Sites and mechanisms of action of lidocaine upon the isolated spinal cord of the frog.

نویسندگان

  • M Kuno
  • S Matsuura
چکیده

The sites of action of lidocaine on the responses evoked by stimulation of lateral column (LC) and dorsal root (DR) were studied in the isolated, intra-arterially perfused spinal cord of the bullfrog. When the ventral root volley produced by stimulation was abolished by lidocaine, the presynaptic focal potential was almost unchanged. Intracellular recordings from motoneurons clearly demonstrated a marked reduction in amplitude of the EPSPs before the block of conduction of presynaptic fibers and the block of invasion of the neuron soma by antidromic spike potential. At low concentrations of lidocaine, the EPSPs elicited by LC stimulation produced shortening in time to peak, slowing in the decay time, decrease in amplitude and smaller changes in the later EPSPs of a train than the earlier ones. From the observations, it was concluded that the low concentrations of lidocaine affected primarily synaptic transmission in the spinal cord. The possible mechanisms of action of lidocaine were discussed.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Compound Action Potential of Isolated Spinal Cord: A Biophysical Analysis to Address Activity of Individual Fibers Following Contusion Injury

Compound action potential (CAP) of spinal cord represents valuable properties of neural fibers including excitability, rate of myelination and membrane integrity. These properties are measured using amplitude, latency and area under curve of CAPs recorded from spinal cord. Here, the isolated spinal cord was set in a double sucrose gap (DSG) chamber and its response to intracellular stimulation ...

متن کامل

GABAergic system for Ptychodiscus brevis toxin-induced depression of synaptic transmission elicited in isolated spinal cord from neonatal rats

The involvement of inhibitory transmitters for Ptychodiscus brevis toxin (PbTx)-induced depression of spinal synaptic transmission in neonatal rats was investigated. Stimulation of a dorsal root evoked monosynaptic reflex (MSR) and polysynaptic reflex (PSR) potentials in the segmental ventral root. The PbTx depressed the reflexes in a concentration-dependent manner and this depression was block...

متن کامل

GABAergic system for Ptychodiscus brevis toxin-induced depression of synaptic transmission elicited in isolated spinal cord from neonatal rats

The involvement of inhibitory transmitters for Ptychodiscus brevis toxin (PbTx)-induced depression of spinal synaptic transmission in neonatal rats was investigated. Stimulation of a dorsal root evoked monosynaptic reflex (MSR) and polysynaptic reflex (PSR) potentials in the segmental ventral root. The PbTx depressed the reflexes in a concentration-dependent manner and this depression was block...

متن کامل

Intrathecal Amylin and Salmon Calcitonin Affect Formalin Induced c-Fos Expression in the Spinal Cord of Rats

Background: Amylin and Salmon Calcitonin belong to the calcitonin family of peptides and have high affinity binding sites in the rat spinal cord. The aim of this study was to characterize receptors for Amylin and Salmon Calcitonin functionally in the spinal cord of rats. We assessed the expression of c-Fos in response to intraplantar formalin in the lumbar regions of the spinal cord in consciou...

متن کامل

A Review of the Occurrence and Mechanisms of Induction of Osteoporosis Following Spinal Cord Injury

Introduction: Spinal cord injury (SCI) causes devastating injuries in patients. The main mechanisms of the pathogenesis of secondary injury include nerve degeneration, gliosis, and inflammation. Spinal cord injury induces a disorder or failure in several organs due to the vital role of the spinal cord in regulating bodily functions. Osteoporosis is a consequence of spinal cord injury that occur...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • Brain research

دوره 249 1  شماره 

صفحات  -

تاریخ انتشار 1982