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D L Cheney

Publications and source records attributed to D L Cheney.

At least 37 records · Page 2Linked to original sources
PubMed1990

The representation of social relations by monkeys.

Monkeys recognize the social relations that exist among others in their group. They know who associates with whom, for example, and other animals' relative dominance ranks. In addition, monkeys appear to compare types of social relations and make same/different judgments about them. In captivity, longtailed macaques (Macaca fascicularis) trained to recognize the relation between one adult female and her offspring can identify the same relation among other mother-offspring pairs, and distinguish this relation from bonds between individuals who are related in a different way. In the wild, if a vervet monkey (Cercopithecus aethiops) has seen a fight between a member of its own family and a member of Family X, this increases the likelihood that it will act aggressively toward another member of Family X. Vervets act as if they recognize some similarity between their own close associates and the close associates of others. To make such comparisons the monkeys must have some way of representing the properties of social relationships. We discuss the adaptive value of such representations, the information they contain, their structure, and their limitations.

Animals↗
PubMed1988

Constant infusion of [13C6]glucose: simultaneous measurement of turnover of GABA and glutamate in defined regions of the brain of individual animals.

A new method has been developed to measure simultaneously the turnover rates of glutamate and GABA in individual areas of the brain of the rat. Rats received a constant infusion of [13C6]glucose, such that the flux of this stable isotope label through the pools of glucose, glutamate and GABA in the central nervous system (CNS) could be monitored by gas chromatography-mass fragmentography. The ratios of glucose/GABA and glucose/glutamate labelling were then used to calculate the fractional rate constants for GABA and glutamate, respectively. Using this approach, baclofen (20 mg/kg) decreased the turnover rates of both glutamate and GABA in the cerebellum, prefrontal cortex, striatum and hippocampus of the rat. In contrast, only the turnover of GABA was decreased in the septum and superior colliculus. Muscimol decreased the turnover rates of both amino acids in all regions of the brain examined. These data, therefore, provide in vivo support for the results of previous in vitro studies which indicated that cortical glutamatergic nerve endings and/or cell bodies possess inhibitory GABAB receptors. The present data further suggest that not all glutamatergic projections possess these receptors.

Amino Acids↗
PubMed1987

Antagonism of N-methyl-D-aspartate (NMDA) evoked increases in cerebellar cGMP and striatal ACh release by phencyclidine (PCP) receptor agonists: evidence for possible allosteric coupling of NMDA and PCP receptors.

A comparison was made of the actions of phencyclidine receptor agonists and N-methyl-D-aspartate (NMDA) receptor antagonists in two well-defined neurochemical test systems. These included (i) [3H]acetylcholine release from striatal cholinergic interneurons in vitro, a system known to be positively modulated by corticostriatal excitatory amino acid inputs in vivo; and (ii) cerebellar cGMP levels in vivo, an indicator of cerebellar Purkinje cell activity, which is also modulated by excitatory amino acid inputs. Using these neuronal systems, we report that phencyclidine receptor agonists demonstrated a noncompetitive antagonism of NMDA receptor agonist actions.

Acetylcholine↗
PubMed1984

On the neurotoxicity of chlordecone: a role for gamma-aminobutyric acid and serotonin.

Rats receiving the chlorinated insecticide, chlordecone (80 mg/kg i.p.), exhibit hyperexcitability, exaggerated startle response and tremors within a few hours after the injection. Since the chlordecone-elicited tremors are relieved by injections of muscarinic receptor blockers, acetylcholine has been implicated indirectly in the mechanism of chlordecone toxicity. Our studies on acetylcholine steady-state levels and turnover in several brain structures failed to detect evidence for an involvement of cholinergic presynaptic mechanisms in the chlordecone toxicity. We then investigated whether GABA is involved by measuring the rate of its accumulation following intraventricular injection of gabaculine. Chlordecone reduced the rate of GABA accumulation in striatum, but not in cerebellum, brainstem or hippocampus. Such inhibition appeared 4 h after drug injection thereby preceding the onset of tremors. Since tremors elicited by chlordecone are attenuated by the administration of serotonin receptor blockers and since chlordecone increases serotonin (5-HT) turnover, we studied whether 5-HT recognition sites are modified following chlordecone administration. We have found a reduction of the Bmax of 5-HT1 receptors in striatum and hippocampus without any modification in the kinetic characteristics of 5-HT2 receptors. We have also shown that the temporal relationship between down regulation of 5-HT1 recognition sites, reduction of striatal GABA turnover and tremors caused by chlordecone allows one to consider these 3 phenomena as reciprocally dependent. In conclusion our results favor the possibility that tremors may result from a decrease in the striatal GABergic tone which probably is elicited by an increase of serotonergic activity caused by chlordecone by a yet unknown mechanism.

Acetylcholine↗
PubMed1984

An immunohistochemical study on the location of GABAergic neurons in rat septum.

Antisera against L-glutamate decarboxylase (GAD), the synthesizing enzyme of gamma-aminobutyric acid (GABA) were used to locate GABAergic neurons and nerve terminals in the septal complex of the rat by using the peroxidase-antiperoxidase method. Varying densities of immunoreactive terminals were observed in saline-treated rats but nerve cell bodies were only demonstrated after interventricular or intraseptal injections of colchicine. Small and medium-sized GAD-positive neurons were found in lateral septal nuclei, the largest number of these cells being in the pars dorsalis, and in the bed nucleus of the stria terminalis. Several GAD-immunoreactive neurons were located in the medial septal nucleus and the nucleus of the diagonal band of Broca (DB), where the cells were larger in the ventral than dorsal parts of the region. In the medial septal nucleus and in DB the GAD-positive cell bodies were distributed similarly to cholinergic neurons. Large GAD-positive neurons were also found in the septofimbrial nucleus. Intense immunoreactivity in nerve terminals was observed in the lateral septal nucleus, around the island of Calleja magna, between the DB and nucleus accumbens, and in the septofimbrial and triangular septal nuclei. In contrast, the medial septal nucleus, the DB, and the bed nucleus of the stria terminalis only showed weak to moderate immunoreactivity. These results provide direct morphological evidence for the presence of neurons capable of synthesizing GABA in septal nuclei. We suggest that there are two different GABAergic neuronal systems operating in the septum: a population of small cells in the lateral septal nucleus and a group of large cells in the medial septum and DB.

Animals↗
PubMed1984

In vitro characterization of agonist, antagonist, inverse agonist and agonist/antagonist benzodiazepines.

The efficacy of coupling between the benzodiazepine receptor and chloride channel as well as the coupling to the GABA receptor is differentially affected by different benzodiazepine ligands. In general, the order of efficacy with regard to allosteric effects of benzodiazepine ligands on the chloride channel ([35S]TBPS) and GABA receptor ([3H]muscimol), is: agonist greater than agonist/antagonist greater than partial agonist greater than antagonist; with inverse agonists acting in a manner opposite to the classical benzodiazepine agonists. The chloride ionophore is allosterically modulated both by benzodiazepine and GABA receptors.

Animals↗
PubMed1984

The acoustic features of vervet monkey grunts.

East African vervet monkeys give short (125 ms), harsh-sounding grunts to each other in a variety of social situations: when approaching a dominant or subordinate member of their group, when moving into a new area of their range, or upon seeing another group. Although all these vocalizations sound similar to humans, field playback experiments have shown that the monkeys distinguish at least four different calls. Acoustic analysis reveals that grunts have an aperiodic F0, at roughly 240 Hz. Most grunts exhibit a spectral peak close to this irregular F0. Grunts may also contain a second, rising or falling frequency peak, between 550 and 900 Hz. The location and changes in these two frequency peaks are the cues most likely to be used by vervets when distinguishing different grunt types.

Acoustics↗
PubMed1984

In vitro characterization of benzodiazepine receptor agonists, antagonists, inverse agonists and agonist/antagonists.

Using an extensively washed membrane preparation and standardized incubation conditions, the actions of benzodiazepine (BZ) receptor ligands were evaluated on [3H]flunitrazepam [+/- 10 microM gamma-aminobutyric acid (GABA)], [3H]muscimol (+/- 2.5 microM etazolate) and [35S]butyl bicyclophosphorothionate (TBPS) binding. Classical BZ receptor agonists stimulated [35S]TBPS binding and [3H]muscimol binding in the presence of etazolate. These agents also possessed ratios for [3H]flunitrazepam binding in the absence and presence of GABA (GABA ratio) of 2 to 5. BZ antagonists and inverse agonists had GABA ratios less than 1 and did not alter, or reduced, both [35S]TBPS and [3H]muscimol (+etazolate) binding. The nonsedating BZ agonist/antagonist agents CGS 9896, CL 218872, PK 8165 and PK 9084 all possessed GABA ratios between 1.1 and 1.4 and only stimulated [35S]TBPS and [3H]muscimol (+etazolate) binding to approximately 50% of the level of classical BZ agonists. The BZ partial agonists CGS 9895 and RU 39419 both were unique in that they possessed GABA ratios of 1 or less, stimulated [35S]TBPS binding and had no effect on [3H]muscimol binding (+etazolate). Therefore, by monitoring the major components of the BZ receptor complex (BZ receptor, GABA receptor and chloride channel), we were able to distinguish between different BZ drugs and to support suggestions that these drugs act via unique BZ receptor populations which possess differential couplings to the GABA receptor and chloride channel.

Animals↗
PubMed1983

A comparison of the analgesic activities of 4,5,6,7-tetrahydroisoxazolo[5,4-c]pyridin-3-ol (THIP) and 6-chloro-2[1-piperazinyl]pyrazine (MK 212).

Both the gamma-aminobutyric acid (GABA) mimetic, THIP (4,5,6,7-tetrahydroisoxazolo[5,4-c]pyridin-3-ol and the serotonergic agonist, MK 212 (6-chloro-2[ 1-piperazinyl ]pyrazine) are effective analgesic agents in the mouse hot plate assay. Naltrexone, however, fails to reverse the analgesia elicited by either compound. Acute injection of THIP potentiates the morphine analgesia and chronic administration of THIP produces a functional tolerance to its analgesic effects. MK 212 antagonizes the analgesia induced by either morphine or THIP. These results support the postulate that GABAergic and serotonergic synapses represent two synaptic mechanisms which participate in the modulation of pain threshold in a manner that is independent from opioid receptors. Moreover, GABA and serotonin appear to be able to modulate opioid-mediated analgesia in an opposing manner with GABAergic mechanisms facilitating and serotonergic mechanisms inhibiting morphine-induced antinociception.

Analgesics↗
PubMed1983

The transsynaptic regulation of the septal-hippocampal cholinergic neurons.

There is not yet a complete understanding of the functional interactions among various septal nuclei which regulate hippocampal function. Nevertheless, much has been learned histologically and biochemically about the major connections of the distinct areas of the septal complex and the chemical character of some of these pathways. The cholinergic septal-hippocampal pathway serves as a well defined link between these two important structures of the limbic system. Acetylcholine turnover rates in the hippocampus have been shown to increase or decrease proportionally to the activity of the cholinergic neurons originating in the septum. Moreover, these turnover rates have been shown to be modulated by intraseptal injections of agonists or antagonists of various neurotransmitters or neuromodulators which are stored in various cell groups located in the septum. By coupling this biochemical approach with techniques to study the receptor organization, greater detail concerning the transmitter and cotransmitter interactions among the various neuromodulators can be obtained.

Acetylcholine↗
PubMed1983

Interstrain comparison of avoidance behavior and neurochemical parameters of brain cholinergic function.

Five rat strains (Long-Evans Hooded, Zivic Miller, Lewis, Buffalo and Fischer-344) were tested in a shuttlebox conditioned avoidance task and the differences in the performance levels among the strains were noted. In parallel experiments using naive rats, the acetylcholine concentrations in eight brain regions and the acetylcholine turnover rate in five brain regions were determined for these strains. Interstrain differences in these parameters were found but no correlation between avoidance performance and either of these measures was apparent in any brain region studied. In separate experiments, no differences were found in the hippocampal acetylcholine concentration or the turnover rate among good performing Hooded, poor performing Hooded or untested Hooded rats. Similarly, no differences in regional acetylcholine turnover rates were found between naive rats of the Iowa Reactive and Nonreactive strains. [3H]-QNB (quinuclidinyl benzilate) binding was studied in three brain regions in the five strains, but no large interstrain differences in binding characteristics were found. In contrast to interpretations of other workers based on less direct assay methods involving fewer strains, we conclude that no strong correlation exists between avoidance performance ability and basal levels of brain cholinergic activity.

Acetylcholine↗
PubMed1983

Simultaneous modulation of hippocampal cholinergic activity and extinction by intraseptal muscimol.

The relationship between regulation of acetylcholine metabolism in the septal-hippocampal pathway and extinction of a food reinforced lever press response was investigated by comparing the turnover rate of acetylcholine (TRACh) in the rat hippocampus with the amount of responding during extinction after intraseptal injection of the gamma-aminobutyric acid receptor agonist muscimol. Doses (0.3-3.0 nmol) which decreased the TRACh in the hippocampus also increased the responding during extinction over that of saline controls. Responding during the continuous reinforcement schedule before extinction was also increased, but to a lesser extent. Higher doses (10-30 nmol) further decreased the TRACh in the hippocampus, decreased it in the cortex and were accompanied by irregular responding and sedation. The TRACh in the hippocampus was also measured in drug-free rats undergoing extinction after training on a continuous reinforcement or variable interval 60 sec reinforcement schedule. Although the variable interval 60 sec reinforcement schedule rats responded more than the continuous reinforcement rats during extinction, there were no differences between the TRACh in the hippocampus. The present results indicate that the decrease in the hippocampal TRACh which is produced by intraseptal muscimol is accompanied by an increase in the response rate during extinction, but that operantly induced differences in this behavior are not accompanied by detectable changes in hippocampal TRACh.

Acetylcholine↗
PubMed1982

The dimethylheptyl derivative of (-)-delta 8-tetrahydrocannabinol reduces the turnover rate of gamma-aminobutyric acid in the septum and nucleus accumbens.

Accumulating evidence suggests that the cannabinoids exert their action to reduce the turnover rate of acetylcholine in the hippocampus by an action in the septum via inhibitory gamma-butyric acid (GABA) containing interneurons. In the studies presented here administration of the potent dimethylheptyl derivative of (-)-delta-tetrahydrocannabinol, which has previously been shown to reduce the turnover rate of acetylcholine in the hippocampus, reduces the turnover rate of GABA in the septum. A simple model in which cannabinoids transsynaptically activate inhibitory GABAergic septal neurons impinging on cholinergic septal neurons does not explain the data. A more complex model suggesting that inhibitory GABAergic septal interneurons innervate other inhibitory GABAergic septal interneurons has been hypothesized.

Acetylcholine↗
PubMed1982

Neuronal location of N6-cyclohexyl[3H]adenosine binding sites in rat and guinea-pig brain.

N6-cyclohexyl[3H]adenosine, ([3H]CHA), was used to label adenosine A1 receptors in crude synaptic membranes prepared from rat and guinea pig brain. The density of [3H]CHA binding sites was highest in the rat hippocampus and cerebellum and in the guinea-pig hippocampus. A micro-dissection of coronal sections of guinea-pig hippocampus revealed that the specific binding capacity for [3H]CHA in area CA-1 was 20-30% higher than in area CA-3, dentate gyrus and subiculum. Selective neuronal lesions of serotonergic, noradrenergic and cholinergic afferents to the hippocampus failed to alter [3H]CHA binding to hippocampal membranes. These results suggest that [3H]CHA binding sites are not associated with axons or terminals of these neurones in the hippocampus. Intrahippocampal injection of kainic acid reduced the number of [3H]CHA recognition sites by 30% with no alteration in the affinity of [3H]CHA for these receptors. Thus, a significant portion of A1 receptors may be associated with intrinsic neurones of the hippocampus which do not appear to be innervated by noradrenergic, cholinergic or serotonergic axons.

Adenosine↗
PubMed1982

Increase in exogenous choline fails to elevate the content or turnover rate of cortical, striatal, or hippocampal acetylcholine.

The present experiments were designed to test whether increasing the availability of choline to rat brain increases the rate of acetylcholine synthesis in that organ. The content of choline and acetylcholine and the turnover rate of acetylcholine in striatum, hippocampus, and cerebral cortex were measured following changes in dietary choline, intraperitoneal choline, or intravenous infusion of choline. Increasing plasma choline caused some increase in tissue choline but did not increase acetylcholine levels nor acetylcholine turnover rate in any of the areas of brain studied. Indeed, in hippocampus, choline decreased the turnover rate of acetylcholine.

Acetylcholine↗
PubMed1982

Inhibition of acetylcholine turnover rate in rat hippocampus and cortex by intraventricular injection of adenosine analogs.

The effects of i.c.v. administration of adenosine receptor agonists and antagonists on the turnover rate of acetylcholine (TRACh) in various areas of the rat brain were examined in an effort to better understand the role of adenosine as a neuromodulator or cotransmittr. TRACh was determined by gas chromatographic-mass fragmentographic analysis of the rate of deuterium incorporation into ACh and choline during a constant rate infusion of deuterated phosphorylcholine. The i.c.v. administration of the adenosine receptor agonist, 2-chloroadenosine (2-CIAdo), in a dose of 82 nmol failed to change the ACh or choline content of any of the brain areas examined. This dose of 2-CIAdo elicited significant reductions in the TRACh in both the hippocampus and frontal cortex, but not in the striatum. The extent of the TRACh reduction was 67 and 36% in hippocampus and cortex, respectively. This inhibition of TRACh elicited by 2-CIAdo was antagonized by pretreatment (i.c.v.) with theophylline (278 nmol), suggesting that an activation of adenosine receptors is operative in the action of 2-CIAdo. Further support for a participation of adenosine receptors in the action of 2-CIAdo was obtained by comparing the effects of the L- and D-isomers of phenylisopropyladenosine (PIA) on TRACh. The i.c.v. administration of L-PIA (65 nmol) elicited a 79% reduction in the TRACh in the hippocampus, whereas D-PIA (65 nmol i.c.v.) had no significant effect on hippocampal TRACh. This finding supports the view that these effects on TRACh may be mediated by adenosine A1 receptors, but not by A2 receptors, because the former, but not the latter, display marked stereoselectivity toward PIA. It also was demonstrated that intraseptal injections of L-PIA or theophylline failed to reduce the TRACh in the hippocampus, suggesting that adenosine receptors located in the septum are not operative in mediating the i.c.v. action of PIA.

2-Chloroadenosine↗