Search PubMed⌕ Search

Biomedical subjects

G D Bittner

Publications and source records attributed to G D Bittner.

At least 73 records · Page 4Linked to original sources
PubMed1985

Quantal mechanism of long-term synaptic potentiation.

Intracellular recordings were used to demonstrate the occurrence and to analyze the microphysiology of long-term synaptic potentiation (LTP) in the crayfish opener neuromuscular synapse. Brief stimulation of the single excitor motor axon enhanced the amplitudes of subsequent postsynaptic potentials for several hours. Three methods of quantal analysis were used to evaluate the mechanism responsible for LTP. The results of all three methods supported predictions of the hypothesis that LTP results from a presynaptic mechanism that increases the average of neurotransmitter quanta evoked by nerve impulses in the excitor axon.

Animals↗
PubMed1981

Intracellular recordings from crustacean motor axons during presynaptic inhibition.

Action potentials intracellularly recorded from near the nerve terminals of the opener excitor motor axon in crayfish are reduced in amplitude during presynaptic inhibition. The amplitude and sign (hyperpolarizing or depolarizing) of presynaptic inhibitor potentials (PIPs) depends upon the relationship between the resting membrane potential of each excitor axon and its PIP equilibrium potential (which equals the equilibrium potential for gamma-aminobutyric acid).

Action Potentials↗
PubMed1981

Long term survival of enucleated segments of glial cytoplasm in the leech Macrobdella decora.

Enucleated cytoplasmic segments of the giant connective glial cell (GCGC) survive morphologically intact for at least 10 weeks in the leech Macrobdella decora. Enucleated GCGC segments isolated from regenerating nerve axons show some degenerative changes after 4 weeks compared to GCGC segments which surround intact or regenerating nerve axons. Survival of GCGC cytoplasm is associated with an increase in the number of microglia. Relatively few (10-30%) nerve axons degenerate after severance from their cell body.

Animals↗
PubMed1981

Morphology and number of neurons in two species of polychaetes.

Neurons of the ventral nerve cord (VNC) in the polychaete species Clymenella torquata and Nereis virens were ultrastructurally distinguished from glial cells by the smaller diameter and elongated shape of glial nuclei in adult organisms. In contrast to neurons, beta-glycogen-like particles and densely packed microfilaments were found in glial cytoplasm. Using these and other criteria, glial cells were distinguished from nerve cells in histologic preparations. All neuronal nuclei were counted in specified regions of the CNS of both polychaetes. In both species, the number of neuronal nuclei in various CNS regions remained constant in animals of very different body size. Since Clymenella has a set number of ganglia in the VNC and a set number of body segments, the total number of CNS neurons remains constant in adult members of this species. Since adult Nereis adds VNC ganglia in newly forming body segments, the total number of CNS neurons continuously increases, but the total number of CNS neurons in a ganglion does not change after it is formed.

Animals↗
PubMed1981

Regeneration of axons and nerve cell bodies in the CNS of annelids.

The neuron addition hypothesis predicts that species that add CNS neurons during a particular ontogenetic stage should regenerate ablated somata better than species that add few, if any, neurons to the CNS during that same stage. We report that CNS nerve cells do not regenerate in three species of adult (reproductively competent) leeches (Hirudo medicinalis, Haemopus grande, and Macrobdella decora), which do not increase the number of neurons in any portion of the CNS. Nereis virens, a polychaete that adds CNS neurons to newly forming ganglia in the adult stage, also does not regenerate CNS neurons. Conversely, CNS neurons, including a pair of uniquely identifiable somata, do regenerate in Clymenella torquata, a polychaete that has a constant number of neurons in the adult stage. Hence, the results of our study suggest that several versions of the neuron addition hypothesis cannot predict CNS regenerative abilities in adult annelids. Finally, we report that severed stumps of CNS axons do not degenerate rapidly in Nereis or Clymenella, and that both species can regenerate severed CNS axons presumably by morphologic fusion or physiologic activation of surviving stumps.

Animals↗
PubMed1981

An examination of the residual calcium theory for facilitation of transmitter release.

Computer simulations suggest that the simplest versions of the residual calcium model do not predict facilitation during trains of equal-interval stimuli at frog neuromuscular junctions or other synapses. Various modifications of the residual calcium model (e.g. continuous increase in number of active release sites or changes in calcium influx) could account for the observed data.

Animals↗
PubMed1981

Regeneration of motor axons in crayfish limbs: distal stump activation followed by synaptic reformation.

Severed distal stumps of limb motor axons in the crayfish Procambarus clarkii remain ultrastructurally intact for at least 2-3 ms after being severed from their cell body. Initial regeneration of a motor axon is associated with the appearance of up to 200 small profiles (satellite axons) having no glial sheath adjacent to the large surviving stump for about 1 cm distal to the lesion at 4-5 wks postoperatively. These satellite axons are seen 2-4 cm distally at the target muscles 3-4 ms postoperatively. By 14-15 ms postoperative, the motor sheaths from the lesion site to the target muscles contain small axonal processes having thick glial sheaths. Behavioral tests show that some axons that are reconnected to the CNS at 4-5 wks may not be connected at 14-15 ms, whereas other axons not connected by 3-4 ms may be connected at 14-15 ms when the original distal stumps have degenerated. We suggest that all these data can best be explained by the view that motor axons in crayfish limbs initially regenerate via activation of the surviving distal stump by satellite axons which grow out from proximal stump. In most cases, these satellite axons continue to activate the surviving distal stump as they slowly grow to the target muscle. Eventually the satellite axons reform synapses on the target muscle and the original distal stump degenerates.

Animals↗
PubMed1980

Ultrastructural studies of severed medial giant and other CNS axons in crayfish.

The distal stumps of severed medial giant axons (MGAs) and of nongiant axons (NGAs) in the CNS of the crayfish Procambarus clarkii show long-term (5--9 months) survival associated with disorientation of mitochondria and thickening of the glial sheath. However, the morphological responses of the two axonal types differ in that neither the proximal nor the distal stump of severed MGAs ever fills with mitochondria as is observed in some severed NGAs. Furthermore, the adaxonal glial layer never completely encircles portions of MGA axoplasm as occurs in many severed NGAs; in fact, ultrastructural changes in the adaxonal layer around severed MGAs are often difficult to detect. No multiple axonal profiles are ever seen within the glial sheath of the proximal or distal stumps of severed MGAs whereas these structures are easily located within severed NGAs.

Animals↗
PubMed1980

Ultrastructural changes at gap junctions between lesioned crayfish axons.

In crayfish, the severed distal segment of single lateral giant axon (SLGA) often survives for at least 10 months after lesioning if this segme;t retains a septal region of apposition with an adjacent, intact SLGA. In control (unsevered) SLGAs, this septal usually contains gap junctions and 50-60 nm vesicles near the axolemma of both SLGAs. From 1-14 days after lesioning, the distal segment of a severed SLGA undergoes obvious ultrastructural changes in mitochondria and neurotubular organization compared to control SLGAs or to adjacent, intact SLGAs in the same animal. Gap junctions are very difficult to locate in severed SLGAs within 24 h after lesioning. From two weeks to ten months after lesioning, the surviving stumps of severed SLGAs often appear remarkably normal except that structures normally associated with the presence of gap junctions remain very difficult to find. These and other data suggest that SLGA distal segments receive trophic support from adjacent, intact SLGAs. The mechanism of this support probably could not be via diffusion across gap junctions between intact and severed SLGAs since gap junctions largely disappear after lesioning. However, trophic maintenance could occur via the exocytotic - pinocytotic action of 50-60 nm vesicles which are always present on both sides of the septum between an intact SLGA and a severed SLGA distal segment.

Animals↗
PubMed1978

Histological studies of trophic dependencies in crayfish giant axons.

Medial giant (MGA) and lateral giant (LGA) axons of crayfish were doubly cut in order to selectively isolate axonal segments from perikaryal and transsynaptic sources of trophic input. Isolated MGA segments remained morphologically intact for over 43 days, whereas isolated LGA segments usually degenerated within one week. The glial sheaths around isolated MGA segments had significantly increased in thickness within one week, but severed LGA segments showed no increase in sheath thickness at any time after lesioning. These data suggest that cells of the surrounding glial sheath can provide trophic support to isolated MGA segments but not to isolated LGA segments. Extent of glial hypertrophy seems dependent upon specific spatiotemporal parameters. The diameters of isolated MGA segments decreased more rapidly than the diameters of singly cut MGA segments. These data suggest that the MGA also receives some trophic support from pre- or postsynaptic sources. Conversely, some singly cut LGA segments completely degenerated within one week, whereas other singly cut LGA segments remained intact for at least 43 days after lesioning. Such results suggest that the LGA receives a significant trophic input from pre- or postsynaptic structures.

Animals↗
PubMed1978

Biochemical studies of trophic dependences in crayfish giant axons.

Data from previous histological studies indicate that long-term survival of crayfish medial giant axons might be due in part to trophic support from cells of the surrounding glial sheath which often hypertrophy in response to transection of the medial giants. The biochemical studies reported herein show that segments from transected ventral nerve cords (VNC) always incorporate more [3H]leucine into protein than do corresponding segments from intact VNCs. Furthermore, the relative amount of [3H]leucine incorporation in severed segments seems to be influenced by distance and direction from the lesion site as well as time after lesioning. Similar spatiotemporal parameters were previously shown to be correlated with extent of glial hypertrophy around severed medial giant axons. Quantitative autoradiography of medial giant axons after incubation in [3H]leucine revealed that the grain density of label in glial sheaths surrounding severed medial giants was over two-fold greater than in sheaths around corresponding control axons. Moreover, the grain density in the axoplasm of severed medial giants was nearly four-fold greater than the grain density in the axoplasm of control axons. Data from experiments using short or long labeling intervals suggests that labeling in the medial giant axoplasm may be due more to transfer from glial sheath cells than from inherent axonal synthetic mechanisms. In light of this and other data, we concluded that long-term survival of severed medial giant axons is probably due to the direct transfer of trophic substances from cells of the glial sheath into the axon.

Animals↗
PubMed1978

Developmental abnormalities of identifiable neurons in the crayfish Procambarus simulans.

We report anomalies of lateral giant neurons in field-caught animals. In one case, both lateral giant neurons arising from the fifth abdominal ganglion did not terminate in the next-most anterior ganglion, but rather continued to the third abdominal ganglion. In another case, an additional large neuron arising in the fifth abdominal ganglion coursed in a posterior direction. All othe CNS structures appeared normal in animals having either anomaly.

Animals↗