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PubMedDate not supplied

Effects of antiepileptic drugs on GABA responses and on reduction of GABA responses by PTZ and DMCM on mouse neurons in cell culture.

The mechanisms of action of antiepileptic drugs effective against generalized absence seizures (antiabsence AEDs) remain uncertain. Antiabsence AEDs are generally effective against seizures induced in experimental animals by pentylenetetrazol (PTZ) and methyl-6,7-dimethoxy-4-ethyl-beta-carboline-3-carboxylate (DMCM), drugs which reduce GABAergic inhibition. Thus, antiabsence AEDs have been suggested to enhance GABAergic inhibition. We studied the effects of several AEDs on GABA responses recorded from mouse spinal cord neurons grown in primary dissociated cell culture. Four antiabsence AEDs were included: ethosuximide (ESM), dimethadione (DMO), sodium valproate (VPA), and diazepam (DZP). Two experimental AEDs, CGS 9896 and ZK 91296, with anticonvulsant action against PTZ- or DMCM-induced seizures were also included. Possible effects of the antiabsence and experimental AEDS on PTZ- and DMCM-induced inhibition of GABA responses were also evaluated. PTZ and DMCM reversibly reduced GABA responses in a concentration-dependent manner. PTZ completely inhibited GABA responses at 10 mM (IC50 of 1.1 mM), whereas DMCM-induced inhibition of GABA responses reached a plateau level of 39% of control values at 1 microM (IC50 of 33 nM). ESM (1,200 microM), DMO (6 mM), VPA (200 microM), CGS 9896 (2 microM), and ZK 9896 (2 microM) did not alter GABA responses. DZP enhanced GABA responses in a concentration-dependent manner. The inhibition of GABA responses produced by PTZ 1 mM was unaltered by ESM (600 microM), DMO (6 mM), CGS 9896 (1 microM), or ZK 9896 (1 microM). Coapplication of VPA (200 microM) and PTZ (1 mM) slightly enhanced the PTZ effect. DZP (greater than 10 nM), however, reversed the PTZ-induced reduction of GABA responses.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

Chemosensory responses of Acanthamoeba castellanii: visual analysis of random movement and responses to chemical signals.

A visual assay slide chamber was used in conjunction with time-lapse videomicroscopy to analyze chemotactic behavior of axenically grown Acanthamoeba castellanii. Data were collected and analyzed as vector scatter diagrams and cell tracks. Amebas responded to a variety of bacterial products or potential bacterial products by moving actively toward the attractant. Responses to the chemotactic peptide formyl-methionyl-leucyl-phenylalanine (fMLP), lipopolysaccharide, and lipid A were statistically significant (P < or = 0.03), as was the response to fMLP benzylamide (P < or = 0.05). Significant responses to cyclic AMP, lipoteichoic acid, and N-acetyl glucosamine were also found. Chemotactic peptide antagonists, mannose, mannosylated bovine serum albumin, and N-acetyl muramic acid all yielded nonsignificant responses (P > 0.05). There was no single optimal concentration for response to any of the attractants tested, and amebas responded equally over the range of concentrations tested. Pretreatment of amebas with chemotactic peptides, bacterial products, and bacteria reduced the directional response to attractants. Amebas that had been grown in the presence of bacteria appeared more responsive to chemotactic peptides. Treatment of amebas with trypsin reduced the response of cells to chemotactic peptides, though sensitivity was restored within a couple of hours. This suggests the ameba membrane may have receptors, sensitive to these bacterial substances, which are different from the mannose receptors involved in binding bacteria to the membrane during phagocytosis. The rate of movement was relatively constant (ca. 0.40 microns/s), indicating that the locomotor response to these signals is a taxis, or possibly a klinokinesis, but not an orthokinesis. Studies of the population diffusion rate in the absence of signals indicate that the basic population motility follows the pattern of a Levy walk, rather than the more familiar Gaussian diffusion. This suggests that the usual mathematical models of ameboid dispersion may need to be modified.

Acanthamoeba↗

PubMed2001

Factors predicting interferon treatment response in patients with chronic hepatitis c: late viral clearance does not preclude a sustained response.

OBJECTIVES: Because of the suboptimal efficacy, cost, and adverse effects of interferon in chronic hepatitis C (HCV), predictors have been sought to detect patients with a good treatment response. Also, markers for determining a poor response early in the course of therapy, such as the lack of early viral clearance, have been proposed. METHODS: Ninety-seven patients with chronic hepatitis C were enrolled to receive leukocyte alpha-interferon according to a stepped-care management protocol. The final virological treatment response was evaluated in 74 patients after a 6-month post-treatment follow-up. The relationship between pretreatment and during-treatment variables and the long-term response was assessed. RESULTS: Non-1 viral genotype, higher pretreatment ALT levels, and lower gamma-glutamyl transferase (GGT)/ALT ratios and GGT as well as younger age were significantly associated with a sustained response; a trend was also detected for lower serum ferritin levels. Normalization of ALT by 3 months was also a significant predictor of a long-term response. Of the 27 patients carrying the HCV genotype 3a, seven (26%) were still HCV RNA positive at 6 months. Of these patients, however, five (19%) still achieved a sustained virological response after treatment for up to 12 months. CONCLUSIONS: In contrast to some previous reports, our results suggest that a late viral clearance after 6 months of interferon monotherapy may not preclude a favorable long-term response after a 12-month treatment, especially in patients carrying a non-1 HCV genotype. A low pretreatment GGT/ALT ratio is a predictor of a good treatment response.

Adolescent↗

PubMed1983

Pattern-evoked responses and luminance-evoked responses in the human electroretinogram.

Electrical potentials were recorded from the cornea of the human eye in response to the onset and offset of square-wave stripe patterns varying in spatial frequency, luminance and contrast. Under high retinal illumination (50119 photopic td) the response to pattern onset was a positive wave (pattern-onset wave) followed by a negative after-potential. As long as the pattern was presented, a steady potential of positive polarity (plateau potential) was observed. The response to pattern offset was a biphasic negative-positive wave followed by a negative after-potential. A comparison between wave forms obtained with pattern onset-offset stimuli and luminance increase-decrease stimuli suggests: (a) the pattern-onset wave is the result of an interaction between a luminance-increase and a luminance-decrease response; (b) the plateau potential is mainly an additive superposition of two receptor processes originating from retinal areas that receive increases and decreases in local luminance; (c) the negative-positive potential is an a-wave and a b-wave originating from retinal areas that receive increases in local luminance. The amplitude of the pattern-onset wave was greatest at a spatial frequency around 3-4 c/deg. This behaviour was closely correlated with contrast sensitivity determined psychophysically by previous investigators. Therefore, the pattern-onset wave seems to be a pattern-evoked response. The amplitude of the b-wave following pattern offset showed a monotonic decrease with increasing spatial frequency. It is mainly a luminance-evoked response. Under low retinal illumination (457 photopic td) the pattern-onset wave and the b-wave at pattern offset were smaller. However, the pattern-onset wave had its maximum amplitude at a lower spatial frequency. When increases or decreases in space-average luminance were combined with pattern onset or offset, transitions between pattern- and luminance-evoked responses could be observed. The results suggest that a decrease in local luminance is the essential stimulus for evoking a pattern-related response while increases in local light intensity generate luminance-evoked responses.

Cornea↗

PubMed1998

Intestinal immune responses to an inactivated oral enterotoxigenic Escherichia coli vaccine and associated immunoglobulin A responses in blood.

An inactivated oral enterotoxigenic Escherichia coli (ETEC) vaccine against ETEC diarrhea was given to 25 adult Swedish volunteers. The vaccine consisted of formalin-killed E. coli bacteria expressing the most common colonization factor antigens (CFAs), i.e., CFA/I, -II, and -IV, and recombinantly produced cholera B subunit (CTB). Immunoglobulin A (IgA) antibody responses in intestinal lavage fluid to CTB and CFAs were determined and compared with corresponding responses in stool extracts and serum as well as with IgA antibody-secreting cell (ASC) responses in peripheral blood. Two doses of vaccine induced significant IgA responses to the different CFAs in lavage fluid in 61 to 87% of the vaccinees and in stool in 38 to 81% of them. The most frequent responses were seen against CFA/I. The magnitudes of the antibody responses against CTB and CFA/I in stool correlated significantly (CTB, P < 0.01; CFA/I, P < 0. 05) with those in intestinal lavage. Intestinal lavage responses against CFAs were best reflected by the ASC responses, with the sensitivity of the ASC assay being 80 to 85%, followed by stool (sensitivity of 50 to 88%) and serum antibody (sensitivity of 7 to 65%) analyses. CTB-specific immune responses were seen in >90% of the vaccinees in all assays.

Administration, Oral↗

PubMed1976

Glucose disappearance rate, insulin response and growth hormone response in the small for gestational age and premature infant of very low birth weight.

The purpose of the present investigation was to study the disappearance rate of intravenously administered glucose, plasma insulin, plasma growth hormone (GH) and their responses to an intravenous glucose load in 29 infants who were small for gestational age (SGA). The findings were compared to those in 19 premature babies of similar birth weight who were appropriate for gestational age (AGA); in all the weights were below 2,000 g. The babies were divided in two groups according to their age when tested, at less than 24 and 25-48 h. SGA infants cleared glucose more rapidly than AGA infants (p less than 0.01) whose clearance rates were similar to those previously reported in normal full-size and full-term newborns. Arterial insulin values before glucose loading were similar in all groups. The insulin response to glucose was poor in both SGA and AGA infants, but there was no significant difference between these two groups of infants. The response in the two groups at 24 and 25-48 h was similar. In 8 SGA babies insulin response was studied shortly after glucose injection to determine beta-cell release, but there was no significant difference of insulin level before and after glucose administration. In 5 AGA and 8 SGA babies insulin response was studied simultaneously in portal vein and aorta. In AGA babies the insulin response was completely different in the two vessels with a high response in the vein; on the contrary, in SGA infants response was variable. Growth hormone levels were high before test in SGA and AGA; after a glucose load the plasma GH levels increase, but the response was identical in SGA and AGA.

Birth Weight↗

PubMed1997

Lipopolysaccharide depresses cardiac contractility and beta-adrenergic contractile response by decreasing myofilament response to Ca2+ in cardiac myocytes.

Lipopolysaccharide (LPS) plays a key role in the pathogenesis of sepsis. Cardiac function and the inotropic response to beta-adrenergic stimulation are impaired in sepsis. We hypothesized that LPS, in clinically relevant levels (1 ng/mL), directly depresses contractility and beta-adrenergic responses in cardiac myocytes. Cardiac myocytes were isolated from the left ventricle of adult rabbits using digestive enzymes (collagenase and protease). We depyrogenated the enzymes (LPS contamination lowered from 100 to 300 ng/mL to < 0.7 ng/mL) to minimize development of LPS tolerance during cell isolation. After 6 hours of incubation with 1 ng/mL LPS, there was a decrease in the extent of active cell shortening with no change in Ca2+ transients (measured with indo 1 fluorescence), indicating decreased myofilament responsiveness to Ca2+. This was related to NO pathways, since cGMP (a second messenger of NO) increased in cardiac myocytes and LPS effects were completely reversed with a 1 mmol/L NG-monomethyl-L-arginine (L-NMMA, a NO synthase inhibitor). LPS did not alter the intracellular Ca2+ response to beta-adrenergic stimulation with isoproterenol but attenuated the contractile response (maximal cell shortening, 15.5 +/- 1.0% versus 23.3 +/- 1.1% in control myocytes; P < .001). LPS attenuation of the contractile response to isoproterenol was restored completely by L-NMMA and almost completely restored (to 86% of the control response) by an inhibitor of cGMP-dependent protein kinase. We conclude that LPS depresses cardiac contractility and the contractile response to beta-adrenergic stimulation by a NO-cGMP-mediated decrease in myofilament responsiveness to Ca2+. The direct effects of low levels of LPS on cardiac myocytes may contribute to cardiac depression and hemodynamic decompensation during sepsis.

Actin Cytoskeleton↗

PubMed1991

Allergen-induced asthmatic responses. Relationship between increases in airway responsiveness and increases in circulating eosinophils, basophils, and their progenitors.

The inflammatory response during allergen-induced asthma was assessed using serial measures of peripheral blood eosinophils (Eo), basophils (B), and Eo/B progenitor cells (Eo/B-CFU). A group of 14 stable asthmatic individuals (beta 2-agonists only as needed) had inhalation provocation tests with allergen (18 tests in total) and with diluent. Serial blood samples were taken before and 1 and 24 h after the tests; methylcellulose cultures for Eo/B-CFU and granulocyte-macrophage (GM-CFU) were scored at 14 days. Circulating Eo, B, and Eo/B-CFU were increased at 24 h after allergen inhalation when this resulted in increased histamine airway responsiveness (n = 13). In the 5 subjects with isolated early asthmatic responses the Eo, B, and Eo/B-CFU counts did not change. There was no change in the GM-CFU after allergen. The ratio change in circulating Eo/B-CFU was negatively correlated with baseline histamine airway responsiveness (r = -0.8, p less than 0.05). Four subjects who had an isolated early response and no blood changes to one allergen developed an increase in histamine airway responsiveness and an increase in Eo, B, and Eo/B progenitors after inhalation of a second different allergen. The results indicate that in subjects with an allergen-induced increase in histamine airway responsiveness, an inflammatory response occurs that includes an increase in the number of Eo/B progenitors. This response, possibly mediated by Eo/B growth and differentiation factors, could lead to the accumulation of these cells in the airway and contribute to the airways inflammation present in asthma.

Allergens↗

PubMed1992

Increase in airway responsiveness and effect of deep inhalation on airway caliber in allergen-induced asthma. Relationship to the late-phase response.

The airway responsiveness to methacholine (MCh) and the effect of deep inhalation (DI) on airway caliber were determined in 18 asthmatic patients at baseline and 3 and 24 h after an allergen inhalation challenge. The dose of MCh causing a 20% fall of FEV1 (PD20) was used as an index of airway responsiveness; the ratio of forced expiratory flow at 40% of FVC from maximal and partial flow/volume curves (MEF40M/P) was used to assess the effect of DI on airway caliber. Thirteen patients showed a dual asthmatic response (DAR) to allergen, 5 patients an isolated early-phase asthmatic response (EAR). In the DAR patients, 3 h after allergen challenge, when the early-phase response had resolved and the late-phase response had yet to develop, MChPD20 (geometric mean) was reduced from 202 to 71 micrograms (P less than 0.001) whereas MEF40M/P at the MCh end point was unchanged (p greater than 0.4). Twenty-four hours after allergen challenge, when late-phase response had developed, MChPD20 was further reduced to 51 micrograms (p less than 0.02), and this reduction was accompanied by a decrease of MEF40M/P at the MCh end point (p less than 0.01). In the EAR patients, neither MChPD20 nor MEF40M/P was significantly changed at any time during the study. We conclude that most of the increase in airway responsiveness that follows acute exposure to allergen precedes the late-phase response and is not determined by the same mechanisms that impair the ability of the lung to dilate airways with a DI.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗

PubMed1979

Prostaglandin E modulation of the mitogenic response of human T cells. Differential response of T-cell subpopulations.

Prostaglandins (PG) of the E series, PGE(1) and PGE(2) (PGEs), can induce elevations of intracellular cyclic AMP (cAMP) among thymus-derived (T) lymphocytes (T cells) and inhibit their reactivity. For example, 0.1 muM of PGEs induces a two- to threefold increase of intracellular cAMP among human peripheral blood T cells and a 20-30% suppression of their blastogenic response to phytohemagglutinin. However, this suppression actually represents the net reactivity of T-cell populations demonstrating quite different responses to PGEs. Fractionation of T-enriched populations on a discontinuous density gradient yields a population of high density cells whose phytohemagglutinin-induced blastogenic response is suppressed 60%; a population of intermediate density cells whose response is suppressed 20%; and a population of low density T cells whose response is not suppressed, but is enhanced 20% by both of the PGEs. The diametrically opposite responses of low and high density T cells to the PGEs is not related to any difference in their intrinsic mitogen reactivity nor is it influenced by interactions with other T cells, bone marrow-derived (B) cells, or monocytes. Moreover, the distinct blastogenic response of low and high density T cells to PGEs does not simply correlate with PGE-mediated activation of adenylate cyclase. PGE(2) induced comparable absolute and identical relative increases of intracellular cAMP among the low and high density T cells. Cholera toxin, a potent activator of adenylate cyclase, and exogenous 8-bromo cAMP mimicked the effects of the PGEs on these two T-cell populations. These data demonstrate that T cells are heterogeneous with regard to their response to the PGEs. Thus, PGEs should be considered as potential regulators rather than as universal suppressors for T-cell reactivity. Moreover, the effect of PGEs on the blastogenic response of a given T-cell population depends upon intracellular events which occur subsequent to elevations of cAMP.

Cell Count↗

PubMed2000

The effects of some antidepressant drugs on prepulse inhibition of the acoustic startle (eyeblink) response and the N1/P2 auditory evoked response in man.

Both the acoustic startle (eyeblink) response and the N1/P2 complex of the auditory evoked potential can be suppressed by presentation of a brief low-intensity stimulus 30-500 ms before the 'startle-eliciting' stimulus ('prepulse inhibition', PPI). We examined the effects of three antidepressants on PPI of these two responses. Fifteen males (19-30 years) participated in four weekly sessions, in which they received placebo, amitriptyline (100 mg), fluvoxamine (100 mg), and reboxetine (4 mg) (p.o.), according to a balanced double-blind design. Twenty minute simultaneous recordings of electromyographic (EMG) responses of the orbicularis oculi muscle of the right eye and vertex auditory evoked potentials were carried out 195 min after drug ingestion. Sound stimuli (1 kHz) were presented in 40 trials separated by variable intervals (mean 25 s): (1) 40 ms, 115 dB ('pulse alone', 20 trials) and (2) 40 ms, 85 dB, followed after 120 ms by 40 ms, 115 dB ('prepulse/pulse', 20 trials). Under the placebo condition, both the EMG response and the N1/P2 complex showed >50% PPI. Fluvoxamine and reboxetine did not significantly alter the amplitude or PPI of either response. Amitriptyline significantly reduced the amplitudes of both responses; it had no effect on PPI of the EMG response, but significantly attenuated PPI of the N1/P2 complex. Amitriptyline also reduced arousal, as indicated by an increase in power of low-frequency electroencephalographic waves. The results confirm the susceptibility of the N1/P2 complex to PPI. The reduction of the amplitudes of the EMG response and N1/P2 complex by amitriptyline may be related to its sedative action. The differential effect of amitriptyline on PPI of the N1/P2 complex supports the suggestion that different mechanisms may be involved in PPI of this response and PPI of the N1/P2 complex.

Administration, Oral↗

PubMed2004

Effects of quetiapine and haloperidol on prepulse inhibition of the acoustic startle (eyeblink) response and the N1/P2 auditory evoked response in man.

Contraction of the orbicularis oculi muscle in response to a sudden loud sound (acoustic startle response) and the N1/P2 component of the auditory evoked potential are both attenuated when a brief low-intensity stimulus is presented 30-500 ms before the 'startle-eliciting' stimulus (PPI). Here, we report the effects of the 'atypical' antipsychotic drug quetiapine and the 'conventional' antipsychotic haloperidol on these responses. Sixteen males (aged 19-38 years) participated in four sessions at 7-day intervals, in which they received quetiapine 12.5 mg, quetiapine 25 mg, haloperidol 3 mg and placebo, according to a balanced double-blind design. Electromyographic (EMG) responses of the orbicularis oculi muscle and N1/P2 auditory evoked potentials were recorded in a 20-min session, 2 h after treatment. Subjects received 40 trials in which 1-kHz sounds were presented: (i) 40 ms, 115 dB ('pulse alone' trials) and (ii) 40 ms, 85 dB, followed after 120 ms by 40 ms, 115 dB ('prepulse/pulse' trials). Mean amplitudes of the EMG response and the N1/P2 potential were derived from the pulse-alone trials and, in each case, percentage PPI was calculated. Serum prolactin was measured after each treatment, and autonomic (heart rate, blood pressure, salivation) and psychological (visual analogue self-ratings of mood and alertness, critical flicker fusion frequency) measures were taken before and after each treatment. Quetiapine 12.5 mg and 25 mg significantly reduced the amplitude of the EMG response without altering its inhibition by prepulses; haloperidol had no effect on EMG response amplitude or PPI. Neither drug affected N1/P2 amplitude or PPI of this response. Quetiapine, but not haloperidol, reduced subjective alertness and critical flicker fusion frequency. Haloperidol, but not quetiapine, elevated serum prolactin level. The ability of quetiapine to attenuate the startle response may reflect its sedative action.

Acoustic Stimulation↗

PubMed1995

Retinoid-X receptor (RXR) differentially augments thyroid hormone response in cell lines as a function of the response element and endogenous RXR content.

Retinoid-X receptor (RXR) forms heterodimers with thyroid hormone receptor (TR) and significantly enhances binding to thyroid hormone response elements (TREs). Expression of RXR in a transient transfection assay augments the T3 response, but the influences of the specific cell line and TRE used have not been systematically studied. We determined RXR alpha and -beta augmentation of the TR alpha-mediated T3 response in transient transfection assays of COS, JEG, and mouse embryonic stem (ES) cell lines for a series of eight wild-type thyroid hormone (T3) and retinoic acid response elements (previously shown to bind TR). RXR augmented T3-induced expression in COS and ES cells (1.5- to 4-fold greater expression with added RXR compared to TR alone), but had minimal effect on augmentation of response in JEG cells. For most elements studied there was a proportional augmentation of basal and T3-stimulated expression. TREs from rat GH and laminin-B1, however, had relatively higher levels of T3-induced expression as a result of RXR cotransfection (T3 induction ratios increased 2-fold or greater). Previous characterization of these elements demonstrates that they contain more than two hexameric binding domains, all of which can simultaneously bind TR. The influence of endogenous RXR expression in a cell line on RXR augmentation of the T3 response was determined. RXR alpha and -beta messenger RNA (mRNA) expression was quantitated by Northern blot in each cell line. COS and JEG cells expressed almost exclusively RXR alpha mRNA, although expression was almost 2-fold higher in JEG compared to COS cells (12 +/- 2.5 vs. 6.8 +/- 0.5 density units relative to actin; mean +/- SE; P < 0.05). ES cells expressed only RXR beta mRNA, but at a very low level (0.4 +/- 0.1). Nuclear extracts prepared from JEG and COS cells augmented TR binding proportional to the endogenous RXR mRNA expression, and the heterodimer band was supershifted by the addition of antibody to RXR alpha. Nuclear extracts from ES cells had no detectable TR heterodimer binding to a range of response elements. RXR augmentation of the T3 response differs among cell lines and is greater in those with reduced endogenous RXR. Furthermore, the functional augmentation of the T3 response ratio by RXR is likely to require additional sequences contained in only a subset of elements in which RXR augments TR binding.

Animals↗

PubMed1983

Gonadotropin responses to gonadotropin-releasing hormone and prolactin responses to thyrotropin-releasing hormone and metoclopramide in women with amenorrhea and insulin-treated diabetes mellitus.

Gonadotropin responses to GnRH and PRL responses to TRH and metoclopramide (MTC) were investigated in nine consecutive women with amenorrhea and insulin-treated diabetes mellitus. Nine normal menstruating diabetic women, 12 normal women in the early follicular phase, and nine consecutive nondiabetic women with functional amenorrhea served as controls. No significant differences were found in relation to diabetes regulation within the two diabetic groups. Amenorrheic patients with diabetes mellitus had significantly lower basal PRL levels than normal women and estradiol levels compared to the other groups. Basal plasma LH concentrations were significantly lower in women with amenorrhea and diabetes mellitus than in nondiabetics with amenorrhea, whereas plasma FSH levels were similar in all groups. The LH response to GnRH was significantly lower in amenorrheic patients with diabetes mellitus than in normal women, and a significant correlation (r = 0.81, P less than 0.01) was found between the LH response to GnRH and the basal estradiol level in these women. The FSH response to GnRH and the PRL response to TRH were similar in all groups. Amenorrheic diabetics had significantly lower PRL responses to MTC compared to other groups, and nondiabetics with amenorrhea had significantly lower PRL response than normal women. It is concluded that diabetic patients with functional amenorrhea have low basal and MTC-stimulated PRL levels, low basal LH levels, and decreased LH response to GnRH despite low estrogen levels. These hormonal changes may in part be caused by a raised central dopaminergic activity leading to a depression of pituitary ovulatory mechanisms.

Adult↗

PubMed1997

Individual differences in alcohol responsivity: physiological, psychomotor and subjective response domains.

OBJECTIVE: Psychometrically stable measures of individual differences in response to consuming alcohol were developed as part of an ongoing project investigating "high-tolerant" drinking drivers. The derived measures were correlated with diagnostic criteria of alcohol abuse and dependence, as well as drinking frequency, heavy drinking and tolerance estimations. METHOD: Male subjects (N = 94), 21 to 59 years old, participated in each of two identical alcohol consumption sessions (mean dose = 0.78 g/kg). Multiple response measures obtained before and after drinking (mean BAC = 78 mg/dl, descending) were used to compute postconsumption regression residuals that were factor analyzed. RESULTS: Factors reflecting psychomotor, subjective and physiological responsivity to alcohol were extracted. Confirmatory factor analyses indicated consistent psychomotor and physiological factor structures across the two testing sessions, but a bifurcation of the subjective measures. Test-retest correlations of the responsivity residuals indicated medium to moderately large effect sizes (mean = .32, range = .15-.51). Residuals summated within each response domain indicate moderate internal consistency (mean = .56, range = .45-.72) and higher reliabilities than single measure indices (range = .53-.59). Summated residuals within the response domains suggest diminished responsivity is associated with more severe alcohol-use diagnoses and were differentially predictive of self-reported drinking practices. CONCLUSIONS: Alcohol responsivity is multidimensional. Individual differences across different domains can be measured reliably and are associated with different patterns of alcohol use and abuse. Greater attention should be given to the specific domain of alcohol responsivity measures obtained in past and future research that relates individual differences to alcohol-related problems.

Adult↗

PubMed1992

Further characterization of the steroidogenic responsiveness of purified zona fasciculata/reticularis cells from bovine adrenal cortex before and after primary culture: changing responsiveness to phosphoinositidase C agonists.

When bovine adrenocortical cells from the zona fasciculata/reticularis (zfr) are maintained in primary culture, cortisol secretion in response to acute stimulation with ACTH and adrenaline (which activate adenylate cyclase) is seen to increase steadily over the first 48 h, while secretion in response to angiotensin II and acetylcholine (which activate phosphoinositidase C) shows an initial decline in the first 24 h and a recovery to maximum after 48 h. We have investigated whether these discrepant changes in cortisol secretory response to the different agonists are due to changes in formation of the associated second messengers (cAMP or inositol phosphates), or altered coupling of these second messenger signals to steroid secretion. Increases in steroid secretion in response to ACTH and adrenaline were paralleled by increased cAMP. Steroid secretion in response to exogenous 8-bromoadenosine 3':5'-cyclic monophosphate also increased steadily during this 48-h period. Thus increased responsiveness was due to both increased second messenger formation and increased coupling to the steroid secretory response. The decreased steroid secretory response to angiotensin and acetylcholine after 24 h, and subsequent recovery after 48 h in culture, were accompanied by an increased formation of phosphoinositols after 24 h and a further increase by 48 h. However, the steroid secretory response to a combination of calcium ionophore and the protein kinase C activator, phorbol 12-myristate 13-acetate, was reduced after 24 h and recovered by 48 h of culture. Fura-2-loaded cells also showed an increase in intracellular [Ca2+] after 24 h in culture.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2002

Influence of sex and gonadal status of sheep on cortisol secretion in response to ACTH and on cortisol and LH secretion in response to stress: importance of different stressors.

There are sex differences in the response to stress and in the influence of stress on reproduction which may be due to gonadal steroids but the nature of these differences and the role of the gonads are not understood. We tested the hypotheses that sex and the presence/absence of gonads (gonadal status) will influence the cortisol response to injection of ACTH, insulin-induced hypoglycaemia and isolation/restraint stress, and that sex and gonadal status will influence the secretion of LH in response to isolation/restraint stress. Four groups of sheep were used in each of three experiments: gonad-intact rams, gonadectomised rams, gonad-intact ewes in the mid-luteal phase of the oestrous cycle and gonadectomised ewes. In Experiment 1 (n=4/group), jugular blood samples were collected every 10 min for 6 h; after 3 h, two animals in each group were injected (i.v.) with ACTH and the remaining two animals were injected (i.v.) with saline. Treatments were reversed 5 days later so that every animal received both treatments. Experiment 2 (n=4/group) used a similar schedule except that insulin was injected (i.v.) instead of ACTH. In Experiment 3 (n=5/group), blood samples were collected every 10 min for 16 h on a control day and again 2 weeks later when, after 8 h of sampling, all sheep were isolated and restrained for 8 h. Plasma cortisol was significantly (P<0.05) elevated following injection of ACTH or insulin and during isolation/restraint stress. There were no significant differences between the sexes in the cortisol response to ACTH. Rams had a greater (P<0.05) cortisol response to insulin-induced hypoglycaemia than ewes while ewes had a greater (P<0.05) cortisol response to isolation/restraint stress than rams. There was no effect of gonadal status on these parameters. Plasma LH was suppressed (P<0.05) in gonadectomised animals during isolation/restraint stress but was not affected in gonad-intact animals, and there were no differences between the sexes. Our results show that the sex that has the greater cortisol response to a stressor depends on the stressor imposed and that these sex differences are likely to be at the level of the hypothalamo-pituitary unit rather than at the adrenal gland. Since there was a sex difference in the cortisol response to isolation/restraint, the lack of a sex difference in the response of LH to this stress suggests that glucocorticoids are unlikely to be a major mediator of the stress-induced suppression of LH secretion.

Adrenocorticotropic Hormone↗

PubMed1974

Effects of response rate, reinforcement frequency, and the duration of a stimulus preceding response-independent food.

Food-reinforced key pecking in the pigeon was maintained under a four-component multiple schedule. In two components, responding was maintained at high rates under a random-ratio schedule. In the other two components, responding was maintained at low rates under a schedule that specified a minimum interresponse time. For both high and low response rates, one of the schedule components was associated with a high reinforcement frequency and the other components with a lower reinforcement frequency. During performance under these schedules, a stimulus terminated by access to response-independent food was periodically presented. The duration of this pre-food stimulus was 5, 30, 60, or 120 sec. Changes in rate of key pecking during the pre-food stimulus were systematically related to baseline response rate and the duration of the stimulus. Both high and low response rates were increased during the 5-sec stimulus. At longer stimulus durations, low response rates were unaffected and high response rates were decreased during the stimulus. For two of three pigeons, high response rates maintained under a lower frequency of reinforcement tended to be decreased more than high response rates maintained under a higher reinforcement frequency. In general, the magnitude of decrease in high response rates was inversely related to the duration of the pre-food stimulus.

Journal Article↗