Pain at the Slaughterhouse in Ruminants with a Focus on the Neurobiology of Sensitisation

Abstract

We pose, based on a neurobiological examination, that events that occur around the time of slaughter have the potential to intensify the pain response, through the processes of sensitisation and enhanced transmission. Sensitisation, or an enhanced response to painful stimuli, is a well-discussed phenomenon in the human medical literature, which can arise from previous injury to an area, inflammatory reactions, or previous overstimulation of the stress axes. A number of events that occur prior to arrival at, or in the slaughterhouse, may lead to presence of these factors. This includes previous on-farm pathology, injuries arising from transport and handling and lack of habituation to humans. Whilst there is limited evidence of a direct effect of these on the processes of sensitisation in animals at slaughter, by analogy with the human neurobiology literature the connection seems plausible. In this review a neurobiological approach is taken to discuss this hypothesis in the light of basic science, and extrapolations from existing literature on the slaughter of ruminants. To confirm the postulated link between events at slaughter, and processes of hypersensitisation, further dedicated study is required.

Keywords: Halal; Kosher; Shechita; abattoir; animal welfare; cattle; pain; river buffalo; sensitisation; stunning.

Figure 1

Schematic representation of nociceptor stimulation in response to a harmful stimulus produced by an electric drive. The first stage of transduction occurs when the harmful stimulus created by the electric drive activates nociceptors and is converted to an electrical impulse. The second stage is transmission, where the information is channelled through two primary efferent nociceptive neurons; the C-fibres (or C-polymodal nociceptors) and A-delta fibres [18]. Attenuation of the response occurs in the dorsal horn of the spinal cord and is called modulation. Finally, processing and integration of the response occurs so pain is perceived. N-Methyl-D-aspartate receptor (NMDA), and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA).

Figure 2

Peripheral and central sensitisation processes. After tissue injury, multiple chemical mediators (e.g., interleukin (IL), histamine (HI), H⁺, K⁺, bradykinin (BK), prostaglandin (PG), cold, heat, adenosine triphosphate (ATP), nerve growth factor (NGF), serotonin (5-HT), tumour necrosis factor (TNFα) and calcitonin gen related peptide (CGRP)), known as “sensitizing soup”, activate receptors in nociceptors (transient receptor potential cation channel (TRPV), acid-sensing ion channels (ASIC), G-protein-coupled receptors (GPCR), tropomyosin receptor kinase A (TrkA) and ion channel), increasing the ratio of action potentials that results in continuous depolarisation and increased sensitisation of peripheral pain receptors. When harmful stimuli reach second-order neurons in the dorsal horn of the spinal cord, excitatory substances like glutamate (GLU) and substance P (SP) are released by the nociceptors into secondary neurons. Activation of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR), N-Methyl-D-aspartate receptor (NMDAR), neurokinin-1 receptor (NK1R) and simultaneous changes increase intracellular Ca²⁺ concentrations, enhancing transmission and excitation, together with the so-called wind-up phenomenon after repeated activation of nociceptive fibres. Other mediators produced by glial cells (e.g., nitric oxide (NO), IL-1, IL-6, ATP, TNFα and brain-derived neurotrophic factor (BDNF)) contribute to the central sensitisation and amplification of responsiveness to painful sensations and the development of hyperalgesia to sensory inputs.

Figure 3

Schematic representation of the neurophysiological process of pain nociception in relation to the injured tissue and degree of trauma. Grade 1 trauma involves the skin, Grade 2 trauma has muscle involvement with the most severe (grade 3) trauma reflecting bone damage.

Figure 4

Indicators during slaughter caused by the absence, or poor application, of stunning. Visible indicators include vocalisations, movements of the ears, struggling, bristling, shaking, ocular and pupillary reflexes, the painful withdrawal stimulus, body posture, straightening reflexes, respiratory rhythm, the tongue position and the reflex reaction to a painful stimulus.