PubMed Health⌕ Search

Biomedical subjects

G A Cottrell

Publications and source records attributed to G A Cottrell.

At least 19 recordsLinked to original sources
PubMed1992

Effects of intracerebral quinpirole on locomotion in rats.

The effects of the dopamine D2 receptor agonist quinpirole (LY 171555) on locomotor activity and margin time (thigmotaxis or wall-hugging) were measured for 2 h in rats injected either s.c. (vehicle, 0.02, 2.0 mg/kg) or directly into either the dorsal striatum or nucleus accumbens (vehicle, 0.1, 1.0, 10, 20 or 40 micrograms bilaterally in each site). In all groups, margin time decreased as drug dose increased. As in previous research, quinpirole given s.c. decreased locomotor activity at a low dose and had a biphasic effect on locomotor activity at the high dose. Both of these effects were also elicited by quinpirole injected directly into the dorsal striatum; 10 and 20 micrograms decreased locomotion immediately, while 40 micrograms led to both the immediate decrease and a later increase. In contrast, the lowest doses of quinpirole (0.1 and 1.0 microgram) injected into the nucleus accumbens led to an increase in locomotion from 20 to 60 min, while the higher doses led only to the early decrease. Thus, both the locomotor activating and inhibiting effects of quinpirole are found in both the nucleus accumbens and the dorsal striatum, but the differing dose-response relationships indicate that the mechanisms are not the same in these two brain regions.

Animals↗
PubMed1992

Potentiation of the dorsal immobility response following intrastriatal injections of enkephalins.

The effects of bilateral intrastriatal injections (1.0 microgram/side) of leucine5- and methionine5-enkephalins and their related nonopiate fragments upon three measures of immobility over a time course were investigated. Both leucine5-enkephalin and des-Tyr1-leucine-enkephalin potentiated the duration of the dorsal immobility response (DIR) 15 min postinjection and over a 1-h time course. On the other hand, methionine5-enkephalin and des-Tyr1-methionine-enkephalin potentiated the duration of the DIR at 5 and 15 min. These enkephalins and their fragments had no effect upon vertical cling and bar catalepsy. In a second study, an SC injection of 4 mg/kg naloxone 15 min prior to the central injections blocked the potentiation of the DIR effects of the enkephalins.

Animals↗
PubMed1992

Dopamine D1 antagonists potentiate the durations of bar and cling catalepsy and the dorsal immobility response in rats.

The effects of dopamine D1 antagonists SCH 23390 or SK&F 83566 (at SC doses of 0.00, 0.01, 0.05, and 0.1 mg/kg) were tested for 2 h on bar and cling catalepsy and the dorsal immobility response. Each of the drugs potentiated the duration of each of the three measures of immobility in a dose- and time-dependent manner. Each of the drugs had rapid but brief effects on all three response measures; the peak effect of SK&F 83566 took place at 20 min and that for SCH 23390 at 40 min for each behavior. At each effective drug dose, SCH 23390 had a greater effect than SK&F 83566 on each behavior. Dopamine D1 antagonists potentiated three different immobility responses, as do dopamine D2 antagonists.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1992

FMRFamide-related peptides potentiate transmission at the squid giant synapse.

The stellate ganglion of the squid Loligo pealli contains the neuropeptides Phe-Met-Arg-Phe-NH2 (FMRFamide), Phe-Leu-Arg-Phe-NH2 (FLRFamide) and at least one N-terminally extended FMRFamide-related peptide that is yet to be fully characterized. Both local application and arterial perfusion of FLRFamide potentiate transmission at the giant synapse. The N-terminally related peptide Ser-Asp-Pro-Phe-Leu-Arg-Phe-NH2 (SDPFLRFamide) produced a similar effect. The threshold for both the tetra- and the hepta-peptides was less than 10 microM. Potentiation could be detected as an increase in rate of rise of the EPSPs, as an increase in amplitude of the EPSP in the absence of spikes, or under voltage clamp as an increase in the EPSC. The effect was most pronounced when the synapse was fatigued by high frequency stimulation. Another molluscan peptide, eledoisin and also leucine enkephalin were without effect. In the absence of any detectable effects of FLRFamide on the resting membrane potential of either pre- or postsynaptic terminals or on the presynaptic spike, it is suggested that the peptide influences transmitter mobilization. However, the peptide could also exert small changes in preterminal calcium currents, which so far we have been unable to detect.

Animals↗
PubMed1992

Modulation of voltage-dependent calcium current in Helix aspersa buccal neurones by serotonin and protein kinase C activators.

In Helix aspersa, activation of the cerebral giant serotonin neurones (GSNs) evokes a biphasic, excitatory synaptic response in the M neurones of the buccal ganglia. Local application of serotonin to the current-clamped M neurones also evokes fast and slow depolarizing responses. The slow response is thought to be dependent on calcium ions, whereas sodium ions have been implicated in the fast response. Here we provide further evidence that the slow response results from an increase in conductance to calcium ions, and show that okadaic acid, an antagonist of protein phosphatases 1 and 2A, potentiates the effect of serotonin, suggesting that the response is phosphorylation dependent. Further, agents known to activate protein kinase C, such as 1-oleoyl-2-acetyl-rac-glycerol and active phorbol esters (but not an inactive one) were found to increase the calcium current (actually carried by barium ions) of the M neurones. Such data suggest that the slow synaptic response mediated by serotonin can occur by activation of protein kinase C and phosphorylation of the affected voltage-sensitive calcium channels, or some closely associated protein(s).

Animals↗
PubMed1990

The neuropeptide Phe-Met-Arg-Phe-NH2 (FMRFamide) can activate a ligand-gated ion channel in Helix neurones.

This report presents evidence that the molluscan neuropeptide FMRFamide can directly activate a ligand-gated ion channel in Helix neurones. Using the patch-clamp technique we have observed unitary currents activated by the application of FMRFamide onto outside-out patches. As for the whole-cell response, Na+ ions are the main charge carriers. We conclude that FMRFamide may act as a fast depolarizing neurotransmitter in the Helix nervous system.

Animals↗
PubMed1979

Ionic basis of different synaptic potentials mediated by an identified dopamine-containing neuron in Planorbis.

A specified dopamine neuron in Planorbis corneus produces dopamine-mediated e.p.s.ps, i.p.s.ps or biphasic, depolarizing-hyperpolarizing p.s.ps in different follower neurons. The excitatory potentials were of three types. Some follower neurons exhibited slow e.p.s.ps (ca 1 s), and a long-lasting, slowly desensitizing, depolarizing response to iontophoresed dopamine. Others showed rapid (ca. 150 ms) e.p.s.ps, often of variable amplitude, and a rapid, quickly desensitizing, response to iontophoresed dopamine. The rapid e.p.s.ps were sometimes followed by the inhibitory response (biphasic potential). The e.p.s.ps were potentiated by hyperpolarization and reduced by depolarization, though they could not be inverted. The slow e.p.s.p. was shown to be associated with an increase in membrane conductance, but it has proved difficult to elucidate the ions involved. A third type of e.p.s.p. was produced by electrical transmission. The inhibitory potentials were generally reduced in amplitude by artificial hyperpolarization but could rarely be inverted. This is probably due in part to the presence of of electrotonic coupling between these follower neurons. The i.p.s.ps were associated with an increase in conductance which appeared small when measured in the cell body. However, the i.p.s.ps produced considerable shunting of electrotonic transmission between coupled followers indicating a large increase in conductance at the synapse. I.p.s.ps were unaffected by Cl-free solution but they were greatly reduced, though rarely inverted, by increasing the external K concentration. They were blocked by intracellular tetraethylammonium, or cooling. The effects on corresponding responses to iontophoresed dopamine were in each case the same as on the i.p.s.ps. It is concluded that the i.p.s.ps mediated by the dopamine neuron are produced by an increase in permeability to K+. On a few occasions i.p.s.ps mediated by the dopamine neuron were potentiated by hyperpolarization. This appeared to be caused by a sharp increase in membrane resistance with hyperpolarization of these particular neurons. However, mediation by a mechanism of conductance decrease could not be completely excluded.

Animals↗
PubMed1978

Cellular accumulation of amines and amino acids in the central ganglia of a gastropod mollusc, Planorbis corneus: an autoradiographic study.

The distribution of radioactivity was examined autoradiographically in ganglia exposed to 10 different tritium-labelled compounds, some putative transmitters and the others transmitter precursors. The autoradiographic pattern was found to vary greatly for different substances, suggesting the presence of several different accumulating systems in the ganglia. Identified amine-containing neurons take up their own transmitter substance specifically. However, whereas uptake by dopamine-containing, and presumed histamine-containing neurons occurs over both perikarya and processes, in 5-HT-containing neurons it appears restricted to axon processes. The transmitter precursors L-DOPA and 5-hydroxytryptophan were taken up by the perikarya of both dopamine- and 5-HT-containing neurons, possibly by the same uptake system. In high concentrations, tyramine was selectively accumulated by cells containing dopamine and by non-dopamine (possibly octopamine- or tyramine-containing) neurons, but in low concentrations it labelled only the latter. GABA labelled a separate population of neurons and was particularly concentrated in their processes. Some, if not all, of the neurons specifically labelled after exposure to glutamic acid are neurosecretory cells. Tyrosine and glycine appeared to be accumulated in a non-specific manner and many of the substances were also accumulated by glial cells or by parts of the connective tissue capsule.

5-Hydroxytryptophan↗
PubMed1977

Effect of corticosteroids in the hippocampus on passive avoidance behavior in the rat.

The site of action of corticosteroids in avoidance learning was investigated in 110 rats. Injection of cycloheximide, 30 min before one-trial training on a passive avoidance task suppressed corticosteroid secretion in response to footshock, and produced an avoidance deficit in a test 6 days later. However, an additional injection of hydrocortisone, either subcutaneously or intra-hippocampally within 5 min of training, restored the avoidance response in the test. Septal and hypothalamic injections of the hormone were ineffective in reversing the cycloheximide effect, whereas the effect of hormone injection into the amygdala was equivocal because of an increased level of activity. Corticosteroids secreted following an aversive experience appear to act upon the steroid-sensitive neurons in the hippocampus to influence the animal's later performance of passive avoidance response.

Adrenal Cortex Hormones↗
PubMed1975

Excitatory, inhibitory and biphasic synaptic potentials mediated by an identified dopamine-containing neurone.

1. A giant dopamine-containing cell, situated in the left pedal ganglion of the water snail Planorbis corneus, was identified in isolated living preparations of the central nervous system. Spectrophotofluorimetric analysis confirms that the cell contains dopamine, whereas noradrenaline appears to be absent. The cell is unique in being a repeatedly identifiable dopamine-containing neurone. 2. Stimulation of the giant dopamine-containing cell resulted in excitatory, inhibitory or biphasic (depolarizing-hyperpolarizing) synaptic potentials in a number of follower neurones. The duration of the e.p.s.p.s and i.p.s.p.s was 0-3-5 sec; they ranged from barely detectable responses to ones 7 mV in amplitude in different cells. The depolarizing phase of a biphasic synaptic potential (b.p.s.p.) was usually less than 1 mV in amplitude (max. 3mV) and lasted 40-400 msec. The latency of i.p.s.p.s was long (70-120 msec) compared with that of e.p.s.p.s and b.p.s.p.s (20 msec). Abolition of the depolarizing phase of b.p.s.ps. by tubocurarine left a long-latency (70-120 msec) i.p.s.p. All responses showed summation and marked facilitation. 3. Evidence is presented that the post-synaptic potentials are produced by direct connections from the giant cell and result from a release of dopamine. Of eight putative transmitter substances tested on these different groups of neurones, only dopamine produced a potential change which in each case was of the same polarity as the post-synaptic potential when this was monophasic. However, generally applied dopamine produced only a hyperpolarization in follower cells showing b.p.s.p.s. This result is probably partly due to rapid desensitization of the receptors mediating the depolarization and also to a masking of the depolarization by the more effective hyperpolarizing response. 4. Erogometrine and 6-hydroxydopamine specifically antagonized the i.p.s.p.s and dopamine receptors mediating inhibition. Neither the e.p.s.p.s nor the excitatory dopamine response were blocked by high concentrations of hexamethonium. Hexamethonium was also ineffective in blocking the depolarizing phase of a b.p.s.p., which was, however, selectively eliminated by tubocurarine. 5. It is suggested that dopamine is the transmitter released from the giant cell and that it can mediate excitatory, inhibitory or biphasic responses in different follower neurones.

Acetylcholine↗