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D O Carpenter

Publications and source records attributed to D O Carpenter.

At least 181 records · Page 10Linked to original sources
PubMed1981

Fine structure and organization of the infrared receptor relay, the lateral descending nucleus of the trigeminal nerve in pit vipers.

The morphology of the nucleus of the lateral descending tract of V has been studied in species of two genera of pit vipers, cottonmouth moccasin (Agkistrodon piscivorus piscivorus), and rattlesnake (Crotalus ruber and Crotalus horridus horridus). The nucleus is the site of termination of primary afferent neurons forming the infrared receptors in the facial pits. It is located on the external surface of the common descending tract of V and contains somata that range in size from 7 to 22 micrometer in A. p. piscivorus and 7 to 27 micrometer in C. ruber. Electron microscopy reveals that the lateral descending tract contains both A delta and C fibers. Degeneration experiments indicate that the A delta fibers are primary afferents. The source of the C fibers is unknown. The lateral descending nucleus in both the cottonmouth and rattlesnake is fundamentally similar in organization. Afferent terminals containing clear spherical vesicles make synaptic contact with dendritis processes within the main neuropil. These axon terminals are also postsynaptic to boutons containing pleomorphic vesicles and some large dense-core vesicles. The C fibers terminate in a neuropil at the margin of the lateral descending tract on small dendritic processes that appear to come from neurons within the nucleus. This neuropil is found external to the tract in the cottonmouth and internal to the tract in the rattlesnake. The terminals contain clear spherical vesicles and large dense-core vesicles. The singularity of input to this nucleus is apparently reflected in the morphology. This is discussed in relation to the subnucleus caudalis of the mammalian brainstem.

Afferent Pathways↗
PubMed1981

Cyclic AMP induces a voltage-dependent current in neurones of Aplysia californica.

A voltage-dependent inward current is elicited by intracellular application of cyclic AMP in some neurons of Aplysia. The current has a slow time course and is present only at potentials more depolarized than -30 mV. Two other methods of increasing cellular cyclic AMP (phosphodiesterase inhibitors and sodium fluoride activation of adenylate cyclase) also induce an inward current at depolarized potentials.

Animals↗
PubMed1981

Effects of furosemide on neural mechanisms in Aplysia.

The effects of furosemide on action potentials and responses to several neurotransmitters have been studied in the neurons of Aplysia. Furosemide (10(-7) and 10(-3) M) does not visibly affect the normal action potential in R15 neurons. However, when TTX (30 microM) is used to block the sodium component in R15, the remaining spike (presumably the calcium component) is increased in amplitude in the presence of furosemide. Furosemide also alters transmitter-induced conductances. Furosemide greatly reduces the amplitude and shifts, in a depolarizing direction, the reversal potential of chloride-dependent responses to gamma-aminobutyric acid (GABA) and acetylcholine (ACh). This suggests that furosemide both blocks the chloride channel and inhibits a chloride pump. ACh-induced sodium responses were also reduced by furosemide but to a lesser extent than chloride responses. The potassium response to ACh and a voltage-dependent calcium response to serotonin were not altered. These results indicate that furosemide could alter synaptic responses both presynaptically by enhancement of calcium flux during the action potential and postsynaptically by blockade of chloride and sodium conductances.

Acetylcholine↗
PubMed1981

Biphasic responses to acetylcholine in mammalian reticulospinal neurons.

Acetylcholine (ACh) responses were elicited by ionophoresis from neurons, located in the medial pontine reticular formation, which were antidromically identified as having axons projecting in the reticulospinal tracts. Most neurons were silent at rest and could be caused to discharge at a regular, slow rate by a constant application of glutamate. ACh altered this slow rate of firing in 28 of 29 cells but showed three different patterns of effect: approximately one-third were excited, one-third were inhibited, and one-third showed biphasic inhibition-excitation. The ACh responses were not sensitive to atropine. These observations suggest that reticulospinal neurons have ACh receptors mediating both inhibition and excitation, perhaps located on different portions of the same neuron.

Acetylcholine↗
PubMed1981

Lateral olfactory tract transmitter: glutamate, aspartate, or neither?

Aspartate and glutamate are the principal candidates for the excitatory neurotransmitter released by the lateral olfactory tract (LOT) in prepyriform cortex of the rat. Identity of action of the natural transmitter with exogenous glutamate and/or aspartate, however, has not yet been demonstrated. We show that bath-applied 2-amino-4-phosphonobutyric acid, a presumed specific glutamate antagonist, blocks LOT-stimulated prepyriform field potentials and single unit activity but not the single unit response to ionophoretically applied glutamate or aspartate in rat olfactory cortex slices. These results suggest that neither aspartate nor glutamate is the LOT transmitter. Responses to ionophoretically applied N-methyl-DL-aspartate, kainic acid, and DL-homocysteate were clearly decreased by 2-amino-4-phosphonobutyric acid. This suggests that these agents, usually presumed to be aspartate or glutamate agonists, act at different receptors than aspartate and glutamate.

Aminobutyrates↗
PubMed1980

Thyrotropin-releasing hormone has multiple actions in cortex.

The responses to application of TRH were examined on 38 identified neurons in sensory motor cortex of cat. Two pyramidal tract (PT) and 3 nonpyramidal tract (NPT) neurons were directly excited by TRH. Two other NPT neurons were inhibited by TRH. TRH potentiated the excitatory action of ACh on 4 of 12 PT neurons and 1 of 2 unidentified cells. None of these neurons showed a direct effect of TRH. TRH did not potentiate the response to Glu on 12 cells tested, even when the same cell showed TRH modulation of the ACh response. None of the NPT cells examined showed TRH modulation of the excitatory ACh response. These results demonstrate that TRH has multiple actions in mammalian cerebral cortex, but that these actions, such as the modulation of the ACh responses, appear to exist on discrete populations of neurons.

Acetylcholine↗
PubMed1980

Choroidal blood flow as a heat dissipating mechanism in the macula.

We studied the possible role of the choroidal circulation in stabilizing the temperature environment of the retina and the retinal pigment epithelium. Temperature measurements were taken from the retina and choroid of the monkey eye while the ambient illumination and choroidal blood flow were varied. The results showed that the choroidal circulation plays a significant role in dissipating heat generated by the focusing of light at the macula and suggest that this function may be a primary reason for the relatively high values of choroidal blood flow.

Animals↗
PubMed1979

Neurotransmitter receptors on gill muscle fibers and the gill peripheral nerve plexus in Aplysia.

Isolated pinnules of the gill of Aplysia contract when dopamine (DA) is perfused through the bath. The contraction is not blocked by high-Mg2+ seawater, and reflects excitatory receptors for DA on the smooth muscle cells of the gill. The pinnule often shows irregular, spontaneous contractions which are blocked by high-Mg2+ seawater and 30 mM CoCl2. These contractions reflect spontaneous activity of a peripheral nerve plexus. No other transmitter was found to be directly excitatory on the muscle fibers, although there are inhibitory receptors for serotonin (5-HT). Tactile stimulation of the pinnule evoked a two-component contractile reflex contraction due to activation of the peripheral nerve plexus. Acetylcholine, octopamine, and 5-HT but not several other transmitters depressed these responses, presumably due to inhibitory receptors on the neurons of the peripheral plexus.

Animals↗
PubMed1978

Receptors for gamma-aminobutyric acid (GABA) on Aplysia neurons.

Aplysia neurons show 5 different types of response (three excitatory and two inhibitory) to iontophoretic application of gamma-aminobutyric acid (GABA). Four of these are associated with a membrane conductance increase, but one is associated with a conductance decrease. The most common response is a fast hyperpolarization which reverses at about--58 mV and is sensitive to manipulation of external Cl- concentration, and thus is due to a specific increase in Cl- conductance. There is an infrequent, slower hyperpolarizing response which does not reverse above about--80 mV and is insensitive to external Cl-. This response appears to result from a conductance increase to K+. Two types of depolarizing responses are associated with conductance increases. These responses differ in their latency, duration and sensitivity to curare. The more frequent is relatively rapid (peak at 1-2 sec) and is depressed by curare at high concentrations. In other neurons, GABA causes a slower response, peaking at 6-10 sec, which is not curare-sensitive. Usually for both types of response, the voltage and conductance changes are completely abolished by perfusion with Na+-free seawater, and the responses cannot be reversed with depolarization. In other neurons such as L11, the response can be reversed with depolarization, and appears to result from a conductance increase to both Na+ and Cl-. In neuron R15, GABA causes a slow depolarizing response (peak at about 9 sec) which is associated with a decreased membrane conductance, probably to K+. The classical GABA antagonists, picrotoxin and bicuculline, block Cl- responses but no others, while the fast Na+ and Cl- responses are depressed by curare. Strychnine does not affect any GABA response. The multiplicity of GABA responses, the specificity of their organization and the fact that only some neurons have receptors for GABA, argue that GABA may have a role as a neurotransmitter in Aplysia. Furthermore, the existence of several types of excitatory GABA response suggests that GABA may function both as an inhibitory and excitatory neurotransmitter.

Acetylcholine↗
PubMed1978

A comparison of similar ionic responses to gamma-aminobutyric acid and acetylcholine.

1. Fast Na+-, Cl-, and K+-Conductance increase responses to gamma-aminobutyric acid (GABA) show times to peak similar to the comparable ionic responses to acetylcholine (ACh). 2. On some identified neurons, both putative transmitters elicit responses due to the same conductance change. For example, in cell R2 both substances cause an increase in Cl- conductance. Receptors for GABA and ACh on R2 do not cross desensitize and therefore are distinct. The ACh but not the GABA response is blocked by alpha-bungarotoxin and strychnine. 3. In R2 both responses reverse at -58 mV, and the Cl- ionophore (for both responses) appears to be partially permeant to propionate and isethionate, but impermeant to acetate, sulfate, and methylsulfate. 4. The Cl- responses but not the Na+ responses to both ACh and GABA are blocked by both picrotoxin and bicuculline, the classical GABA antagonists. 5. These results are compatible with the hypothesis that the ionophores associated with receptors to different neurotransmitters but mediating the same ionic conductance change have many common properties and may, in fact, be identical. Bicuculline and picrotoxin may be specific blockers of the Cl- ionophore, not the GABA receptor.

Acetylcholine↗
PubMed1978

Ionic mechanisms of pacemaker activity in cardiac Purkinje fibers.

Rhythmic activity in cardiac Purkinje fibers can be analyzed by using the voltage clamp technique to study pacemaker currents. In normally polarized preparations, pacemaker activity can be generated by two distinct ionic mechanisms. The standard pacemaker potential (phase 4 depolarization) involves a slow potassium current, IK2. Following action potential repolarization, the IK2 channels slowly deactivate and thus unmask a steady background inward current. The resulting net inward current causes the slow pacemaker depolarization. Epinephrine accelerates the diastolic depolarization by promoting more complete and more rapid deactivation of IK2 over the pacemaker range of potentials. The catecholamine acts rather selectively on the voltage dependence of the gating mechanism, without altering the basic character of the pacemaker process. The nature of the pacemaker depolarization is altered by intoxication with high concentrations of cardiac glycosides or aglycones. These compounds promote spontaneous impulses in Purkinje fibers by a mechanism that supersedes the ordinary IK2 pacemaker. The digitalis-induced depolarization is generated by a transient inward current that is either absent or very small in untreated preparations. The transient inward current is largely carried by sodium ions. Its unusual time course probably reflects an underlying subcellular event, the oscillatory release of calcium ions from intracellular stores.

Animals↗