visual cortical pathways.

Push-pull cannulae were inserted into both medial and lateral banks of the suprasylvian sulcus and used for local perfusion with artificial extracellular fluid (aECF). Electrical stimulations of regions of cortex projecting to the lateral suprasylvian area (LSA) were accompanied by enhanced levels of release of excitatory amino acids. Electrical stimulation of the area 17/18 border evoked a greater release of aspartate relative to glutamate in the medial bank of the LSA (posteromedial lateral suprasylvian: PMLS), of glutamate over aspartate in the lateral bank (posterolateral lateral suprasylvian: PLLS) while in the fundus, both were released equally or glutamate levels were slightly elevated over those of aspartate.

Vasopressin: its role in antipyresis and febrile convulsion.

When pyrogenic substances are injected intravenously into experimental animals, a sequence of events is set in motion which involves the hypothalamus and perhaps other portions of the diencephalon to produce a febrile response. We now present evidence that the brain produces its own endogenous antipyretic which may serve as a means of controlling the extent of the fever. When arginine vasopressin is perfused through the lateral septal area of the hypothalamus of the sheep, fever is suppressed.

Peptide neurohormones: their role in thermoregulation and fever.

The neural elements of the rostral diencephalon in the mammal have been implicated in the regulation of body temperature. Moreover, it may be the neural elements within this region of the brain which activate the febrile mechanisms in response to pyrogen. Is it possible that the neuropeptides located within this area of the brain serve as neurochemical intermediaries involved in temperature regulation, fever, and (or) antipyresis? Central administration of several neuropeptides can elicit marked changes in the core temperature of an animal.

Alcohol drinking induced in the monkey by tetrahydropapaveroline (THP) infused into the cerebral ventricle.

In the female macaque monkey acclimated to a primate chair, Collison cannulae were stereotaxically implanted bilaterally in the lateral cerebral ventricle. The voluntary self-selection of ethyl alcohol versus water was determined repeatedly during a series of 12-day test sequences in which the concentration of the alcohol solution offered to the primate was increased systematically over 12 successive days from 3% to 30%. Following control preference sequences, the dopamine-dopaldehyde condensation product, tetrahydropapaveroline (THP), was infused daily in each monkey's cerebral ventricle (ICV) in a volume of 200-400 microliter.