PubMed · 4973321
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
D G Kline, B R DeJonge. 1968. Evoked potentials to evaluate peripheral nerve injuries.. https://pubmed.ncbi.nlm.nih.gov/4973321/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
The effects of galanin (GAL) on magnocellular neurosecretory cells (MNCs) were examined during microelectrode recordings from supraoptic neurons in superfused hypothalamic explants. Application of the full-length peptide (GAL1-29) or of the N-terminal fragment GAL1-16 produced reversible membrane hyperpolarization with an IC50 near 10 nM. These effects were associated with an increase of membrane conductance, with a reversal potential near -70 mV, and were not blocked by tetrodotoxin, indicating that the receptors mediating these effects are located postsynaptically. Hyperpolarizing responses were also observed in response to the GAL-like chimeric ligands M35 and M40, suggesting that these behave as partial agonists at galanin receptors. The reversal potential of the GAL-mediated effect was unaffected by reducing extracellular chloride or by intracellular chloride injection, indicating that the effects of galanin are not mediated by modulation of chloride conductances. In contrast, reducing the external concentration of potassium ions from 3 to 1 mM shifted the reversal potential of the responses to -85 mV, suggesting the involvement of a potassium conductance. When tested on spontaneously active MNCs, the hyperpolarizing effects of galanin were associated with a suppression of firing in both continuously active and phasically active neurons. Inhibition of phasic bursts was mediated both through the inhibitory effects of the hyperpolarization and through a GAL-mediated inhibition of the depolarizing afterpotential that is responsible for the production of individual bursts. These results suggest that galanin may be a potent endogenous modulator of firing pattern in hypothalamic neuroendocrine cells.
A series of related new models for the local dynamics of cardiac tissue is introduced. The models are based on a simple memory-like quantity that is used to determine the relationship among the durations and amplitudes of the stimulated action potentials. The first of these models produces period-doubling and chaos, consistent with constant pacing experiments, when standard restitution dynamics would predict stability of the primary 1:1 pattern. Analysis of the associated one-dimensional map suggests how various physiological parameters affect the period-doubling sequence. Many of these relationships have been observed in experiments. The remaining models extend the formalism of the first to account for the Hopf bifurcation of 2:2 patterns observed in experiments. One of these models reproduces the bifurcation sequence, 1:1, 2:2, Hopf bifurcation of 2:2, 2:2 and 2:1 seen in experiments as the pacing interval is decreased. The models clarify the dynamics involved in determining the amplitudes and durations of successive action potentials. Results from these models together with comparison with the experiment strongly suggest that quantities with time constants of the order of 50 and 400 ms exist and affect action potential formation in heart tissue.
Detailed information regarding the contribution of individual gamma-aminobutyric acid (GABA)-containing inhibitory neurons to the overall synaptic activity of single postsynaptic cells is essential to our understanding of fundamental elements of synaptic integration and operation of neuronal circuits. For example, GABA-containing cells in the thalamic reticular nucleus (nRt) provide major inhibitory innervation of thalamic relay nuclei that is critical to thalamocortical rhythm generation. To investigate the contribution of individual nRt neurons to the strength of this internuclear inhibition, we obtained whole-cell recordings of unitary inhibitory postsynaptic currents (IPSCs) evoked in ventrobasal thalamocortical (VB) neurons by stimulation of single nRt cells in rat thalamic slices, in conjunction with intracellular biocytin labeling. Two types of monosynaptic IPSCs could be distinguished. "Weak" inhibitory connections were characterized by a significant number of postsynaptic failures in response to presynaptic nRt action potentials and relatively small IPSCs. In contrast, "strong" inhibition was characterized by the absence of postsynaptic failures and significantly larger unitary IPSCs. By using miniature IPSC amplitudes to infer quantal size, we estimated that unitary IPSCs associated with weak inhibition resulted from activation of 1-3 release sites, whereas stronger inhibition would require simultaneous activation of 5-70 release sites. The inhibitory strengths were positively correlated with the density of axonal swellings of the presynaptic nRt neurons, an indicator that characterizes different nRt axonal arborization patterns. These results demonstrate that there is a heterogeneity of inhibitory interactions between nRt and VB neurons, and that variations in gross morphological features of axonal arbors in the central nervous system can be associated with significant differences in postsynaptic response characteristics.