Bradykinin (BK) Research
Introduction
Migraine is a debilitating condition with symptoms ranging from head pain and visual disturbances to nausea and vomiting. Migraine aetiology is little understood, although the involvement of abnormal electrical activity in the trigeminal neurones and the release of Calcitonin Gene Related Peptide (CGRP) are probable. Bradykinin is known to elicit neurological changes through direct stimulation and also sensitisation of neurones, leading to action potentials and possible neurosecretion within the Dorsal Root Ganglia cells. These effects are similar to the events thought to underlie the development of migraine and hence experimental procedures have been undertaken to investigate the actions of bradykinin within trigeminal neurones. If bradykinin acts in a similar manner in this setting then it may be a strong research target for the further understanding and treatment of migraine.
The experiments used trigeminal neurones, which were classified to ensure consistency in results, and their electrophysiological responses were tested before and after the administration of bradykinin. Once the action of BK was established the experiment aimed to narrow down the findings in order to identify the mechanisms by which it does so.
The research is split into a number of sections:
- Practical Methodology – This section outlines the practical steps taken throughout the experiment.
- Perforated Patch Clamp – This method was used throughout the experiment and this section provides some background information on the technique.
- Neuronal Classification – A number of measurements and observations were made of the neurones tested in order to classify them; the tests and results are outlined here.
- BK Effects – The initial research to establish the effects of BK are investigated and discussed in this section.
- BK Receptors – Once BK was found to have effects further experiments were undertaken to establish which receptor BK was eliciting its effects through.
- BK Mechanisms – BK is known to act through intracellular mechanisms and this was investigated in order to establish how BK establishes neuronal sensitisation and activation in trigeminal neurones.
